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M. Kerry O'Banion

Researcher at University of Rochester

Publications -  113
Citations -  7847

M. Kerry O'Banion is an academic researcher from University of Rochester. The author has contributed to research in topics: Neuroinflammation & Microglia. The author has an hindex of 41, co-authored 100 publications receiving 7022 citations. Previous affiliations of M. Kerry O'Banion include State University of New York System & University of Münster.

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Inflammatory processes in Alzheimer's disease.

TL;DR: While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle.
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ALS-causing SOD1 mutants generate vascular changes prior to motor neuron degeneration

TL;DR: It is reported here that amyotrophic lateral sclerosis–linked superoxide dismutase 1 (SOD1) mutants with different biochemical characteristics disrupted the blood–spinal cord barrier in mice by reducing the levels of the tight junction proteins ZO-1, occludin and claudin-5 between endothelial cells.
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The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective.

TL;DR: Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease.
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Sustained hippocampal IL-1β overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology

TL;DR: A transgenic mouse model of sustained IL-1 beta overexpression that was capable of driving robust neuroinflammation lasting months after transgene activation is described, characterized by astrocytic and microglial activation in addition to induction of proinflammatory cytokines.
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Neuroinflammatory processes in Alzheimer's disease.

TL;DR: Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD and a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or in concert account for the epidemiologically observed protection.