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.
Our event with Dr. Wendy Suzuki explaining how higher levels of physical fitness are associated with better brain structure and higher cognitive function. Highlights video.
Our event with Dr. Wendy Suzuki explaining how higher levels of physical fitness are associated with better brain structure and higher cognitive function. Full video.
Two blood markers, phosphorylated tau 217 (p-tau217) and phosphorylated tau 181 (p-tau181), showed strong diagnostic performances for Alzheimer’s disease and discriminated Alzheimer’s from frontotemporal lobar denervation (FTLD) syndromes and normal cognition, a retrospective study...
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