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Alzheimer's disease (AD) or senile dementia of Alzheimer's type is a neurodegenerative disease which results in a loss of mental functions due to the deterioration of brain tissue. Its exact aetiology (cause) is still unknown, but environmental as well as genetic factors are thought to contribute (mutations in at least four genes predisposing to AD have been identified). Dementia (from Latin demens) is progressive decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging. ...
In the anatomy of animals, the brain, or encephalon, is the supervisory center of the nervous system. ...
Biological tissue is a group of cells that perform a similar function. ...
Etiology (alternately aetiology, aitiology) is the study of Greek words aitia = cause and logos = word/speech) is used in philosophy, physics and biology in reference to the causes of various phenomena. ...
This article is about mutation in biology, for other meanings see: mutation (disambiguation). ...
This stylistic schematic diagram shows a gene in relation to the double helix structure of DNA and to a chromosome (right). ...
Until the 1960s, the disease was thought to be uncommon, but later it was realized that much of what had been regarded as the normal process of aging was actually the result of this disease. Centuries: 19th century - 20th century - 21st century Decades: 1900s 1910s 1920s 1930s 1940s 1950s - 1960s - 1970s 1980s 1990s 2000s 2010s Years: 1960 1961 1962 1963 1964 1965 1966 1967 1968 1969 Events and trends The 1960s was a turbulent decade of change around the world. ...
In biology, senescence is the state or process of aging. ...
Clinical features The typical visible symptom is progressive and chronic memory loss. Alzheimer's disease is also manifested in behavorial changes, which may include confusion, disorientation, sudden periods of defiance, abusive behavior, or violence, etc. in people who have no previous history of such behavior (rarely, an affected person experiences euphoria). Thus, Alzheimer's disease presents a considerable problem in patient management. Average duration is approximately 10 years. The disease duration has been noted to vary as very roughly half of the normal life expectancy of a healthy person of the same age as the patient in whom the Alzheimer's is diagnosed, subject to a maximum of 10 to 12 years for those diagnosed at a young age. Memory loss can be caused by many things. ...
Pathology There are several changes found in the brain in AD. - The deposition of an abnormal protein outside nerve cells in the form of amyloid. These are called diffuse plaques and amyloid also forms the core of more organized plaques called senile or neuritic plaques.
- The accumulation of abnormal filaments of protein inside nerve cells in the brain. The protein is called tau and is normally present to stabilise microtubules. In AD, an abnormally phosphorylated form of tau protein accumulates as paired helical filaments. Tau accumulates
- As masses of filaments inside nerve cell body termed neurofibrillary tangles
- Inside nerve cell processes in the brain termed neuropil threads
- Inside nerve cell processes that surround amyloid plaques - termed plaque neurites.
- Amyloid accumulation in the walls of small blood vessels in the brain. Termed amyloid angiopathy (also called congophilic angiopathy)
- Diffuse neuropathology, nerve cells and their processes including synapses die and are lost from key brain regions. This results in atrophy of the affected areas and enlargement of the ventricles.
- Loss of synaptic contacts between neurons. May be related to the regulation of cell adhesion proteins by presenilins. The presenilins have been identified as part of the processing apparatus that produces the amyloid beta protein.
There is also regional involvement of gross atrophy, and enlarged ventricles in the brain. Massive synaptic and dendritic loss is expected. The neurotransmitters serotonin, acetylcholine, norepinephrine, and somatostatin are at decreased levels. Glutamate levels are usually elevated. Amyloid describes various types of protein aggregations that share specific traits when examined microscopically. ...
Neuropathology is the study of diseases of the nervous system. ...
Atrophy is the partial or complete wasting away of a part of the body. ...
Schematic of cell adhesion The study of cell adhesion is part of cell biology. ...
Serotonin (5-hydroxytryptamine, or 5-HT) is a monoamine neurotransmitter synthesised in serotonergic neurons in the central nervous system and enterochromaffin cells in the gastrointestinal tract. ...
The chemical compound acetylcholine, often abbreviated as ACh, was the first neurotransmitter to be identified. ...
Norepinephrine, known as noradrenaline outside the USA, is a catecholamine and a phenethylamine with chemical formula C8H11NO3. ...
Somatostatin is a hormone. ...
Glutamic acid or glutamate is one of the 20 most common natural amino acids. ...
