LC3 overexpression reduces Aβ neurotoxicity through increasing α7nAchR expression and autophagic activity in neurons and mice.pdf.pdf

Neuropharmacology 93 (2015) 243e251
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Neuropharmacology
journal homepage: ate/neuropharm
LC3 overexpression reduces Ab neurotoxicity through increasing
a7nAchR expression and autophagic activity in neurons and mice
*
Shih-Ya Hung a, b, Wei-Pang Huang c, Houng-Chi Liou d, Wen-Mei Fu d,
a Department of Medical Research, China Medical University Hospital, Taichung 40447, Taiwan
b Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan
c Department of Life Science, National Taiwan University, Taipei 10617, Taiwan
d Pharmacological Institute, College of Medicine, National Taiwan University, Taipei 10051, Taiwan
article info abstract
Article history: Autophagy is an intracellular degradation pathway with dynamic interactions for eliminating damaged
Received 24 June anelles and protein aggregates by lysosomal digestion. The EGFP-conjugated microtubule-associated
Received in revised form protein 1 light chain 3 (EGFP-LC3) serves to monitor autophagic process. Extracellular b-amyloid peptide
26 January 2015
accumulation is reported as a major cause in Alzheimer's disease (AD) pathogenesis; large numbers of
Accepted 1 February 2015
autophagic vacuoles accumulate in patients' brains. We previously demonstrated that extracellular Ab
Available online 14 February