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Annamalai Prakasam

Researcher at Medical University of South Carolina

Publications -  10
Citations -  830

Annamalai Prakasam is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Alzheimer's disease & Amyloid precursor protein. The author has an hindex of 10, co-authored 10 publications receiving 756 citations.

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High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice.

TL;DR: Cognitive performance in rodent models of hypercholesterolemia in relation to neuroinflammatory changes and amyloid precursor protein (APP) processing, the two key parameters of Alzheimer's disease pathogenesis are evaluated.
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Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model

TL;DR: Evidence is provided that vitamin E delays onset of cognitive and morphological abnormalities in a mouse model of DS, and may represent a safe and effective treatment early in the progression of DS neuropathology.
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Neuronutrition and Alzheimer's disease.

TL;DR: Beneficial dietary techniques in the fight against AD are summarized and several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
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A Partial Failure of Membrane Protein Turnover May Cause Alzheimers Disease: A New Hypothesis

TL;DR: This theory would predict that focussing on specific reagents such as gamma-secretase inhibitors that hamper metabolism of APP, may initially show some beneficial effects on cognitive performance by elimination of acutely toxic ADDLs, but over the longer term may exacerbate the disease process by reducing membrane protein turnover.
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Pigment Epithelium-derived Factor Maintains Retinal Pigment Epithelium Function by Inhibiting Vascular Endothelial Growth Factor-R2 Signaling through γ-Secretase

TL;DR: The hypothesis that misregulation of γ-secretase may not only lead to Aβ deposits in dry AMD but can also be damaging to RPE function by blocking the protective effects of PEDF to prevent VEGF from driving the dry to wet AMD transition is supported.