Many of these features can be seen with the microscope using special histological techniques and are only seen when the brain is examined after death.
Etiology Three competing hypotheses exist to explain the cause of the disease.
The oldest hypothesis is the "cholinergic hypothesis". It states that Alzheimer's begins as a deficiency in the production of acetylcholine, a vital neurotransmitter. Much early therapeutic research was based on this hypothesis, including restoration of the "cholinergic nuclei". The possibility of cell-replacement therapy was investigated on the basis of this hypothesis. All of the first-generation anti-Alzheimer's medications are based on this hypothesis and work to preserve acetylcholine by interfering with acetylcholinesterases (enzymes that break down acetylcholine). Results from these medicines have not been promising. In all cases, they have served to only treat symptoms of the disease and have neither halted nor reversed it. These results and other research have led to the conclusion that acetylcholine deficiencies may not be causal but are a result of widespread brain tissue damage, damage so widespread that cell-replacement therapies are likely to be impractical.
The other two hypotheses are of generally equal acceptance. "Tau-ists" believe that the tau protein abnormalities come first and lead to a full disease cascade. "bA-ptists" believe that beta amyloid deposits are the causative factor in the disease. For example, the presence of the APP gene on chromosome 21 is believed to explain the high incidence of AD in patients with Down syndrome (trisomy 21). The terms "tau-ist" and "ba-ptist" are used (lightheartedly) in scientific publications by Alzheimer's disease researchers. A third protein, alpha synuclein, which has already been shown to be important in Parkinson's disease, has recently been proposed as the etiological candidate, giving rise to the "syn-ners". By 2004, several researchers have come to the conclusion that Alzheimer's disease may be a "triple-protein pathology", wherein interactions among all three lesions are what give rise to Alzheimer's disease, rather than any one of the three. A child with Down syndrome Down syndrome (also called Downs syndrome) encompasses a number of genetic disorders, of which trisomy 21 (a nondisjunction) is the most representative, causing highly variable degrees of learning difficulties and physical disabilities. ...
There is compelling evidence that genetic predispositions underlie the development of Alzheimer's disease. However, the most obviously genetic cases are also the rarest. Most cases identified are 'sporadic' with no clear family history. It is probable that environmental factors have to interact with a genetic susceptibility to cause development of disease. Head injury has been consistently shown to be linked to later development of AD in epidemiological studies. In addition, small cranial diameter has been shown to correlate well with early onset of recognizable symptoms. The most commonly accepted explanation for this last feature is that larger brains simply may have more cells that can afford to be lost. Inheritance of a specific variation of the ApoE gene (epsilon 4) is regarded as a risk factor for development of disease, but large-scale genetic association studies raise the possibility that even this does not indicate susceptibility so much as how early one is likely to develop Alzheimer's. Intriguing work is currently going on investigating the possibility that the regulatory regions of various Alzheimer's associated genes could be important in sporadic Alzheimer's, especially inflammatory activation of these genes. This stylistic schematic diagram shows a gene in relation to the double helix structure of DNA and to a chromosome (right). ...
Studies have not shown strong link with toxins, vitamins, metals or diet, although rabbits fed a high-cholesterol diet in the presence of copper ions in their water did develop amyloid brain lesions and cognitive deficiencies [1] (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12920183), [2] (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=14506299). Likewise, linkage has been found between zinc or copper and reactive oxidative stress contributing to Alzheimer's pathology [3] (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0V-483ST4V-1&_coverDate=04%2F30%2F2003&_alid=187240288&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4872&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=c4bdc9c6cb9a59aa2a676e79124856d3), and the amyloid precursor protein has been shown to alter expression in response to metal supplementation and chelation [4] (http://iospress.metapress.com/app/home/contribution.asp?wasp=nntr48wqwp5xnjarpv5m&referrer=parent&backto=issue,10,17;journal,1,29;linkingpublicationresults,1:105656,1), [5] (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCR-4B37JCB-2&_coverDate=01%2F15%2F2004&_alid=187240616&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=5177&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=f8157cd24891e6a93e263dae23299e96), [6] (http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0002-8614&date=2003&volume=51&issue=8&spage=1143). Therefore, it is hasty and premature to dismiss any and all environmental effects out of hand. There have been studies that link aluminium to the progression of Alzheimer's, but the results from these studies have not been confirmed and are not widely accepted by Alzheimer's experts. Vitamins are organic chemicals that a given living organism requires in trace quantities for good health, but which the organism cannot synthesize, and therefore must obtain from its diet. ...
