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Maya A. Koike

Researcher at University of California, Irvine

Publications -  17
Citations -  2694

Maya A. Koike is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Stroke & Brain ischemia. The author has an hindex of 13, co-authored 17 publications receiving 2180 citations. Previous affiliations of Maya A. Koike include University of Pennsylvania & University of California, San Francisco.

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Colony-Stimulating Factor 1 Receptor Signaling Is Necessary for Microglia Viability, Unmasking a Microglia Progenitor Cell in the Adult Brain

TL;DR: Surprisingly, extensive treatment results in elimination of ∼99% of all microglia brain-wide, showing that microglian homeostasis in the adult brain are physiologically dependent upon CSF1R signaling.
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A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia.

TL;DR: It is demonstrated that TREM2 interacts with endogenous ligands on neurons, forming a receptor–ligand pair connecting microglia with apoptotic neurons, directing removal of damaged cells to allow repair.
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Blocking IL-1 Signaling Rescues Cognition, Attenuates Tau Pathology, and Restores Neuronal β-Catenin Pathway Function in an Alzheimer’s Disease Model

TL;DR: It is reported that chronic dosing of 3xTg-AD mice with an IL-1R blocking Ab significantly alters brain inflammatory responses, alleviates cognitive deficits, markedly attenuates tau pathology, and partly reduces certain fibrillar and oligomeric forms of amyloid-β.
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Essential role of mitochondrial energy metabolism in Foxp3+ T-regulatory cell function and allograft survival

TL;DR: The data show that key OXPHOS regulators are required for optimal Treg function and Treg‐dependent allograft acceptance and give insights into the fundamental mechanisms by which mitochondrial energy metabolism regulates immune cell functions in vivo.
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Oligemic Hypoperfusion Differentially Affects Tau and Amyloid-β

TL;DR: This study indicates for the first time that total tau and amyloid-beta are differentially impacted by mild hypoperfusion, and results in a significant increase specifically in tau phosphorylated at serine and threonine and a tau epitope associated with paired helical filaments in AD patients.