Alternative Ways to Treat Dementia

Super Memory Formula

After the harsh reality that the doctor had to face his son ending his life, he suffered a major irreversible memory loss disease. This caused him to fall into depression and depend on the drugs from the pharma which was devasting for his mental and physical health and on so many other levels. After countless hours of research and experimentation, he realized that the root of all problems of memory loss was an enzyme that eats away the memory cells when the person gets older. This makes the person forget their loved ones, family and friends as if they have never met them. In some cases, they even forget about their past experiences, if they had children, how they came to the place they are in right now and who they are in the first place. This was exactly what the doctor had in his future if he did not make a decision. But he did and met with great people who helped him find the cure. This was a groundbreaking study that no one wanted to believe or endorse because it would go against the large pharma industry. However, the information is in there to protect yourself and your loved ones from such a devastating experience. You only need to follow the link and you will be guided to get the information downloaded to your device and follow the all-natural ways to get rid of memory loss. More here...

Super Memory Formula Summary

Rating:

4.7 stars out of 14 votes

Contents: Ebook
Author: Dr. Michael Duckett
Official Website: supermemoryformula.com
Price: $77.00

Access Now

My Super Memory Formula Review

Highly Recommended

The writer has done a thorough research even about the obscure and minor details related to the subject area. And also facts weren’t just dumped, but presented in an interesting manner.

Purchasing this ebook was one of the best decisions I have made, since it is worth every penny I invested on it. I highly recommend this to everyone out there.

Memory Loss Following Heart Surgery

We think that hypertension impairs memory by damaging tiny blood vessels that terminate in the brain's white matter, the bundles of axons that transmit messages throughout the brain and central nervous system. Lesions, or abnormalities, in white matter occur to some degree in virtually everyone older than age sixty and contribute to age-related memory loss. But people with hypertension have more extensive white matter damage than same-age peers with normal blood pressure. Research suggests that hypertension that is inadequately treated might also predispose you to dementia. There's an additive effect discharge from the hospital. Although the incidence of cognitive problems declined to 24 percent after six months, the authors surprisingly found an increase in problems at a five-year follow-up, with 42 percent of cases exhibiting deficits. In contrast, a German research group included a strong postoperative management approach to control vascular risk factors and found overall...

Aluminum and Alzheimers Disease

You might have heard that exposure to aluminum can cause Alzheimer's disease. Scientists have been studying this issue for many years, ever since finding that aluminum accumulates in the abnormal brain tissue of people with Alzheimer's disease. The evidence has been difficult to sort out, and many studies have offered contradictory findings. You can be exposed to aluminum in drinking water, in foods cooked in aluminum pots and pans, and possibly in foods and beverages packaged in aluminum. Some antiperspirants contain aluminum, which can be absorbed through the skin. But such environmental exposures tend to be extremely small. Although scientists continue to study the Alzheimer's-aluminum connection, most experts discount aluminum as a significant risk factor for the disease.

Memory Myth My Mother Had Alzheimers So Im Bound to Get It

Having a first- or second-degree relative (sibling, parent, aunt, uncle, grandparent) with Alzheimer's disease does not mean that you're destined to get it. Only the rarest form of Alzheimer's disease, the early-onset familial type, is unequivocally genetically transmitted. But even if your mother or another close relative had early-onset Alzheimer's disease, unless you carry one of the genetic mutations that cause it, your risk is no higher than that of someone without a family history of the disease.

Effect of Alzheimers Neuropathology on Communicative Function

By the end stage of the disease, memory loss is extensive, disorientation may extend to self as well as time and place, and problem-solving skills are minimal. Urinary and then fecal incontinence develop, and ultimately ambulatory ability is severely compromised or lost. Nonetheless, a few linguistic skills are intact (Bayles et al., 2000). Most individuals retain some functional vocabulary, although a small percentage are mute. Much of the language produced by those who still speak is nonsensical. Nonetheless, many patients can follow a one-stage command demonstrating comprehension of language. The majority can read a simple word. Many retain common social phrases such as ''I don't care'' and ''I don't know,'' and can contribute to a conversation.

Medications for Mild to Moderate Alzheimers Disease

All of the cholinesterase inhibitors are equally effective in temporarily stabilizing memory and other functions of people in the early to middle stage of Alzheimer's disease, although people's response is highly individual. People who aren't helped by one of the drugs might respond to one of the others. After using one of the cholinesterase inhibitors for several weeks, about half of patients are somewhat more alert and better able to care for themselves and engage in activities. The drugs may have other benefits, according to a 2003 report in the Journal of the American Medical Association. This review of twenty-nine studies found that cholinesterase inhibitors might also ease some of the psychiatric symptoms of Alzheimer's disease, such as depression, anxiety, hallucinations, and delusions.

Treatment for Moderate to Severe Alzheimers Disease

Memantine, either alone or in combination with one of the cholinesterase inhibitors, is used for patients with moderate to severe Alzheimer's disease. Research shows that memantine helps slow the progression of memory loss and other cognitive symptoms for a period of time. A study published in the Journal of the American Medical Association in 2004 compared a group of Alzheimer's disease patients taking donepezil plus memantine with another group, taking donepezil plus a placebo. People taking both medications for six months exhibited a significantly slower pace of decline in cognitive functions. A similar finding was reported with respect to activities of daily living, which refer to bathing, dressing, and other aspects of personal care. Although patients in both groups declined over the six-month study, the decline was steeper in the donepezil plus placebo group. Our clinical experience with memantine is similar to what we see with the cholinesterase inhibitors. Specifically,...

Drugs for Vascular Dementia or Mixed Dementia

Treatment of these types of dementia is two-pronged. First, we aim to prevent further injury to the brain by controlling vascular problems the root cause of vascular dementia and one of the causes of mixed dementia. This means managing hypertension, high cholesterol, and diabetes with a healthier diet, more exercise, and, if necessary, medications. Second, we treat symptoms of vascular dementia with the same medications that are approved for Alzheimer's disease. Clinical trials have found that galantamine, donepezil, and memantine bring about temporary improvements in memory and related cognitive domains, as well as in daily functioning in patients with vascular dementia.

Alternative Remedies for Memory Loss

If medications for Alzheimer's disease can improve memory and related cognitive function in people with the disorder, can they confer the same benefits to people with normal memory The answer is, maybe. A 2001 study compared the performance of a small cohort of commercial airline pilots who took donepezil for one month with those who took a placebo. The pilots who took the Alzheimer's disease drug performed better on difficult flight-simulation tasks. The researchers interpreted the results to mean that donepezil might have improved the pilots' procedural memory their retention and execution of complex skills. ple with Alzheimer's disease, although not for people with normal age-related memory loss.

Alzheimers disease and dementia

Alzheimer's disease (AD) is accompanied by a complex and distributed pattern of neuroanatomical change that is difficult to distinguish clinically from dynamic alterations in normal aging. Diagnosis of AD before death remains one of exclusion. Definitive diagnosis requires postmortem histological findings of diffuse neuronal and synaptic loss, accompanied by characteristic neuro- Although definitive diagnosis of AD requires direct observation of autopsy or biopsy specimens with characteristic neuropathological lesions, the National Institute of Neurological and Communicative Disorders and Stroke Alzheimer's Disease and Related Disorders Association (NINCDS-ARDRA) has defined criteria for probable AD (McKhann et al., 1984). These criteria include an acquired persistent decline involving at least three of the following cognitive domains language, memory, visuospatial skills, cognition, emotion, and personality. The accuracy of these criteria has been evaluated at autopsy and has been...

Cortical Circuitry and Alzheimers Disease

In the absence of AD, there does not appear to be a significant neuron loss in the entorhinal cortex in aged humans (Gomez-Isla et al., 1996 Hof et al., 2003 West, 1993), nor is there loss of neurons in the entorhinal cortex in aged monkeys (Gazzaley et al., 1997). However, a lack of quantifiable neuron loss does not necessarily mean that degenerative changes are not occurring in the entorhinal cortex as humans age. In fact, virtually all humans over the age of 55 have some NFTs in layer II of the entorhinal cortex (Bouras et al., 1994), making it difficult to distinguish qualitatively between age-related degenerative events in the entorhi-nal cortex that represent early progressive AD and those that are more stable. Many of the NFTs in this region in normal adults or patients with mild cognitive impairment (MCI) are ''transitional neurons,'' that is, neurons that are still intact and are included in an analysis of total neuron counts, yet have transitional intraneuronal pathology...

