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Jae-sung Bae

Researcher at Kyungpook National University

Publications -  142
Citations -  9000

Jae-sung Bae is an academic researcher from Kyungpook National University. The author has contributed to research in topics: Mesenchymal stem cell & Microglia. The author has an hindex of 31, co-authored 129 publications receiving 7881 citations. Previous affiliations of Jae-sung Bae include Gwangju Institute of Science and Technology & University College London.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Human umbilical cord blood-derived mesenchymal stem cells improve neuropathology and cognitive impairment in an Alzheimer's disease mouse model through modulation of neuroinflammation.

TL;DR: It is suggested that hUCB-MSC produced their sustained neuroprotective effect by inducing a feed-forward loop involving alternative activation of microglial neuroinflammation, thereby ameliorating disease pathophysiology and reversing the cognitive decline associated with Aβ deposition in AD mice.
Journal ArticleDOI

Mesenchymal stem cells enhance autophagy and increase β-amyloid clearance in Alzheimer disease models

TL;DR: It is suggested that mesenchymal stem cells significantly enhance autolysosome formation and clearance of Aβ in AD models, which may lead to increased neuronal survival against Aβ toxicity.
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Bone marrow-derived mesenchymal stem cells reduce brain amyloid-β deposition and accelerate the activation of microglia in an acutely induced Alzheimer's disease mouse model

TL;DR: Evidence is provided that BM-MSCs can promote the reduction of Abeta through the microglial activation in this acutely induced AD brain, suggesting a potential therapeutic agent against AD.