General Name, Symbol, Number aluminium, Al, 13 Chemical series poor metals Group, Period, Block 13 (IIIA), 3, p Density, Hardness 2700 kg/m3, 2. ...
Rare cases are caused by dominant genes that run in families. These cases often have an early age of onset. Mutations in presenilin-1 or presenilin-2 genes have been documented in some families. Mutations of presenilin 1 (PS1) lead to the most aggressive form of familial AD (FAD). Evidence from rodent studies suggests that the FAD mutation of PS1 results in impared hippocampal-dependent learning which is correlated with reduced adult neurogenesis in the dentate gyrus ( Wang et al, 2004 (http://www.sciencedirect.com/science/article/B6T0F-4CB0G5C-B/1/f88958872d2aed83eebc6cbd76f9341f)). Mutations in the APP gene on chromosome 21 can also cause disease. The location of the hippocampus in the human brain. ...
Neurogenesis literally means birth of neurons. Neurogenesis is most prevalent during pre-natal development and is the process by which neurons are created to populate the growing brain. ...
The location of the hippocampus in the human brain. ...
Figure 1: Chromosome. ...
Prevalence Alzheimer's disease is the most frequent reason for dementia in the elderly and affects almost half of all patients with dementia.
2-3% of persons aged 65 show signs of the disease, while 25% or more of persons aged 85 have symptoms of Alzheimer's and an even greater number have some of the pathological hallmarks of the disease without the characteristic symptoms. The proportion of persons with Alzheimer's begins to decrease after age 85 because of the increased mortality due to the disease, and relatively few people over the age of 100 have the disease.
Diagnosis While expert clinicians who specialize in memory disorders can diagnose AD with an accuracy of 85-90%, a definitive diagnosis of Alzheimer's disease must await an autopsy. Many increasingly sophisticated diagnostic tests are also used (including: brain scans, behavioral tests and testing for genetic predisposition) but these are, at present, used mainly to identify or rule out possible alternative explanations for the symptoms. For the former Death Metal band called Autopsy, see Autopsy (band). ...
Brain imaging is a fairly recent discipline within medicine and neuroscience. ...
Psychological testing generally focuses on memory, attention, abstract thinking, the ability to name objects, and other cognitive functions. However, results of psychological tests do not easily distinguish between Alzheimer's Disease and other types of dementia such as normal pressure hydrocephalus. Psychological testing can be helpful in establishing the presence of and severity of dementia. It can also be useful in distinguishing true dementia from temporary (and more treatable) cognitive impairment due to depression or psychosis, which has sometimes been termed pseudodementia. Normal pressure hydrocephalus (NPH) is a neurological disorder often misdiagnosed as Parkinsons disease, Alzheimers disease, and senility. ...
Prevention Efforts to find a cure Alzheimer's after-the-fact have so far been disappointing. Meanwhile, the apparent great success of preventive strategies remained uncelebrated and almost unnoticed. Age is the primary risk factor for Alzheimer's. The baby boom is approaching its golden years. Indeed, much of the concern about the solvency of the governmental social safety net is founded on estimates of the costs of caring for baby boomers, assuming that they develop Alzheimer's in the same proportions as earlier generations. Most preventive strategies appear to work far better (or at all) only if begun long before the symptoms of overt Alzheimer's appear. Thus wide dissemination of information about the availablility of effective preventive strategies appears a public health strategy of high benefit and high urgency.