Alzheimers Disease And The Ubiquitinproteasome System

The first connections between the ubiquitin protein and Alzheimer's disease were made some years prior to the observations of van Leeuwen and his co-workers. In the late 1980s, two research groups independently noted that neurofibrillary tangles and plaque neurites stained intensely with antibodies against the ubiquitin protein6-8. The era of ubiquitin immunohistochemistry had begun. Therein followed significant activity in the field of ubiquitin and neurodegeneration, and it soon became clear that immunoreactivity to the ubiquitin protein was not limited to Alzheimer's disease. Inclusions in a range of other neurodegenerative disorders, including (but not limited to) Parkinson's disease, dementia with Lewy bodies, Pick's disease, amyotrophic lateral sclerosis, and Huntington's disease, were subsequently found to stain with antibodies to ubiquitin9-11. Outside of the nervous system, ubiquitin immunoreactivity was detected in mallory bodies in alcoholic liver disease, as well as...

Genetics of Alzheimers Disease

Moghaddam, B. and Bunney, B.S., Ionic composition of microdialysis perfusing solution alters the pharmacological responsiveness and basal outflow of striatal dopamine, J. Neurochem., 53, 652, 1989. 12. Perry, E.K., Kilford, L., Lees, A.J., Burn, D.J., and Perry, R.H., Increased Alzheimer pathology in Parkinson's disease related to antimuscarinic drugs, Ann. Neurol., 54, 235, 2003. 15. Tuszynski, M.H. and Blesch, A., Nerve growth factor from animal models of cholinergic neuronal degeneration to gene therapy in Alzheimer's disease, Prog. Brain. Res., 146, 441, 2004. 21. Hardy, J. and Selkoe, D.J., The amyloid hypothesis of Alzheimer's disease progress and problems on the road to therapeutics, Science, 297, 353, 2002. 22. Luo, Y., Bolon, B., Kahn, S., Bennett, B.D., Babu-Khan, S., Denis, P., Fan, W., Kha, H., Zhang, J., Gong, Y., Martin, L., Louis, J.C., Yan, Q., Richards, W.G., Citron, M., and Vassar, R., Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and...

Alzheimers Disease Dementia

Alzheimer's disease is a disorder that impairs the brain's intellectual functions (memory, orientation, and calculation). Memory gradually deteriorates, causing impaired judgment and other problems that affect a person's ability to perform normal daily activities. Alzheimer's disease is the most common cause of dementia, accounting for more than half of all cases in people age sixty-five and older. Alzheimer's disease and other forms of dementia may disrupt sleep regulation and other brain functions. Sleep is usually fragmented, with more awakenings and more time spent awake as the night progresses. Deep sleep is reduced, and REM sleep is less well organized. Wandering, disorientation, and agitation during the evening and night, a phenomenon known as sundowning, can require constant supervision and place great stress on caregivers. In such cases, benzodiazepine drugs or small doses of antipsychotic medications such as haloperidol (Haldol) and thioridazine (Mel-laril) are often...

Script Theory and Semantic Memory Loss

The data on semantic-autobiographical interactions point to limitations of cognitive models that represent concepts purely in terms of a static network of properties of words and objects. There are other facets of performance in semantic dementia patients that are not easily accommodated by traditional semantic memory models. One of our patients, L.B., was consistently unable to name a pair of glasses on confrontation. In comprehension tests he would comment, Glasses, what's glasses I don't know what that is. He could not match the spoken word with the real object or provide descriptive or gestural information. To all intents and purposes he had total loss of knowledge of the word glasses. Nevertheless, when intending to read or carry out close work he would remark I'll just go and get my glasses, would proceed to find his glasses and use them appropriately. Parallel findings have been reported in relation to object use. Objects that fail to be recognized in an artificial test setting...

New Learning in Semantic Dementia

If the medial temporal lobes have a role in new learning of semantic information, then it should be possible to demonstrate new learning in semantic dementia patients in whom medial temporal lobe function is preserved. In their daily lives, patients do show evidence of new learning (Snowden et al., 1996b). One patient, on moving house, had no difficulty in learning the names of new neighbours. Another patient had no difficulty learning to use an electric toaster for the first time, despite initial lack of recognition. A patient, reported by Graham et al. (1999b), was able to relearn lost vocabulary. Nevertheless, retention is unstable and information is lost without constant use and rehearsal. Patients retain information only so long as it is linked to ongoing daily experience.

Models Of Memory Disorders In Dementia

Alzheimer's Dementia A few models have specially addressed the issue of the progressive development of memory disorders in Alzheimer's disease. One example is the model by Ruppin & Reggia (1995 see also Carrie, 1993), who model memory performance during progressive Alzheimer's disease, using a model of the cortex in which synapses are gradually lost. At the same time a mechanism of synaptic compensation (Bertoni-Freddari et al., 1990 DeKosky & Scheff, 1990) causes the remaining synapses to increase their strengths (effectiveness), thus counteracting general loss of input excitation. In contrast to an earlier model by Carrie (1993), which showed a flat Ribot gradient, the model by Ruppin & Reggia (1995) is able to produce Ribot gradients, because remote memories benefit more from the synaptic compensation process than recent memories. This work constitutes an important contribution in that it presents and investigates yet another possible factor that may underlie Ribot...

Normal Aging or Dementia A Questionnaire

How do you know when memory loss is an early symptom of Alzheimer's disease or another type of dementia There's no question that severe, progressive memory loss is a hallmark of dementia, but recent research suggests that forgetfulness alone is not a perfect predictor of Alzheimer's disease. In an article published in the Archives of Neurology in 2000, researchers at Harvard Medical School found that responses to eight standard clinical questions predicted with a high degree of accuracy whether people with memory impairment would remain stable, decline, or improve. The eight questions were derived from three categories judgment and problem solving, home and hobbies, and personal care as follows

Cholinergic hypothesis of Alzheimers disease

The theory that there is a link between memory loss and the decrease in activity of choline acetyl-transferase (ChAT) in the brain of Alzheimer's patients. ChAT is a crucial ingredient in the chemical process that produces acetylcholine, a neurotransmitter linked to learning and memory. There has been a link between this change in neuro-chemical activity, changes in memory loss, and the physical appearance of Alzheimer brains (especially in the number of plaques). Researchers have found a loss of nerve cells in a part of the base of the brain called the nucleus basalis some patients with classical Alzheimer's disease have been shown to lose as many as 90 percent of these cells. The nucleus basalis is a major site of cholinergic neurons in the brain its projections reach a number of brain areas associated with learning and memory. cholinesterase inhibitors Medications designed to enhance memory and other cognitive functions by influencing certain chemical activities in the brain,...

Alzheimers Disease

Alzheimer's disease is undoubtedly and with good reason the most widely known neurological illness that causes memory loss. Alzheimer's disease is the leading cause of dementia, affecting an estimated four and a half million Americans at a cost of 100 billion per year, with the number of cases in the United States expected to reach between eleven and sixteen million by 2050. Alzheimer's disease causes substantial loss of neurons along with the appearance of characteristic pathological features in the brain amyloid plaques and neurofibrillary tangles. These plaques and tangles contain beta-amyloid, the sticky proteinaceous substance that is thought to be central to the Alzheimer's disease process. Early in the course of the disease, these features are concentrated in the hippocampus and cause the hallmark memory deficits. As 165 the disease progresses, most areas of the cortex become involved, and cognitive function becomes globally affected. You'll learn more about Alzheimer's disease...

Dementia

The most common cause of dementia is Alzheimer disease, which accounts for approximately 60 percent of cases. Alzheimer disease is a diagnosis of both inclusion and exclusion. Inclusion criteria are the gradual development of cognitive decline over months or years, impairments in memory, and at least one other cognitive dysfunction (i.e., aphasia, apraxia, or agnosia). The exclusion criterion is that other causes (e.g., cerebrovascular disease, Parkinson disease, major depression, hypothyroidism, pernicious anemia, subdural hematoma) have been ruled out. Cerebrovascular disease is the second most common cause of dementia and accounts for 10-20 percent of cases. Unfortunately, valid diagnostic criteria have not been well established, and even expert clinicians are wrong about 50 percent of the time when making this diagnosis. The physician should suspect vascular dementia when the history suggests that cognitive deficits began suddenly the physical examination identifies focal...

Vascular Dementia

Dementia can be produced by disease of the brain's vascular system, and the distribution of disease defines the nature of the neuropsychological deficits. However, the many possible variations in the nature and distribution of vascular disease make it impossible to specify a typical profile of neuropsychological deficits. For example, individuals with an infarct in the territory of the left posterior cerebral artery involving the temporo-occipital region might exhibit amnesia, whereas an individual with an infarcts in the left anterior cerebral artery involving the medial frontal region may have prominent executive dysfunction, with both nonetheless meeting the criteria for dementia. Similarly, individuals with cortical infarct differ from those with subcortical infarcts. Individuals at greatest risk for developing vascular dementia are those who have experienced one or more clinically evident ischemic strokes (Desmond et al., 1999). In fact, one-fourth to one-third develop dementia...

