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Xinglong Wang

Researcher at Case Western Reserve University

Publications -  88
Citations -  15966

Xinglong Wang is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Mitochondrion & Neurodegeneration. The author has an hindex of 46, co-authored 88 publications receiving 13265 citations. Previous affiliations of Xinglong Wang include University of Nebraska Medical Center & University of Nebraska–Lincoln.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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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Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's Disease

TL;DR: DLP1 overexpression, likely through repopulation of neuronal processes with mitochondria, prevented ADDL-induced synaptic loss, suggesting that abnormal mitochondrial dynamics plays an important role in ADDL -induced synaptic abnormalities.
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Oxidative stress and mitochondrial dysfunction in Alzheimer's disease

TL;DR: Evidence not only demonstrates the full spectrum of oxidative damage to neuronal macromolecules, but also reveals the occurrence of oxidative events early in the course of the disease and prior to the formation of the pathology, which support an important role of oxidative stress in AD.
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Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins

TL;DR: APP, through amyloid β production, causes an imbalance of mitochondrial fission/fusion that results in mitochondrial fragmentation and abnormal distribution, which contributes to mitochondrial and neuronal dysfunction.
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Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease.

TL;DR: Changes in mitochondrial DNA and mitochondrial dynamics, two aspects critical to the maintenance of mitochondrial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD are focused on.