Many studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and aspirin delay the onset, and lower the ultimate risk, of Alzheimer´s disease. According to population studies, low but consistent daily NSAID use over a period of years of NSAIDs such as ibuprofen (Advil, Motrin) seems to significantly slow the progress of Alzheimer's, and eventually to dramatically decrease the risk of the disease in those who have not yet developed it. Quite large daily doses of aspirin also appear to slow the progression towards Alzheimer's, and reduce the eventual risk of developing the disease, but to a lesser degree, and with a much greater risk of potentially fatal stomach ulceration. It seems that NSAIDs are of great use in preventing or delaying the onset of the disease but of little use for treating it once it has progressed to early or full-blown Alzheimer's. Daily NSAID users experience greater risk reduction over time, with some reduction after two years of regular ibuprofen use, and marked reduction after five or more years. It should be noted that some similar drugs such as acetaminophen, naproxen, and the 'COX-2 inhibitors' were found to have no demonstrated benefit (and some evidence of cardiac harm). This ineffectiveness and the increase in adverse cardiac events associated with these agents was reported in various studies in 2004 and highlights the key role of ibuprofen in the original studies showing moderated risk associated with NSAID use. These studies leave ibuprofen as the NSAID most likely to reduce Alzheimer's risk. Ibuprofen is also the nonprescription NSAID with the lowest risk of promoting gastrointestinal bleeding and stomach ulcers. Cyclooxygenase (COX) is an enzyme that is responsible for formation of important biological mediators called prostanoids (including prostaglandins, prostacyclin and thromboxane). ...
A study (Archives of Neurology 2004; 61:82-88) has reported that the combination of vitamins E and C might, over time, sharply reduce the risk of Alzheimer's disease. Marked reduction (up to 80% risk reduction) was achieved after a period of more than five years, but only if dosage was 400 i.u. per day of vitamin E plus 500 mg or more per day of vitamin C. Lesser amounts, such as those found in multivitamin pills, appeared markedly less effective. Large doses of vitamin E without vitamin C had only a mild effect, while large doses of vitamin C without vitamin E had no benefit. However in one small study, 2000 i.u. per day of vitamin E did appear to delay the progression of early Alzheimer’s by several months. Other evidence suggests that vitamin E becomes a damaging pro-oxidant if given in isolation (without other antioxidants). In isolation vitamin E is not recharged after absorbing a free radical by another antioxidant such as vitamin C or Alpha-Lipoic Acid. Some studies suggest that a ratio of at least 1000 mg of vitamin C to 400 i.u. of vitamin E is ideal. Recent studies suggest that the most common forms of E sold in supplements, the dl-alpha or d-alpha tocopherol form, are of little value, and that the gamma form of vitamin E, or a mixture of all the tocopherols and tocotrienols that collectively make up vitamin E from food, provide the most benefit. Vitamin E is markedly less effective unless taken with oil.
In a number of retrospective studies, regular physical exercise has appeared to be inversely related to the development of Alzheimer’s. The Alzheimer's risk of those exercising regularly was half that of the least active. This research is consistent with the observation that virtually all measures designed to promote cardiac fitness and reduce stroke risk also seem to reduce Alzheimer's risk. However in one study, dance appeared to be the only exercise effective in reducing risk. The presence of cardiovascular risk factors -- diabetes, hypertension, high cholesterol and smoking -- in middle age (ages 40 to 44) was found very strongly associated with late-life dementia, as reported in Neurology 2005;64:277-281.
Improved nutritional status of the B vitamin folic acid was found to reduce Alzheimer's incidence in a study of an order of nuns, many of whom volunteered to have their mental status assessed and donated their brains for study after death. The "Nun's study" also revealed nuns who, in life, showed little or no dementia, but upon autopsy were found to have extensive Alzheimer’s plaques. The unimpaired nuns’ brains were free of evidence of stroke, including micro-strokes. Nuns whose brains revealed both plaques and stroke damage, however, were severely impaired in functioning while alive. Thus avoidance of risk factors for stroke may be a key element in preventing final progression to being disabled by Alzheimer's dementia. The discovery of the co-founding role of stroke supports other research showing that quitting smoking, weight reduction, and avoidance of diabetes all reduce Alzheimer's risk. Diabetes greatly increases Alzheimer's risk, and one factor at work may be that the enzyme charged with removing excess insulin from the blood, the Insulin Degrading Enzyme (IDE), also has the responsibility for removing Beta-amyloid plaques from the brain. Perhaps the excess insulin involved in the pre-diabetic metabolic syndrome, as well as insulin used to treat existing diabetes, may demand more IDE than the body is able to produce, leaving none to remove accumulating beta amyloid plaques from the brain.
Some evidence suggests that Alzheimer's risk may also be reduced by inclusion of fish in the weekly diet.