Mixed Dementia

Mixed dementia refers to a syndrome with underlying pathological features of both Alzheimer's disease and vascular dementia. The diagnosis is often made in someone with symptoms of dementia who has a personal history of vascular risk factors and a family history of Alzheimer's disease. The link between vascular dementia and Alzheimer's disease may be more than just a coincidence research suggests that vascular problems play a role in the development of Alzheimer's. A study published in the Archives of Neurology in 2003 found that adults who'd had strokes were at higher risk of developing Alzheimer's disease than people without a history of stroke. This finding added weight to an earlier, well-known National Institute ,131 on Aging-funded study involving 678 nuns that uncovered an association between strokes and Alzheimer's disease. The women who had had strokes plus plaque and tangle pathology were more likely to be diagnosed with Alzheimer's disease than women who had plaque and...

Pseudodementia

Scientists are also investigating the role of pKc in memory disorders such as Alzheimer's disease. one recent study at the university of california, San Diego found that the brains of 11 Alzheimer's victims contained only half as much pKc as the brains of seven people who had died of natural causes. pseudodementia A disorder that mimics dementia but that includes no evidence of brain dysfunction nearly one out of 10 of those thought to be suffering from true dementia in fact have a depressive illness. Unlike dementia, depression is treatable many people respond well to antidepressant drugs. Not surprisingly, pseudodementia is found most often in elderly patients.

Parkinsons Dementia

Parkinson's disease is associated with a loss of striatal dopaminergic neurons, particularly in the pars compacta region of the substantia nigra. Tremor is the best recognized symptom and is present in approximately half of individuals with PD (Martin et al., 1983). Often tremor begins unilaterally, increasing with stress and disappearing in sleep. Other early symptoms include aching, paresthesias, and numbness and tingling on one side of the body that ultimately spread to the other side. Other classic motor symptoms are rigidity, slowness of movement, and alterations in posture. Not all individuals with PD develop dementia, and prevalence estimates vary. Marttila and Rinne (1976), in one of the most comprehensive studies of prevalence, reported it to be 29 . Other investigators have reported similar estimates of dementia prevalence (Rajput and Rozdilsky, 1975 Mindham, Ahmed, and Clough, 1982 Huber, Shuttleworth, and Christy, 1989). Widely debated is the cause of the dementia, with...

Semantic Dementia

Semantic dementia might reasonably be regarded as the prototypical semantic memory disorder. It is a relatively rare clinical syndrome, resulting from focal degeneration of the temporal neocortex and associated with a non-Alzheimer pathology, in which there is a circumscribed and progressive loss of semantic knowledge. The name semantic dementia was introduced in 1989 to encapsulate the multimodal nature of the semantic disorder (Snowden et al., 1989). The designation has been adopted by others (Hodges, et al., 1992a Saffran & Schwartz, 1994) and criteria for the disorder have been outlined (Neary et al., 1998). Patients with selective semantic loss, described in seminal papers by Warrington (1975) and Schwartz et al. (1979), would now be regarded as examples of semantic dementia. Patients commonly present to medical attention complaining of problems in memory. However, in keeping with the fact that medial temporal lobe structures are relatively preserved, patients are not amnesic...

Contemporary Neuroscience

Highly Selective Neurotoxins Basic and Clinical Applications, edited by Richard M. Kostrzewa, 1998 Neuroinflammation Mechanisms and Management, edited by Paul L. Wood, 1998 Neuroprotective Signal Transduction, edited by Mark P. Mattson, 1998 Clinical Pharmacology of Cerebral Ischemia, edited by Gert J. Ter Horst and Jakob Korf, 1997 Molecular Mechanisms of Dementia, edited by Wilma Wasco and Rudolph E. Tanzi, 1997 Neurotransmitter Transporters

Why is a guide to the dentate gyrus necessary

Ohm discusses the diverse anatomical changes in the dentate gyrus that occur in Alzheimer's disease. Leyla DeToledo-Morrell, Travis Stoub, and Changsheng Wang review their studies of Alzheimer's disease, providing a persuasive argument that a major contributing factor is pathology that develops in the entorhinal area. Finally, Ed Dudek and Tom Sutula review a large and active area of research epileptogenesis in the dentate gyrus.

Hallucinations Illusions and Delusions

Hallucinations and delusions are rare among people living in the community, and their presence should lead the physician to consider disorders such as delirium, dementia, manic-depressive illness, schizophrenia, and drug abuse. Hallucinations are perceptions without stimuli and can occur in any sensory modality. Auditory and visual hallucinations are the most common types, and the physician can ask about them while reviewing the patients hearing and vision (e.g., Have you been hearing noises or voices that people who were with you couldn't hear Have you been seeing things with your eyes open that people who were with you couldn't see ). Remember that hallucinations are experienced as real perceptions, so questions such as Did you ever hear see feel something that wasn't there may not elicit an accurate response.

American Society for Stereotactic and Functional

Amnesia following an injury (such as a concussion) in areas of the brain concerned with memory function is known as traumatic amnesia. Degenerative disorders such as Alzheimer's disease or other types of dementia may also cause amnesia, as can infections such as encephalitis or a thiamine deficiency in alcoholics. Amnesia could also be caused by a brain tumor, a stroke or a subarachnoid hemorrhage, or certain types of mental illness for which there is no apparent physical damage.

Two Specialties For The Price Of

The average medical student does not know that a unique integrative career option exists becoming a physician trained in two specialties (Table 7-1). Any doctor can complete two separate residency programs and earn board certification in both disciplines. For example, a small subset of anesthesiologists, who have already completed 1 internship year of general medicine, also finish the 2 final years of internal medicine residency and become board certified in anesthesiol-ogy and internal medicine. Likewise, in other areas of medicine, different specialists take their own approaches to treating the same disease, such as the management of dementia by psychiatrists versus neurologists.

Proteasome And The Brain

The CNS is a highly complex system composed of both mitotic cells (astrocytes, microglia) and postmitotic cells (neurons). The functions of UPP in the CNS are not as defined as compared to other systems, such as the immune system. Studies in Alzheimer's disease (AD) and other age-related neurodegener-ative disorders have provided evidence that the function of the proteasome is impaired and may contribute to both neuropathology and neuron death (40-42). The dysfunction of the proteasome may also lead to the dysfunction of specific organelles including mitochondria, and potentially generate crosstalk with the lysosome system (15,43,44). Developing a better understanding of the protea-some system in the CNS is likely to aid in the development of therapeutic interventions for neurodegenerative disorders as well as normal brain aging.

Alveolar cell Cell of the air sac of the lung

Alzheimer's disease A presenile dementia characterized cellularly by the appearance of unusual helical protein filaments in nerve cells (neurofibrillary tangles) and by degeneration in cortical regions of brain, especially frontal and temporal lobes. See also senile plaques.

Memory Myth Once Brain Cells Die Theyre Gone for Good

This finding has transformed the way neuroscientists think about the aging brain and memory. We now believe that, in most cases, no matter how old you are, your brain is capable of producing new brain cells that have the potential to support pathways that enable you to form new memories. And if the brain is able to generate new neurons, there's hope that one day it may be possible to offset the damage and severe memory loss brought on by degenerative brain disorders, such as Alzheimer's disease.

Amyloid precursor protein app Individuals with

Alzheimer's disease are characterized by extensive accumulation of amyloid in the brain, referred to as senile plaques. These consist of a core of amyloid fibrils surrounded by dystrophic neurites. The principal component of the amyloid fibrils is B A4, a peptide derived from the larger APP. The specific role of amyloid protein is unclear but it is thought that amyloid deposits may cause neurons to degenerate. Amyloid deposits also occur in brains of older Down's syndrome patients. amyloidogenic glycoprotein A4 protein An integral membrane glycoprotein of the brain and related to the Drosophila vnd-gene product. A precursor of ( -amyloid that accumulates in Alzheimer's disease and Down's syndrome. See amyloid precursor protein.

Is Your Brain Shrinking

Only in the presence of memory disorders, such as Alzheimer's disease, does the brain suffer dramatic destruction and loss of neurons. Loss of neurons in the hippocampus and eventually other areas of the brain directly contributes to the pronounced difficulty with short-term memory that's typical of people with Alzheimer's disease.

