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S. M. Sumi

Researcher at University of Washington

Publications -  35
Citations -  7658

S. M. Sumi is an academic researcher from University of Washington. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 24, co-authored 35 publications receiving 7274 citations.

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The Consortium to Establish a Registry for Alzheimer's Disease (CERAD): Part II. Standardization of the neuropathologic assessment of Alzheimer's disease

TL;DR: The Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed a practical and standardized neuropathology protocol for the postmortem assessment of dementia and control subjects, which provides neuropathologic definitions of such terms as “definite Alzheimer's disease” (AD), “probable AD,” “possible AD” and “normal brain” to indicate levels of diagnostic certainty.
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The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part X. Neuropathology Confirmation of the Clinical Diagnosis of Alzheimer's Disease

TL;DR: Despite the relatively high level of clinical diagnostic accuracy, further refinement of assessment batteries may facilitate distinction of non-AD dementias from AD.
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Absence of linkage of chromosome 21q21 markers to familial Alzheimer's disease

TL;DR: No evidence for linkage was found between familial Alzheimer's disease (FAD) and chromosome 21q21 markers (D 21S1/D21S72 and the amyloid beta gene) and data indicate that FAD is genetically heterogeneous.
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Alzheimer's disease: choline acetyltransferase activity in brain tissue from clinical and pathological subgroups.

TL;DR: Multivariate regression analysis showed myoclonus to be the single best predictor of low brain choline acetyltransferase activity in patients with Alzheimer's disease and a history of myOClonus.
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Amyloid β protein (Aβ) deposition in chromosome 14-linked Alzheimer's disease : Predominance of Aβ42(43)

TL;DR: The effects of the mutations in the presenilin 1:PS‐1 (S182) gene may be to cause or at least promote an early and excessive deposition of Aβ42(43) within the brain, a property shared with other inherited forms of AD.