The spice turmeric reduces Alzheimer's incidence in a mouse model and actually dissolves human senile plaques in the test tube. Populations on the Indian subcontinent using turmeric regularly in curry dishes have much lower incidence of Alzheimer's than elsewhere. These factors suggest that inclusion of a bit of turmeric or curry spice in the diet may provide preventive value. Turmeric is a powerful antioxidant and a powerful anti-inflammatory. Binomial name Curcuma longa Linnaeus Turmeric (Curcuma longa, also known as tumeric or curcumin) is a spice commonly used in curries and other south Asian cooking. ...
Presently there are also studies going on testing cholesterol-lowering drugs, so-called statins, like lovastatin, simvastatin etc. as a means of preventing or delaying Alzheimer´s. There seems to be a connection between the cholesterol level inside the brain cells and the deposition of toxic amyloid plaques which make the brain cells die. In addition to lowering cholesterol, the statins may have a beneficial role in reducing inflammation.
The recent observation that nicotine exposure leads to delayed onset of Alzheimer's has stimulated plenty of research into the relationship of nicotine intake and the disease. This is the focus of ongoing debate, and no consensus has been reached.
Nutrition and Alzheimer's Some work is being done to investigate the role of raised levels of homocysteine, and possible nutritional prevention or treatment through taking of foods high in B vitamins and antioxidants to control the levels of homocysteine. Nutrition is interpreted as the study of the organic process by which an organism assimilates and uses food and liquids for normal functioning, growth and maintenance and to maintain the balance between health and disease. ...
An antioxidant is a chemical that prevents the oxidation of other chemicals. ...
This view is supported by Teodoro Bottiglieri, a neuropharmacologist at the Baylor Institute of Metabolic Disease in Dallas, Texas, and Andrew Mc Caddon, a researcher at the University of Wales. (See the Times newspaper, January 31 2004 "Could vitamins help delay the onset of Alzheimer's?" by Jerome Burne). The University of Wales is a federal university founded in 1893. ...
See also: Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med. 2002 Feb 14;346(7):476-83.
Linkage of aluminum products and Alzheimer's Some research suggests a possible link between alumnium intake and risk of Alzheimer's disease. Significant reduction of dietary aluminum intake can be achieved by avoidance of aluminum-based antacids, such as those containing aluminum hydroxide. Aluminum intake might be further reduced by avoiding cooking in aluminum cookware or alumnium foil, and by prefering non-aluminum based deodorants. Aluminum popcans and beer cans generally have plasticized insides to prevent leaching of aluminum into their liquids.
See also: http://www.alzheimers.org.uk/Facts_about_dementia/Risk_factors/info_aluminium.htm
Treatment There is no cure, although there are drugs which reduce neurotransmitter degradation and alleviate some of the symptoms of the disease.
Acetylcholinesterase inhibitors Acetylcholinesterase (AChE) inhibition was thought to be important because there is selective loss of forebrain cholinergic neurons as a result of Alzheimer's. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons). Acetylcholinesterase-inhibitors seemed to modestly moderate symptoms but do not prevent disease progression including cell death. In biochemistry, cholinesterase is a term which refers to one of the two enzymes (EC 3. ...
A synapse is cholinergic if it uses acetylcholine as its neurotransmitter. ...
Examples include:
Recently, a controversy has erupted about cholinesterase inhibitors because a study by Courtney (2004) in the respected medical journal The Lancet has suggested they are ineffective. The pharmaceutical companies dispute the findings of the study. Tacrine is a parasympathomimetic and a centrally acting cholinesterase inhibitor (anticholinesterase). ...
Donepezil, which goes by the trade name Aricept® (Pfizer), is a centrally acting reversible cholinesterase inhibitor. ...
Categories: Stub | Anticholinesterases | Antidementia agents ...
The Lancet is a British medical journal, published weekly by the Lancet Publishing Group. ...
NMDA antagonists Recent evidence of the involvement of glutamatergic neuronal excitotoxicity in the aetiology of Alzheimer's disease let to the development and introduction of memantine. Memantine is a novel NMDA receptor antagonist, and has been shown to be moderately clinically efficacious. (Areosa et al., 2004) Glutamic acid or glutamate is one of the 20 most common natural amino acids. ...
Excitotoxicity is the process by which apoptosis is triggered in neurons by the overactivation of excitatory neurotransmitter receptors such as the NMDA receptor. ...