Commonality of Aggregated Protein Conformations in Neurodegenerative Diseases

Many neurodegenerative diseases and to some extent physiological ageing are characterized by conformational changes and aggregation of specific proteins, resulting in intra or extra neuronal accumulation of amyloid fibrils. Mutations in such aggregate-prone proteins cause inherited forms of disease, as is the case in Alzheimer's, Parkinson's, Huntington's and prion diseases. A common feature of neurodegenerative disorders characterized by protein aggregation is that the aggregate-prone proteins, despite the fact that they are unrelated in size or amino-acid sequence, are detergent-insoluble, and have high P-sheet content and a cross beta structure. These common biochemical features suggest the possibility of a conserved mechanism of pathogenesis in these otherwise phenotypically diverse disorders. The commonality of such aggregate-prone proteins is further supported by the finding that a single antibody can recognize a common conformational epitope displayed by aggregated AP,...

Search for the Toxic Species The Protofibril Hypothesis

As the extracellular or intracellular deposits of neurodegeneration-related proteins are the obvious, dramatic hallmarks of the aggregation process, for a long time the idea had been that such end-products of the aggregation process or, at the very least, the fibrillar forms prior to their incorporation in the deposits, may be the toxic species (23). The possibility that oligomeric species and not the fibril itself could be pathogenic arose when oligomers rich in P-sheet structure termed protofibrils where found to be discrete intermediates in the fibrillization of AP and a-synuclein in vitro (24,25). A role for soluble oligomers in neurodegenerative diseases is further supported by the following observations there is no correlation between fibrillar deposits at autopsy and the clinical severity of Alzheimer's or Parkinson's disease (24), transgenic mouse models of these conditions have disease-like phenotypes before fibrillar deposits can be detected (25) and non-fibrillar AP...

Unconscious Influences and the Body

Freud's work began in neurology, and it became psychological because the clinical phenomena he confronted were incomprehensible with the medical knowledge of that time. Today, neurologists suggest that some of the clinical symptoms Freud observed do have a neurological basis. For example, consider traumatic memory loss. Traumatic experience, in Freud's theory, can cause repression of the traumatic events, so they are unavailable to memory. Neural imaging of the brain shows decreased functioning in the hippocampus and some other areas in people who have been exposed to combat stress and other traumas (Conway & Pleydell-Pearce, 2000).

What are the Targets of the Toxic Effects

Although the toxic oligomer hypothesis has gained considerable ground in recent years, it is not proven, and, as such, it is still possible that frank fibrils and deposits may also exert toxic effects. What could these effects be The major ideas have been that the inclusions either act as physical barriers to information flow in the cell, or that they sequester vital cellular components (23). Such vital components include the monomeric forms of the aggregation-prone proteins. There is more evidence to support this idea in the case of Huntington's Disease, where the depletion of Huntingtin in animal models has been shown to have dramatic consequences on neuronal viability (35). The idea of the physical barrier may make more sense when inclusions, or large aggregates on their way to develop into inclusions, occur at the level of the neuronal processes. Gunawardena et al. (36), demonstrated that in a fly model of Huntington's disease pathogenic polygluta-mine proteins exerted their toxic...

Causes of Memory Problems

His primary care physician referred him to me because he was concerned that he was developing Alzheimer's disease. He anxiously recounted, in minute detail, a half dozen instances of memory failure over the past few months, including a forgotten name, a missed appointment, and a wrong exit on the interstate. Like Michael, many patients with memory problems who come for evaluation discover that the cause is something that they never imagined could impair their ability to think and remember. Often, the cause is a common condition (such as depression) or a disorder that increases the risk of cerebrovascular disease and heart disease (such as poorly controlled high blood pressure or diabetes). Other causes of memory loss are hormonal changes that occur naturally during certain stages of life. For women, hormonal fluctuations following childbirth and around menopause can make them feel less sharp. Men also go through a phase of significant hormonal change as they age a...

Apraxia of Speech Nature and Phenomenology

Cent presented with a seizure disorder and 16 had a diagnosis of degenerative disease, including CreutzfeldtJakob disease and leukoencephalopathy (of the remaining, 9 were unspecified, 4 were associated with dementia, and 3 were associated with primary progressive aphasia). In 15 of cases the AOS was traumatically induced (12 neurosurgically and 3 concomitant with closed head injury), and in the remaining cases the cause was undetermined or was of mixed etiology. Without doubt, these proportions are influenced by the type of patients typically seen at the Mayo Clinic, and may not be representative of other patient care sites.

Chlorpromazine Trade name Thorazine A

Repeated studies of administering choline to treat the memory problems of Alzheimer's disease patients have resulted in conflicting evidence, although most found that giving choline was not helpful. Other studies suggest choline might be useful in heading off some deterioration in the early stages of the disease. Research suggests that levels of choline drop as a person ages and that levels are especially low in people with Alzheimer's disease.

Syndromes of Cognitive Impairment

Decline in cognitive performance can be subdivided into three broad categories delirium, dementia, and focal syndromes. In delirium, several areas of cognitive performance are deficient, but the distinguishing feature is an impairment in the level of consciousness. Level of consciousness refers to a patients alertness, attentiveness, and ability to concentrate. A delirious individual is inattentive and therefore has difficulty remaining focused on a topic during conversation. Patients with delirium are usually drowsy and slowed down in thought and movement. Less commonly (as in delirium tremens), they appear very alert, tense, and restless and are overreactive to stimuli such as sound, light, or touch. Delirium usually has an acute or sub-acute onset, developing over hours or days. It often fluctuates in severity during the course of the day and is usually worse at night. Unpleasant moods (e.g., bewilderment, fear, sadness) and visual illusions and hallucinations are common. 52 PETER...

Referral to Specialists

The primary care physician should consider referral to a neurologist, neu-ropsychiatrist, geriatric psychiatrist, or geriatrician when he or she suspects dementia and the patient is under 65, the neurologic examination suggests an uncommon syndrome, the history and physical examination are atypical, or management is complex because of coexisting medical and neurologic conditions. The physician should consider referral to a psychiatrist when a primary psychiatric disorder is a possible or likely cause of forget- Case Example A 68-year-old retired engineer reported to his physician at his annual examination that he was worried about his memory. He had mixed up the names of his grandchildren, missed an appointment to get his hair cut, and lost several strokes on his golf game. He continued to play bridge, however, to drive, and to do his taxes without problems. There was no change in appetite, sleep, or mood. Physical examination revealed no new abnormalities, mental status examination...

The Search for the HD Gene

To illustrate the challenge of genetic analysis in humans, consider the research quest for a malfunctioning gene responsible for Huntington disease (HD). This inherited malady was named after the young physician George Huntington who in 1872 eloquently described this wrenching condition. HD is a fatal neurological disorder whose symptoms, usually beginning in mid-life, involve uncontrollable movements of the body and progressive dementia. The disease smites nearly ten people in 100,000. In the United States alone, more than 25,000 patients suffer from HD, with about 125,000 more at risk by virtue of being siblings or children of the currently afflicted.

Creutzfeldt Jakob disease

Several common symptoms become evident in CJD patients as the disease runs its course. The duration of CJD from the onset of symptoms to the inevitable death is usually one year however, shorter periods of several months are common, and longer periods of two or more years have been noted, usually in the familial form and with an earlier age of onset. The initial stage of the disease can be subtle, with ambiguous symptoms of insomnia, depression, confusion, personality and behavioral changes, strange physical sensations, and problems with memory, coordination and sight. As the disease advances, the patient experiences a rapidly progressive dementia, and in most cases, involuntary and irregular jerking movements known as myoclonus. Problems with language, sight, muscular weakness, and coordination worsen. The patient may appear startled and become rigid. In the final stage of the disease, the patient loses all mental and physical functions. The patient may lapse into a coma and usually...

Creutzfeldt Jakob Disease Foundation

A new test is being developed to diagnose CJD by examining the cerebrospinal fluid. Additional tests proposed to confirm a diagnosis of CJD include identifying the presence of the deadly prion protein or identifying the prion gene mutation. The difficulties involved in diagnosing CJD may have prevented the identification of the disease in some cases. Because brain biopsy for diagnosing CJD is invasive, costly, and risky, it is often not performed. Moreover, some doctors may not even consider the possibility of a CJD diagnosis since the disease has been rare in the past, and the clinical symptoms of CJD can often be attributed to other ailments. Consequently, CJD may be mistaken for a variety of psychological illnesses and other neurological disorders such as Alzheimer's

The Treatment of Cognitive Symptoms

Cholinesterase inhibitors are the most effective psychopharmacologic agents for enhancing cognition in Alzheimer disease. Tacrine hydrochloride is used only for patients who had significant improvement when the drug was first released and still appear to be benefiting from it. Donepezil hydrochloride is as effective as tacrine but is less likely to cause the gastrointestinal side effects and liver toxicity associated with the latter drug. The initial dose of donepezil is 5 mg po qhs, with an increase to 10 mg po qhs after one month. In clinical studies 50-65 percent of patients have a favorable response. There are no data on whether it is useful to continue the drug with individuals who do not show cognitive or functional improvement, how long the drug should be prescribed, or whether cholinesterase inhibitors are effective in late-stage Alzheimer disease. At 10 mg qhs, the monthly cost of donepezil is approximately 120. Discontinuation studies suggest that some individuals...

