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Trey Sunderland

Researcher at National Institutes of Health

Publications -  231
Citations -  14453

Trey Sunderland is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 59, co-authored 231 publications receiving 14036 citations. Previous affiliations of Trey Sunderland include University of Rochester Medical Center.

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Mood disorders in the medically ill: scientific review and recommendations.

TL;DR: A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between mood disorders and many medical illnesses and there is evidence to suggest that mood disorders affect the course of medical illnesses.
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Clock drawing in Alzheimer's disease. A novel measure of dementia severity.

TL;DR: Although the Clock Drawing Test is certainly not a definitive indicator of Alzheimer's disease, the test is easy to administer and provides a useful measure of dementia severity for both research and office settings where sophisticated neuropsychological testing is not available.
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Diagnosis and treatment of Alzheimer disease and related disorders. Consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer's Association, and the American Geriatrics Society.

TL;DR: A consensus conference on the diagnosis and treatment of Alzheimer disease and related disorders was organized by the American Association for Geriatric Psychiatry, the Alzheimer's Association, and the American Geriatrics Society on January 4 and 5, 1997, and reached consensus.
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Decreased beta-amyloid1-42 and increased tau levels in cerebrospinal fluid of patients with Alzheimer disease.

TL;DR: The findings suggest that the 2 measures, CSF beta-amyloid and tau, are biological markers of AD pathophysiology and may have a potential clinical utility as biomarkers of disease.
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Participation of Presenilin 2 in Apoptosis: Enhanced Basal Activity Conferred by an Alzheimer Mutation

TL;DR: A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity, which might accelerate the process of neurodegeneration that occurs in Alzheimer’s disease, leading to the earlier age of onset characteristic of familial Alzheimers disease.