Etiology (alternately aetiology, aitiology) is the study of Greek words aitia = cause and logos = word/speech) is used in philosophy, physics and biology in reference to the causes of various phenomena. ...
Memantine is an NMDA receptor antagonist used in the treatment of Alzheimers disease. ...
The NMDA receptor (NMDAR) is an ionotropic receptor for glutamate (NMDA is a name of its selective specific agonist). ...
Categories: Biology stubs | Biochemistry | Pharmacology ...
Vaccine There are ongoing tests of an Alzheimer's disease vaccine. This was based on the idea that if you could train the immune system to recognize and attack beta-amyloid placque, the immune system might reverse deposition of amyloid and thus stop the disease. Initial results in animals were promising. However, when the first vaccines were used in humans, brain inflammation occurred in a small fraction of participants, and the trials were stopped. Participants in the halted trials continued to be followed, and some showed lingering benefits in the form of slower progression of the disease. Recent studies in mice continue to show promise that an approach may be found to avoid the inflammation issue. It is hoped that research will provide a better formulation and that in the future it can be of use in families with history of Alzheimer's Disease.
Genetic and population effects Various gene alleles have been associated with Alzheimer's disease, most notably the apolipoprotein E (ApoE) gene. ApoE normally functions to regulate cholesterol metabolism. In addition, it has recently been discovered that Chinese and North American populations differ significantly in development of full-fledged Alzheimer's from early warning symptoms. Whether the reason for this is genetic, dietary, or social has yet to be investigated. An allele is any one of a number of alternative forms of the same gene occupying a given locus (position) on a chromosome. ...
Cholesterol is a steroid lipid, found in the cell membranes of all body tissues, and transported in the blood plasma of all animals. ...
Santorio Santorio (1561-1636) in his steelyard balance, from Ars de statica medecina, first published 1614 Metabolism (from μεταβολισμος(metavallo), the Greek word for change), in the most general sense, is the ingestion and breakdown of complex compounds, coupled with the liberation of energy, and the consequent generation of waste...
Vaccines are helpful to help alzheimer's when they are unhelpful.
Social issues Alzheimer's is considered to be a major public health challenge since the average age of the industrialized world's population is increasing. For this reason, money spent informing the public of available effective prevention methods may yield disproportionate benefits.
History The symptoms of the disease as a distinct nosologic entity were first identified by Emil Kraepelin, and the characteristic neuropathology was first observed by Alois Alzheimer in 1906. In this sense, the disease was co-discovered by Kraepelin and Alzheimer, who worked in Kraepelin's laboratory. Because of the overwhelming importance Kraepelin attached to finding the neuropathological basis of psychiatric disorders, Kraepelin made the generous decision that the disease would bear Alzheimer's name (J. Psychiat. Res., 1997, Vol 31, No. 6, pp. 635-643). Emil Kraepelin (February 15, 1856- October 7, 1926) was a psychiatrist who attempted to create a synthesis of the hundreds of mental disorders classified by the 19th century, grouping diseases together based on classification of common patterns of symptoms, rather than by simple similarity of major symptoms in the manner...
Alois Alzheimer Alois Alzheimer (June 14, 1864 - December 19, 1915), a German neurologist, was a colleague of Emil Kraepelin who first identified the symptoms of what is now known as Alzheimers Disease. ...
Famous Alzheimer's sufferers Enid Blyton (August 11, 1897 - November 28, 1968) was a British childrens author. ...
Carroll Campbell Jr. ...
Hon Alfred Deakin Alfred Deakin (August 3, 1856 - October 7, 1919), intellectual leader of the movement for Australian federation and second Prime Minister of Australia, was born in Melbourne, Victoria, the son of English immigrants. ...
James Montgomery Doohan (born March 3, 1920) is a Canadian actor and linguist best known for his portrayal of Scotty in the television and movie series Star Trek. ...
Ralph Waldo Emerson Ralph Waldo Emerson (May 25, 1803–April 27, 1882) was a famous American essayist and one of Americas most influential thinkers and writers. ...
Barry Goldwater Barry Morris Goldwater ( January 1, 1909 – May 29, 1998) was a United States politician and a founding figure in the modern conservative movement in the USA. Goldwater personified the shift in balance in American culture from the Northeast to the West. ...