The Treatment of Noncognitive Symptoms

Approximately two-thirds of patients with Alzheimer disease will experience a hallucination or delusion at some point in the illness. About 20 percent will have symptoms of major depression. Other common noncognitive symptoms include wandering, pacing, physical aggression, apathy, and sleep disturbance. The assessment of behavior disorder should include a careful evaluation of the environment and the patients medical status. Disordered behavior may be precipitated by newly occurring delirium and by caregivers who are unaware of the patient's specific cognitive deficits. An example of the latter cause is that patients with Alzheimer disease who are asked to perform a task with multiple stages may be unable to comprehend the request because they are aphasic or unable to do it because they are apractic. The frustration that arises from the communication disorder or apraxia may lead to disruptive behavior. In this instance, the most appropriate treatment would be to inform those caring...

Support and Treatment of the Caregiver

Demoralization and depression are present in 40-50 percent of caregivers of individuals with dementia. Some caregivers benefit from educational material or focused discussions on specific symptoms, treatments, and prognoses. Others may benefit from referral to support groups, such as those directed by the Alzheimer Association. (Local telephone numbers can be obtained by calling the Alzheimer Association at 1-800-272-3900.) Well-designed intervention trials demonstrate that a combination of emotional support and educational information benefit caregivers and that such programs can delay nursing home placement for the individuals they look after. When caregivers feel overwhelmed or demoralized despite such measures, the primary care physician should recommend counseling. If the dysphoric

Environmental Contaminants

The fishermen and their families living around Minamata City, in Japan noticed that their cats were ill and dying. They themselves also began to suffer strange symptoms memory loss, ataxic gait, restrictions in their visual field and hearing difficulties. Post-mortem of victims who succumbed showed damage to neurones in the cerebral cortex of the brain.

The Treatment of Focal Syndromes

The treatment of patients with isolated memory impairments (amnestic syndrome) includes searching for an etiology and ensuring safety. If alcohol abuse or thiamine deficiency is possible, the physician should prescribe thiamine, 100 mg im followed by 100 mg po qd. If alcohol abuse or thiamine deficiency is unlikely, cerebrovascular disease may be present and, if identified, should be treated appropriately. About 50 percent of patients who present with isolated memory impairment progress to a dementia syndrome within two years. Patients with aphasia should be referred for speech therapy. Otherwise, patients with focal syndromes should be treated using the general principles described under the treatment of dementia.

Cardiovascular and Neurodegenerative Diseases

Apart from cancer and infectious diseases, cardiovascular diseases cause the highest mortality in the Western world. The development of strategies for the prevention of those diseases is, therefore, of high priority. RNAi is currently used to elucidate the underlying mechanisms of cardiovascular diseases (230,240,241) however, therapy is still way out of reach. Likewise, the number of patients with neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, or amyotrophic lateral sclerosis is growing with the increasing life-span of humans. Many studies support the therapeutic potential of RNAi-based methods for the treatment of diseases like myotrophic lateral sclerosis (242-244). The search for possible candidate genes responsible for Alzheimer's disease (245-251) and Parkinson's disease (252-254) is proceeding at a rapid pace. However, delivery is even more a problem when the trespassing of the blood-brain barrier is involved.

Cytomegalovirus CMV disease

Cytomegalovirus encephalitis encephalitis caused by cytomegalovirus. Studies have shown that CMV encephalopathy is underdiagnosed. It frequently occurs unnoticed in persons with CMV retinitis. Symptoms include dementia, headache, confusion, and fever. The infection progresses rapidly, leading to death within weeks or months.

Enigmas Posed by Malevolent Genes

Many of the rarer inborn metabolic disorders are encoded by mutations not yet eliminated by natural selection, either because the mutations are partially camouflaged, or because their harmful effects are modest in relation to the rate at which the mutations arise. Camouflaging can occur in at least three ways. Alleles responsible for many genetic diseases, such as alkaptonuria, have deleterious consequences only in homozygous individuals. In heterozygotes, these alleles are shielded from natural selection's view because their poor metabolic performance is compensated by the normal allele. Also, many genetic disorders such as Alzheimer disease have postreproductive onset. Contemporary natural selection is blinkered from the scrutiny of genetic defects whose consequences are postponed beyond reproductive age because these defects normally fail to lower an individual's reproductive fitness. In a sense, senescence and death themselves are inborn genetic diseases, and an important...

Researching Druginduced Amnesia

Interest in the cholinergic system originally stemmed from observations of reduced cholinergic markers in post-mortem brains of people who had had Alzheimer's disease (AD), and by demonstrations that this reduction correlated with the degree of cognitive impairment and with cortical pathology (Perry et al., 1978). Around the same time, Drachman & Leavitt (1974) had shown that a drug that antagonizes or blocks the action of acetyl-choline could induce profound memory impairments in healthy young people. Together, this work led to the cholinergic hypothesis of AD (Bartus et al., 1982) and proposals that cholinergic blocking drugs could be pharmacological models of AD (Weingartner, 1985). Although several neurotransmitters are affected in AD (Curran & Kopelman, 1996), cholinergic depletion remains the most clearly documented neurochemical loss, and all drug treatments currently available for AD (e.g. tacrine, donepezil) are designed to ameliorate The degree of amnesia observed also...

Erasistratus of Chios

Estrogen and the brain A growing body of research suggests that the female hormone estrogen may play a protective role against memory loss and Alzheimer's disease and may also improve brain function. in fact, the sharp decrease in estrogen during menopause may be one reason why women are 50 percent more likely to contract Alzheimer's disease at midlife. While the research has not yet clearly proven the role of estrogen as a brain protector, one study of 2,418 women in southern California showed that those who took estrogen supplements after menopause were 40 percent less likely to have Alzheimer's. in this study, the higher the dose of estrogen, the lower the risk of Alzheimer's. in other studies of women over age 65, women who had taken estrogen supplements continuously since menopause had significantly higher scores of verbal memory than other women. regions associated with learning and memory (the basal FOREBRAIN, CEREBRAL CORTEX, and HIPPOCAMPUS) the areas most affected by...

Dideoxycytidine ddC See zalcitabine dideoxyinosine ddl See didanosine

People with HIV are usually advised to take a multiple vitamin-mineral supplement that supplies the basic level of nutrients most important to body function. Many nutritionists believe that additional supplements are necessary. Symptoms that may be related to nutrient deficiencies and may be reversible with appropriate supplementation include serious fatigue, memory loss or other cognitive dysfunction, skin problems, neuropathy, weight loss, loss of the senses of smell or taste, appetite loss, muscle pain or cramps, digestive problems, night blindness, canker sores, constipation, depression anxiety, menstrual cramps, and menopausal problems. Many other symptoms in people living with HIV may be related to nutrient deficiencies.

Federation for Children with Special Needs 107

Other symptoms of this disease include the inability to produce tears or feel pain, as well as poor reflexes and dementia. The lack of sleep leads to other problems, such as hallucinations and coma. There are four stages of the disease, beginning with a progressive insomnia that develops over about four months and includes a collection of psychiatric problems such as panic attacks and bizarre phobias. The second stage includes hallucinations, panic, agitation, and sweating, and lasts about five months. The third stage lasts about three months and involves total insomnia with weight loss. Individuals at this point look much older than they are and may experience incontinence. The fourth stage lasts about six months and is recognized as dementia with total insomnia it ends with sudden death.

Competence and the use of vulnerable groups in research

When an incompetent adult or a child clearly needs treatment, it is given without consent, and its moral justification is duty-based that is, it is in the patient's best interests that the treatment be given. If research is proposed involving incompetent subjects, the duty-based issue of best interests becomes the important deciding factor. In therapeutic research there is the equipoise test together with the consideration of whether the interests of the individual concerned would be best served by receiving treatment as a participant in a trial. Some would regard these criteria as sufficient to make it ethical to enrol an incompetent patient into a therapeutic trial. Others consider that any randomized controlled trial cannot, by definition, be said to be in each individual patient's best interests, since the treatment is not being tailored precisely to each individual. Non-therapeutic research on people who cannot consent is more difficult to justify, for non-therapeutic research...

Fluent aphasia See Wernickes aphasia fluid balance See thirst

Other scientists suggest that low levels of folic acid are closely tied to psychiatric symptoms in the elderly one study has found that elderly patients with mental disorders (especially DEMENtia) were three times more likely to have low folic acid than others their age. Among healthy aged people, those with low folic-acid intake scored lower on memory and abstract-thinking ability. Studies have also found that low daily doses of folic-acid supplements lifted mood and relieved depression.

