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Published on: April 15, 2012
by Knox News
1900s: – Dr. Alois Alzheimer presents case study and Alzheimer’s disease is named.
1920s: – Amyloid is identified as the core substance of plaques.
1930s: – Familial AD is first suggested.
1940s: – Belief persists that senile dementia is normal part of aging caused by cerebral arteriosclerosis.
1950s: – Biological structure of plaques and tangles is investigated.
1960s: – Landmark study suggests that dementia is directly related to the number of senile plaques present in the cerebral cortex.
– Structure of neurofibrillary tangles is described as “paired helical filaments.”
1970s: – National Institute on Aging is created and assumes lead role in AD research.
– Mini-Mental State Exam is introduced.
– Memory and cholinergic function are linked; reduction of choline acetyltransferase is seen in AD.
– Editorial describes AD as a major public health problem and “Alzheimer’s disease” becomes a common term.
– Coalition of grassroots AD advocacy groups begins to rally public awareness of and interest in AD research.
1980s: – National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria are written.
– Alzheimer’s Disease and Related Disorders Association forms, becomes the Alzheimer’s Association.
– First Alzheimer’s Disease Research Centers are funded by NIA.
– Diagnostic and Statistical Manual of Mental Disorders (DSM III) categorizes AD.
– Clinical Dementia Rating (CDR) scale is established.
– Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) is created by NIA.
– AD is linked to chromosome 21 and amyloid precursor protein.
– Beta-amyloid protein is sequenced.
– NIA forms the Alzheimer’s Disease Education and Referral (ADEAR) Center.
1990s: – Food and Drug Administration approves tacrine (Cognex) following successful clinical trial.
– NIA funds Alzheimer’s Disease Cooperative Study.
– First amyloid precursor protein (APP) mutation is discovered.
– Early onset genes and late onset risk factor gene are discovered.
– First in series of transgenic mice models is created.
– Abnormal tau in neurofibrillary tangles is identified.
– NIA-Reagan criteria for AD pathology diagnosis are developed.
– Mutation in tau gene is cause of some chromosome 17 frontotemporal dementia.
– National Alzheimer’s Coordinating Center is formed.
– Mild Cognitive Impairment (MCI) characteristics are defined.
2000s: – Clinical trials, initiatives, and studies examine cholinesterase inhibitors, anti-inflammatories, vitamins, statins, supplements, valproate, antioxidants, hormones, beta amyloid vaccines and alternative medicines.
– Late Onset Alzheimer’s Disease Genetics Study begins.
– Alzheimer’s Disease Neuroimaging Initiative is launched.
– Pittsburgh B compound is developed, allowing researchers to “see” amyloid plaques in PET scans.
– Triple transgenic mouse is introduced.
– New focus on translational studies to facilitate drug discovery and development begins.
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