Rita Hayworth Rita Hayworth (real name Margarita Carmen Cansino) (October 17, 1918 - May 14, 1987) was a famous American film star during the 1940s who was sometimes called The Love Goddess or The Great American Love Goddess. ...
Charlton Heston (born October 4, 1924), born John Charles Carter, is an American film actor noted for heroic roles. ...
Beatrice Lillie (29 May 1894-20 January 1989) was the outstanding comedic actress of her time. ...
Queen Juliana Juliana Louise Emma Marie Wilhelmina, Duchess of Mecklenburg-Schwerin, (April 30, 1909 - March 20, 2004) of the House of Orange-Nassau was Queen of the Netherlands from her mothers abdication in 1948 to her own abdication in 1980 and Queen Mother (with the title of Princess) from...
Burgess Meredith (November 16, 1909 _ September 9, 1997) was an American actor, perhaps best known for playing the Penguin on the television series Batman. ...
Iris Murdoch Dame Jean Iris Murdoch (July 15, 1919 - February 8, 1999) was an Anglo-Irish novelist and philosopher, famed for her series of novels that combine rich characterization and compelling plotlines usually involving ethical or sexual themes. ...
Joseph-Maurice Ravel (March 7, 1875 – December 28, 1937) was a French composer and pianist, best known for his orchestral work, Boléro, and his famous 1922 orchestral arrangement of Modest Mussorgskys Pictures at an Exhibition. ...
Walker Smith Jr. ...
Dame Margaret Rutherford (May 11, 1892 – May 22, 1972) was a British character actress who first came to prominence following World War II in the film adaptations of Noel Cowards Blithe Spirit, and Oscar Wildes The Importance of Being Earnest. ...
Robert Sargent Shriver, Jr. ...
Charles A. Steen, Uranium King Charles A. Steen (b. ...
Cyrus Roberts Vance (March 27, 1917–January 12, 2002), was the United States Secretary of State under President Jimmy Carter from 1977 to 1980. ...
Elwyn Brooks White (July 11, 1899–October 1, 1985) was an American essayist, author, and noted prose stylist. ...
James Harold Wilson, Baron Wilson of Rievaulx, KG, OBE, PC (March 11, 1916 - May 24, 1995) was one of the more successful Labour Prime Ministers of the United Kingdom and a 1960s icon. ...
See also Chi-Ming Yang is the director of Neurochemistry and Physical Organic Chemistry Laboratory at Nankai University, Tianjin, China. ...
Nankai University (pinyin: Nankai Daxue; simplified: 南开大学 traditional: 南開大學), located in Tianjin, is one of the leading universities in China. ...
Tianjin (Chinese: 天津; pinyin: tiān jīn; Postal System Pinyin: Tientsin) is a harbour municipality in China on the Hai He River (from Beijing) and Bohai Gulf of the Yellow Sea (Pacific Ocean). ...
The Great Wall of China, stretching over 6,700 km, was erected beginning in the 3rd century BC to guard the north from raids by men on horses. ...
Creutzfeldt-Jakob Disease (CJD) is a lethal brain disorder characterized by memory loss, personality changes, hallucinations, speech impairment, jerky movements, changes in gait, rigid posture, and seizures due to a rapid loss of neural cells caused by transmissible proteins called prions. ...
In chemistry, an amino acid is any molecule that contains both amino and carboxylic acid functional groups. ...
Familial Alzheimers disease is an uncommon form of Alzheimers disease that comes on earlier in life (usually between 30 and 60 years of age) and is inherited in an autosomal dominant fashion. ...
Reference - Areosa SA, McShane R, Sherriff F. Memantine for dementia. Cochrane Database Syst Rev 2004(4);CD003154.pub2. PMID 15495043
- Courtney C, Farrell D, Gray R, Hills R, Lynch L, Sellwood E, Edwards S, Hardyman W, Raftery J, Crome P, Lendon C, Shaw H, Bentham P; AD2000 Collaborative Group. Long-term donepezil treatment in 565 patients with Alzheimer's disease (AD2000): randomised double-blind trial. Lancet 2004;363:2105-15. PMID 15220031.
The Cochrane Collaboration developed in response to Archie Cochranes call for systematic, up-to-date reviews of all relevant randomized clinical trials of health care. ...
The Lancet is a British medical journal, published weekly by the Lancet Publishing Group. ...
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