Harsh Words High Stakes

Former first lady Nancy Reagan spoke out on the topic of stem cells in May 2004 at a star-studded dinner held by the Juvenile Diabetes Research Foundation in Los Angeles. She emphasized the need to de-politicize the debate over stem cell research, noting that the research held the potential to cure illnesses like Alzheimer's. Science has presented us with a hope called stem cell research, which may provide our scientists with many answers that for so long have been beyond our grasp, she said, I just don't see how we can turn our backs on this.

Laboratory Tests Ignored

A 75-year-old white female with a past medical history significant for hypertension, Alzheimer's disease, and chronic diarrhea presented to the emergency department (ED) with a complaint of 5 days of watery diarrhea (four to five stools per day), fever, and weakness. She reported that a week ago she had attended a funeral where she had some Lebanese food, and 4 days prior to arrival at the ED she began having loose bowel movements, some with bright red blood in them. The patient denied vomiting, but reported some nausea. The patient denied having shortness of breath or chest pain, but did admit to some diffuse abdominal pain associated with the diarrhea. She has had a fever of 100.9 F, generalized weakness, anorexia, and malaise, and her diarrhea has been sporadic over the past few months. This complaint had been extensively worked up in two previous admissions to the ED, but besides mild chronic inflammation seen on biopsy, no other cause for the symptoms was determined.

Refractory Epilepsy A Progressive Intractable but Preventable Condition

Summary The authors propose a hypothesis for the conceptual understanding and prevention of refractory epilepsy based on accumulated laboratory findings and an improved knowledge of the natural history of treated epilepsy. Refractory epilepsy can be recognized as a distinct condition with multifaceted dimensions, including neurobiochemical plastic changes, cognitive decline and psychosocial dysfunction, leading to dependent behavior and a restrictive lifestyle. The biological basis of refractoriness may be multifactorial, and may include the severity of the syndrome and or underlying neuropathology, abnormal reorganization of neuronal circuitry, alteration in neurotransmitter receptors, ion channelopathies, reactive autoimmunity, and impaired antiepileptic drug (AED) penetration to the seizure focus. Recurrent seizures may be the cause of some of these changes. The authors hypothesize that refractory epilepsy may be prevented by interrupting this self-perpetuating progression....

Memory Myth Alcohol Destroys Memory

Large amounts of alcohol are toxic to the brain, but small amounts appear to be beneficial. In recent studies, people who consumed alcohol in moderation had a reduced rate of Alzheimer's disease compared with people who did not drink at all. The exact mechanism of alcohol's beneficial effect is uncertain. One hypothesis is that alcohol reduces cardiovascular risk factors by altering blood lipids. Another hypothesis is that alcohol stimulates the release of the neurotransmitter acetylcholine in the hippocampus. Korsakoff's syndrome, a disorder marked by sudden, dramatic (and usually permanent) memory loss. Apart from Korsakoff's syndrome, other alcohol-related memory problems are potentially treatable and, in some cases, reversible. Cessation of drinking, maintenance of adequate nutrition, and replenishment of vitamin Bt, if necessary, are the keys to treatment of alcohol-related memory dysfunction.

Retrograde Vs Anterograde Amnesia

Most studies have found a poor correlation between scores on RA and AA tests. This has been found in Korsakoff patients (Shimamura & Squire, 1986 Kopelman, 1989, 1991 Parkin, 1991), a mixed group of amnesic patients (Mayes et al., 1994), and Alzheimer patients (Kopelman, 1989, 1991 Greene & Hodges, 1996). There is suggestive evidence that the correlation may be higher if equivalent forms of anterograde and retrograde tests are used (Mayes et al., 1997 Poliakoff & Meudell, 2000), but this has yet to be clearly established in large groups of amnesic patients.

Intellectual Stimulation

A well-educated brain can more effectively withstand age-related neuronal loss than a poorly educated brain. This added resiliency forms the basis for the concept of cognitive reserve, which is used to explain the finding that people with high baseline intelligence are less likely to be diagnosed with dementia than people with lower baseline intelligence.

Neuropsychology Of Tga During Attack

In addition to the complete incapacity to lay down new memories, patients are unable to recall memories which have been at their disposition before the attack. The degree of retrograde amnesia is variable and is more difficult to assess than that of anterograde amnesia as the patient's recall has to be compared with their own premorbid memories in order to estimate the severity of memory loss. There are two types of impaired access to previously acquired memories which are not mutually exclusive On the one hand, there may be a loss of any recollection for a limited period of time preceding the attack. Personal and public circumstances are believed to be as they had been before this period which may span up to several years (Case 1 Caffarra et al., 1981 Kritchevsky & Squire, 1989 Goldenberg et al., 1991 Kazui et al., 1996). On the other hand there can be a patchy memory loss which has no clear-cut temporal limit but may stretch back as far as some decades or even to childhood (Case...

Learning Disabilities Association of America A

Lecithin Called nature's nerve food, this is the major dietary source of choline, the brain chemical implicated as a possible aid to improving memory. Repeated studies of administering lecithin to treat the memory problems of Alzheimer's disease patients have resulted in conflicting evidence, although the majority found it was not helpful. other studies suggest it might be useful in heading off some deterioration in the early stages of the disease.

Singlecase Studies Of Recovery Of Memory Function

Since only a limited amount of formal cognitive testing was reported, however, this recovery profile needs to be treated with some caution. On the basis of their observations, Benson & Geschwind distinguished between three forms of remote memory loss that for over-learned knowledge and skills, as was manifest in their patient's aphasia that for more recently acquired information, such as memory loss for events that occurred in the previous few years and which they considered to be a primary retrieval deficit and memory loss for events in the preceding minutes and hours before a brain insult, which they regarded as representing a loss of memory consolidation. render TGA a particularly important neurological condition for the study of the evolution and resolution of pure amnesia. Furthermore, single case studies of TGA have the benefit of allowing patients to act as their own controls, which is particularly valuable when memory for public events or autobiographical episodes are...

Box 193 Clinical Trials Testing Of Potential New Treatments

FIGURE 19.7 Alex's pedigree may actually be showing us a family history of Huntington disease that no one realized was going on because the onset of the disease was so late that most affected individuals had simply been considered senile, including her brother and her father. Four of her father's siblings had been diagnosed with either senility or Alzheimer disease. One of her father's brothers has recently developed movement problems as he is approaching ninety years of age. Her sister also had not been diagnosed with Huntington disease, although she demonstrated fairly severe movement problems reminiscent of Huntington chorea. We have to wonder if the many cases of reported senility shown here represent a family history of undiagnosed Huntington disease in which the first symptoms were mental rather than physical. FIGURE 19.7 Alex's pedigree may actually be showing us a family history of Huntington disease that no one realized was going on because the onset of the disease was so...

Inflammation And Neurodegenerative Disorders

Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and amytrophic lateral sclerosis (ALS), found to be associated with the accumulation of ubiquitinated proteins in neuronal inclusions also exhibit signs of inflammation. For example, neurofibrillary tangle

Return To Alexs Story

While they were considering the list of possible diagnoses (called the differential diagnosis list), in addition to Alzheimer disease and several other things, Huntington disease was among the possibilities. Since there is a very simple genetic test for CAG repeat expansions in the Huntington disease gene, the doctors arranged to have a sample of Alex's DNA tested for a CAG repeat expansion in her copies of the HD gene. A very clear answer came back with the genetic testing results that told the doctors that Alex has Huntington disease because of the presence of the expanded CAG repeat.

Brain Imaging Studies Of Recovery Of Memory Function

A potentially important application of modern brain imaging procedures to the study of recovery of memory function also relates to functional activation studies of those patients who have recovered from an initially dense amnesia, or those who are left with selective memory loss as part of their neurological condition. Such studies may highlight those areas of the brain that act as neural compensatory mechanisms, and so offer clues as to the basis of recovery of function in brain disease. Very few such studies have yet been carried out, but one exception is that by Maguire (2001), in which a patient with developmental amnesia was found to show greater bilateral temporal lobe involvement during an autobiographical memory task compared to matched control participants.

HIV encephalopathy 225

HIV encephalopathy was formerly called AIDS dementia complex (ADC) and is still sometimes referred to as HIV encephalomyelopathy. HIV encephalopathy was relatively common in the late stages of HIV disease when HIV first appeared. In the past few years a decrease in the incidence of this illness has led medical doctors and researchers to believe that the protease inhibitors are to some extent crossing the blood-brain barrier and working to decrease this result of the virus.

