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Brittani R. Price

Researcher at University of Kentucky

Publications -  11
Citations -  517

Brittani R. Price is an academic researcher from University of Kentucky. The author has contributed to research in topics: Dementia & Medicine. The author has an hindex of 6, co-authored 8 publications receiving 259 citations. Previous affiliations of Brittani R. Price include Tufts University.

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White matter hyperintensities in vascular contributions to cognitive impairment and dementia (VCID): Knowledge gaps and opportunities

Jessica Alber, +53 more
TL;DR: Outstanding questions about white matter hyperintensities and their relation to cognition, dementia, and AD are identified and answered to improve prevention and treatment of WMHs and dementia.
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Hyperhomocysteinemia as a Risk Factor for Vascular Contributions to Cognitive Impairment and Dementia.

TL;DR: This review focuses on HHcy as a risk factor for VCID, specifically, the different mechanisms proposed for homocysteine-induced cognitive decline and the clinical trials aimed at lowering plasma homocy steine.
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An emerging role of astrocytes in vascular contributions to cognitive impairment and dementia.

TL;DR: This review discusses the existing body of literature regarding the role of astrocytes at the vasculature in the brain, and the known consequences of their dysfunction, as well as hypothesize that astroCytes are key mediators of cognitive impairment because of cerebrovascular disease.
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Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition

TL;DR: It is shown that chronic activation of Trem2, in the 5XFAD mouse model of amyloid deposition, leads to reversal of theAmyloid-associated gene expression signature, recruitment of microglia to plaques, decreased amyloids deposition, and improvement in spatial learning and novel object recognition memory.
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Time-course of glial changes in the hyperhomocysteinemia model of vascular cognitive impairment and dementia (VCID).

TL;DR: Astrocytic end-foot disruption could represent a common cellular mechanism of VCID and may be a target for therapeutic development.