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Dr. Zaven Khachaturian is a neuroscientist and Alzheimer's disease researcher.
Khachaturian previously worked for the National Institute on Aging. [1] He was named the editor of the journal Alzheimer's & Dementia.
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Dr. Zaven Khachaturian is a neuroscientist and Alzheimer's disease researcher.
Khachaturian previously worked for the National Institute on Aging. [1] He was named the editor of the journal Alzheimer's & Dementia.
Dementia manifests as a set of related symptoms, which usually surface when the brain is damaged by injury or disease. The symptoms involve progressive impairments in memory, thinking, and behavior, which negatively impact a person's ability to function and carry out everyday activities. Aside from memory impairment and a disruption in thought patterns, the most common symptoms include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia is not a disorder of consciousness, as that is not usually affected. It ultimately has a significant effect on the individual, caregivers, and relationships in general.
Vascular dementia (VaD) is dementia caused by problems in the supply of blood to the brain, typically a series of minor strokes, leading to worsening cognitive abilities, the decline occurring step by step. The term refers to a syndrome consisting of a complex interaction of cerebrovascular disease and risk factors that lead to changes in brain structures due to strokes and lesions, resulting in changes in cognition. The temporal relationship between a stroke and cognitive deficits is needed to make the diagnosis.
Donepezil, sold as the trade name Aricept among others, is a medication used to treat Alzheimer's disease. It appears to result in a small benefit in mental function and ability to function. Use, however, has not been shown to change the progression of the disease. Treatment should be stopped if no benefit is seen. It is taken by mouth.
Memantine is a medication used to slow the progression of moderate-to-severe Alzheimer's disease. It is taken by mouth.
Amyloid beta denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. The peptides derive from the amyloid precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol dependent process and substrate presentation. Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.
Amyloid-beta precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. It functions as a cell surface receptor and has been implicated as a regulator of synapse formation, neural plasticity, antimicrobial activity, and iron export. It is coded for by the gene APP and regulated by substrate presentation. APP is best known as the precursor molecule whose proteolysis generates amyloid beta (Aβ), a polypeptide containing 37 to 49 amino acid residues, whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients.
Tauopathy belongs to a class of neurodegenerative diseases involving the aggregation of tau protein into neurofibrillary or gliofibrillary tangles (NFTs) in the human brain. Tangles are formed by hyperphosphorylation of the microtubule protein known as tau, causing the protein to dissociate from microtubules and form insoluble aggregates. The mechanism of tangle formation is not well understood, and whether tangles are a primary cause of Alzheimer's disease or play a peripheral role is unknown.
Neurodegeneration is the progressive loss of structure or function of neurons, which may ultimately involve cell death. Many neurodegenerative diseases—such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, and prion diseases—occur as a result of neurodegenerative processes. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the sub-cellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.
Latrepirdine, is an antihistamine drug which has been used clinically in Russia since 1983.
Gantenerumab is a monoclonal antibody for the treatment of Alzheimer's disease being developed by Hoffmann-La Roche pharmaceuticals.
Steven T. DeKosky is the Aerts-Cosper Professor of Alzheimer's Research at the University of Florida (UF) College of Medicine, deputy director of UF’s Evelyn F. and William L. McKnight Brain Institute (MBI) and associate director of the 1Florida Alzheimer’s Disease Research Center.
Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.
Early-onset Alzheimer's disease, also called younger-onset Alzheimer's, familial Alzheimer's disease (FAD) or early-onset familial Alzheimer's disease (EOFAD), is Alzheimer's disease diagnosed before the age of 65. It is an uncommon form of Alzheimer's, accounting for only 5–10% of all Alzheimer's cases. About 60% have a positive family history of Alzheimer's and 13% of them are inherited in an autosomal dominant manner. Most cases of early-onset Alzheimer's share the same traits as the "late-onset" form and are not caused by known genetic mutations. Little is understood about how it starts.
The posterior parahippocampal gyrus is a portion of the parahippocampal gyrus.
The Tanz Centre for Research in Neurodegenerative Diseases is a research institute at the University of Toronto, under the umbrella of the Faculty of Medicine, with a focus on the spectrum of neurodegenerative diseases.
Rivastigmine is a cholinesterase inhibitor used for the treatment of mild to moderate Alzheimer's disease. The drug can be administered orally or via a transdermal patch; the latter form reduces the prevalence of side effects, which typically include nausea and vomiting.
Radequinil is a cognitive enhancer which acts as a partial inverse agonist of the benzodiazepine site of the GABAA receptor. It was under development by Dainippon Sumitomo Pharma for the treatment of Alzheimer's disease and made it to phase II clinical trials but development seems to have been halted and it was never marketed.
Carol Elspeth Goodeve Brayne CBE is a British academic and the Professor of Public Health Medicine at the University of Cambridge and Chair of Wellcome's Population and Public Health Review Group. She is Director of the Cambridge Institute of Public Health.
Phenserine is a synthetic drug which has been investigated as a medication to treat Alzheimer's disease (AD), as the drug exhibits neuroprotective and neurotrophic effects.
Constantine G. Lyketsos, is the Elizabeth Plank Althouse Professor in Alzheimer's Disease Research in the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins University, Baltimore, Maryland, United States. He is the founding director of the Richman Family Precision Medicine Center of Excellence in Alzheimer's Disease, and an associate director of the Johns Hopkins Alzheimer's Disease Research Center (ADRC).
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