Do You Need a Memory Evaluation

If you're concerned enough about your memory to wonder if something's wrong, you should see your doctor. Begin with a consultation with your primary care physician. Because this doctor knows you and your medical history, he or she is in an advantageous position to assess the big picture of your health and consider the more common medical and psychological conditions that can cause memory loss. Don't expect to walk out of your primary care physician's office with a diagnosis. There's no single test that can pinpoint the cause of memory loss. A more typical experience is for your doctor to do some preliminary detective work ask you questions about your symptoms, give you a thorough physical examination, review your medications, and run tests for medical conditions that can cause or contribute to memory loss. There is considerable variability among primary care physicians with regard to exper- 99. If your doctor tells you, You don't have Alzheimer's disease, so don't worry it's just...

Definition of Disease

Tertiary disease (or late disease) is the result of organism dissemination throughout the body. It can affect the brain, nerves, eyes, heart, liver, and joints, resulting in awkward muscle movements, paralysis, gradual blindness, and dementia.1 Neurosyphilis was once regarded as a phase of disease exclusive to this category of tertiary syphilis, but it has been shown that neurosyphilis can be present at any stage of the disease process. The diagnosis of the case presented above was secondary syphilis with concurrent neurosyphilis. As mentioned, neurosyphilis is no longer considered to be a distinct phase of disease. It is a manifestation of infection that can occur early with the appearance of the chancre, late in disease when blindness and dementia have set in, or at any point in between. Up to 10 of individuals with neurosyphilis will be asymptomatic, and symptomatology may be different depending on the stage of disease with which it is associated.1 The possible symptoms of...

Clinical Implications

Hippocampal neuronal loss in aging and Alzheimer's disease seems to be different, although some discrepancies exist between the findings of different researchers, perhaps due to interindividual variations in aging, the main site of neuronal loss is described as being either in CA1 and CA4 (Mani et al. 1986 West 1993) or restricted to CA1 and the subiculum (Simic et al. 1997). In Alzheimer's disease, although a lesion of the subiculum is always found, the occurrence of such damage in either CA1 (Bell and Ball 1981 Haigler et al. 1985 Doeb-ler et al. 1987 West 1993) or the gyrus dentatus (Si-mic 1997) is debated. Only the CA2 field seems to escape damage.

Neuropsychological Testing

The purpose of these tests is to determine if your memory and other cognitive abilities fall within normal limits or if the findings suggest a disorder such as depression, mild cognitive impairment, or Alzheimer's disease. But what's normal for you isn't necessarily normal for another person. The neuropsychologist will interpret and analyze the test results within the context of several important variables that influence memory and cognitive ability, such as your age, your estimated baseline intelligence, and your level of education. The distinction between normal and abnormal test performance may be different for a person with a high IQ and an extensive education than for a person with a lower IQ and fewer years of education. Research at Harvard Medical School published in 2004 looked specifically at the effect of IQ on the interpretation of memory test results in a group of highly intelligent elderly individuals. Instead of using general normative data, the researchers found that...

Learning How Patients Handle Illness

It's not just that I had cancer but so much more. I can't have kids. I had memory loss from chemotherapy. . . . What do I ask of my physician Be positive. Give me hope. One doctor said, There's a 50-50 chance and that's all I'd give you. My response was If you're going to focus on statistics, and not on me, I'll change doctors. Be honest. Tell me everything. Tell me over and over again. Tell me about side effects. If I know it's a possibility, I can deal with it later on. Tell me about support groups. Encourage people to go into support groups. If I ask for a second opinion, I'd rather not have my physician threatened by that. Give me a good joke My dadblamed himself because the cancer history was on his side of the family.

Structural Brain Imaging

Several diagnostic tests produce structural images of the brain. Magnetic resonance imaging (MRI), a high-resolution structural imaging technique, can show the shape, size, and contour of the brain. Each new generation of MRI scanners is more sensitive than the one before, and the newest ones can produce spectacular high-resolution images of the brain. Although brain atrophy can be quite subtle in the earliest stages of Alzheimer's disease, high-quality imaging can often reveal tissue loss in key brain structures, including the hippocampus.

Therapeutics Can You Cure Me

Unfortunately, there still remains no effective treatment for many extremely debilitating, and usually fatal, neurologic diseases. These include amyotrophic lateral sclerosis (Lou Gehrig's disease), muscular dystrophy, certain brain tumors, Alzheimer dementia, and Creutzfeldt-Jakob disease. Yet this is part of the reason why neurology is an exciting field for future physician-scientists. Because clinical research in these areas is extremely active, therapies for these diseases may exist by the time current medical students begin their residency training in neurology.

Layers of origin in the entorhinal cortex

In rat, mouse, or monkey, the ipsilateral projection to the dentate gyrus appears to arise mainly, if not exclusively from layer II of the entorhinal cortex (Steward and Scoville, 1976 Schwartz and Coleman, 1981 Ruth et al., 1982, 1988 Witter et al., 1989b van Groen et al., 2003 Chrobak and Amaral, 2006). In humans, fetal material indicates a similar origin (Hevner and Kinney, 1996). It is of interest to note that in the brain of Alzheimer patients, the entorhinal cortex layer II neurons are among the ones preferentially implicated in the disease, such that up to 50 of those neurons apparently disappear. This rather selective loss of layer II neurons has been associated with changes in the outer part of the molecular layer, such as a decrease in free glutamate and a decrease in markers associated with the perforant path, suggesting that in humans also the origin, and obviously termination, of the entorhinal-dentate projection is similar to that reported in other species (Hyman et al.,...

Functional Brain Imaging

If your structural imaging is normal but your doctor suspects that you might have Alzheimer's disease or another type of degenerative condition, he or she might also recommend a single photon emission computed tomography (SPECT) scan or a positron emission tomography (PET) scan. Rather than producing a picture of brain structure, these imaging techniques look at how the brain is functioning. SPECT traces perfusion (blood flow), and PET maps glucose metabolism. Decreased perfusion or energy metabolism in the temporal and parietal regions of the brain is the functional signature of Alzheimer's disease. Other brain disorders produce distinctive functional imaging patterns. These scans can reveal abnormalities even when an MRI appears normal.

Genetic Testing for Memory Impairment

Many of my patients think that having a genetic test for Alzheimer's disease will tell them whether they will get the disorder. But it won't at least not for most people. People with a family history of early-onset familial Alzheimer's disease can learn if they carry one of the genetic markers that convey a 100 percent probability of developing the disease. Inheriting a specific mutation in one of three genes presenilin 1, presenilin 2, and the amyloid precursor protein gene means that you will get the disease not having a mutation means that, despite your family history, your risk is no greater than for a person without the mutation.

Herpes Simplex Encephalitis

Whereas semantic dementia and Alzheimer's disease are progressive disorders arising from intrinsic changes in brain cells, herpes simplex encephalitis (HSE) is an acute, nonprogressive illness. The viral agent attacks principally the frontotemporal regions, and although about one-third of patients make a full recovery, others are left with permanent residual

Other Specialty Consultations

Because memory loss can have such a wide array of causes, the diagnostic process may require input from additional medical specialists. Your primary care physician might refer you to one or more of the following types of doctors to follow up on particular 112 findings from your initial checkup Some patients without a family history of early-onset Alzheimer's disease express a desire to have the ApoE test, which indicates the risk of developing the most common form of Alzheimer's disease but doesn't offer definitive information. I ask them How would knowing this information affect your view of yourself and your life Can you handle the information I'm also concerned about the possibility that some people might be denied employment, health insurance, or access to other resources if they test positive for an e4 allele, the variant of ApoE that conveys increased risk. The genetics of Alzheimer's disease and other memory disorders are a work in progress. Once we have true preventive...

Effects of Lewy Body Pathology on Communicative Function

Lewy bodies are spherical, intracytoplasmic neuronal inclusions that have a dense hyaline core and a halo of radiating filaments composed of proteins containing ubiquitin and associated enzymes (McKeith and O'Brien, 1999). They were first described in the literature by the German neuropathologist Friederich Lewy in 1912. Lewy bodies are classically associated with Parkinson's disease, particularly in the basal ganglia, brain-stem, and diencephalic nuclei. They may also be widespread in the cerebral cortex. Diffuse distribution of Lewy bodies is associated with dementia, and 10 -15 of cases of dementia (Cummings and Benson, 1992 McKeith et al., 1992) have this cause. Patients with LBD often have concomitant Alzheimer's pathology, and some have proposed that LBD is a variant of AD. However, there are cases of pure LBD, which argues for the theory that LBD is neuropathologically distinct (see Cercy and Bylsma, 1997, for a review). Like the dementia of AD, LB dementia has an insidious...

Other pharmacokineticpharmacodynamics considerations

6.2.2.5 Transport of peptides across the blood-brain barrier It has been increasingly recognized that peptides can cross the blood-brain barrier (BBB) as intact molecules. However, for the development of peptides as neuropharmaceuticals, BBB is still a formidable barrier, and strategies must be developed to overcome this barrier. Proteins such as nerve growth factor could be useful for the treatment of degenerative brain diseases such as Alzheimer's disease29 other agents may have relevance to therapy for infections of the central nervous system.30 The BBB represents a complex system of mechanisms that act together to regulate the exchange of fluids and substances between the central nervous system (CNS) and blood. The barrier consists of an endothelial or capillary barrier and the ependymal barrier found at the circumventricular organs and choroid plexus. Circumferential tight junctions exist between the cerebral capillary endothelial cells, which do not allow paracellular transport...

Marilyn A Davies Chiaoying Chang and Bryan L Roth

This chapter first describes the structural changes involved in genetic polymorphisms, mRNA editing, and alternative mRNA splicing of 5-hydroxytryptamine (5-HT) receptors. These structural changes lead to modifications in the production and characteristics of 5-HT receptors and affect protein expression. Functionally, they affect radioligand binding, signal transduction, and receptor sensitivity, thus affecting interindividual variation in responses to therapeutic agents, particularly antipsychotics and antidepressants. Studies indicate that genetic polymorphic and post-transcriptional modifications of 5-HT receptor structure contribute also to pathological processes related to irritable bowel syndrome, cardio-pulmonary problems, psychiatric illness (i.e., schizophrenia and mood disorders), Alzheimer's disease, problems involving increased food and alcohol intake, and behavioral problems such as impulsivity, self-harm, and aggression. In the second part of this chapter, the 5HT2A,...

Neuropharmacology See psychopharmacology

Vascular disease, seizure disorders, neurodegenera-tive diseases (such as Alzheimer's disease or Parkinson's disease), brain tumors, infectious and inflammatory diseases of the central nervous system (CNS), alcohol-induced mental disorders, and developmental disorders involving the brain. A neuropsychologist and a neurologist differ in several ways. A neurologist is a physician (M.D.) who deals with the structural and physiological consequences of brain injury and organic brain disease, while a neuropsychologist (Ph.D) investigates the cognitive and behavioral impact of these conditions. For example, for a person who suffers serious brain damage after a bike accident, a neurologist would assess the physical impact of injuries can the patient walk, move muscles, and maintain hand eye coordination The neuropsychologist would test the person's ability to think and reason clearly and check for memory loss or reading, learning, and comprehension problems. neurosyphilis Infection of the...

Box 221 People With The Same Disorder Can Be Quite Different

Half of the children born with Down syndrome are born with severe heart malformations. These and other life-threatening conditions are so severe that some of these children die before age five. However, for those children who survive the fifth year of life, the average life expectancy is fifty years. Even so, these individuals are at high risk for leukemia and for a degenerative brain disorder similar to Alzheimer disease. Men with Down syndrome are usually sterile, but the women are fertile from the few scattered reports available, it appears that half of their children are born with Down syndrome. On one hand, this result makes good sense half of the eggs produced by such a woman should carry two copies of chromosome 21. However, given that some eighty percent of Down syndrome fetuses spontaneously miscarry, we have to wonder why the final result should be a 1 1 ratio. Although we can imagine models for how this might happen, at this time it is still one of many mysteries about this...

Mental State Examination

Further details on examination of mental state are given in Chapter 1. The Mini-Mental State Examination described in that chapter permits a rapid survey of many areas of cognition, as well as the generation of a summary score that is particularly suitable for description of patients with diffuse global impairment of cognitive function, as occurs in delirium or dementia.

Nuclear magnetic resonance NMR See magnetic Resonance Imaging Mri

Nucleus basalis of Meynert An area near where the optic nerves cross that enters into the cerebral cortex. When this area is destroyed, it causes a drop in acetylcholine activity in the cortex similar to Alzheimer's disease. Scientists suspect that the beginning of Alzheimer's disease may be related to a slow death of cells in the nucleus basalis, which may lead to the formation of the plaques also seen in the disease.

Impairments of Discourse by Level of Processing

With right hemisphere damage, traumatic brain injury, or early-stage Alzheimer's disease. Few studies have looked for impairments at the microstructural level. In one such study, Joanette et al. (1986) showed that both patients with right hemisphere damage and normal controls produced discourse with similar microstructure. Stemmer and Joanette (1998) confirmed this observation but found that individuals with left hemisphere damage tended to produce more fragmented micropropositions, lacking in arguments. This resulted in a disruption of the connective structure of discourse, which requires predicates and arguments to be connected in order to form a semantic network of propositions. Numerous other studies have looked at cohesion, which can be considered representative of the microstructural level. Cohesion refers to the quality of local relationships between the elements of discourse and is frequently expressed through linguistic markers such as pronouns and conjunctions. Patients with...

Crassulacean acid metabolism cam Physiological

Creutzfeldt-Jacob disease Rare fatal presenile dementia of humans, similar to kuru and other transmissible spongiform encephalopathies. Method of transmission unknown. Will induce a neurological disorder in goats 3-4 years after inoculation with CJD brain extract. A new variant, vCJD, has recently been recognized and associated with bovine spongiform encephalopathy. See prions.

Normal Versus Abnormal Forgetting

Tests of memory and related cognitive functions can help distinguish memory disorders from normal, age-related memory loss. And make no mistake age-related memory loss is not a disorder. However, two memory disorders mild cognitive impairment and dementia do become more common with age, leading memory researchers to wonder if there is any relationship between them and age-related memory loss. Experts disagree about the answer. Some say that mild cognitive impairment and dementia are entirely distinct from age-related memory loss. We refer to this view as the discontinuity model. In this view, age-related memory loss is an effect of the normal developmental evolution of the brain in the same way as 118 diminished bone density is the normal and inevitable destiny of the aging human skeleton. On the other hand, discontinuity adherents view dementia as the product of a pathophysiological disease process, a divergence from normal health and development. Other experts view age-related...

Box 222 Partial Aneuploidy Through Translocation Of A Chromosomal Segment

Prediction on the evidence that some of the most profound problems arising from the extra copy of chromosome 21 arise during development before birth, in structures such as the lungs and heart. Once that damage is done, we may simply have to rely on traditional medical and surgical processes for help. However, some of the Down syndrome problems, such as leukemia and Alzheimer diseases, develop after birth, so there may be a chance for prevention or to improve medical intervention if enough is understood about the roles of the particular genes and gene products in these later developments of the disorder. On the other hand, if the most conspicuous component of this disorder, mental retardation, is truly due to the triplication of a single gene, we have to wonder whether it may be possible someday, with early enough prenatal diagnosis, to correct or at least ameliorate that problem through interventions before the baby is even born. It remains to be seen whether the study of triplicate...

Object Knowledge vs Object

Apraxia is the inability to carry out purposeful actions in the absence of weakness or sensory loss. At first sight, consideration of apraxia may seem inappropriate in the context of semantic memory disorders. However, inability to carry out skilled movements can arise for conceptual reasons (De Renzi & Luchelli, 1988 Ochipa et al., 1989 Rothi et al., 1991). A patient may fail to salute or demonstrate the action of combing hair on command because of loss of knowledge of how to carry out the required action. For patients with severe semantic impairment, such as semantic dementia, loss of object knowledge typically entails both an inability to recognize and describe the function of an object, as well as an inability to demonstrate its use. A patient who does not recognize a razor also cannot demonstrate its use by action pantomime. Nevertheless, dissociations between functional knowledge and use can sometimes occur. Moreaud et al. (1998) described a patient who was impaired in his...

The protective effects of alcoholic drinks

It seems clear that alcohol reduces the level of 'bad' cholesterol in the blood (known as LDL) while increasing the level of 'good' cholesterol (HDL). It dilates blood vessels and lowers blood pressure (but chronic alcohol intake increases it). A decrease in colon cancer and Alzheimer's disease have also been associated with moderate drinking. There is evidence, in particular, that one or perhaps two glasses of red wine a day may be beneficial. This is the so-called 'French paradox', for the level of heart disease in France is one of the lowest in the world despite a diet traditionally rich in animal fats. The French also drink more red wine than other countries, and evidence seems to suggest that components in the grapes, polyphenols such as resveratrol, may be partly responsible for the low level of heart disease. One theory put forward is that this is due to the antioxidant effects of the polyphenols. Antioxidants such as vitamins C and E can react with and remove reactive...

More Products

The Great Brain Secret
All About Alzheimers

All About Alzheimers

The comprehensive new ebook All About Alzheimers puts everything into perspective. Youll gain insight and awareness into the disease. Learn how to maintain the patients emotional health. Discover tactics you can use to deal with constant life changes. Find out how counselors can help, and when they should intervene. Learn safety precautions that can protect you, your family and your loved one. All About Alzheimers will truly empower you.

Get My Free Ebook