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Treadmill Exercise Represses Neuronal Cell Death And Inflammation During Amyloid beta‐Induced ER Stress By Regulating Unfolded Protein Response In Aged Presenilin 2 Mutant Mice
Author(s) -
Kang EunBum,
Kwon InSu,
Koo JungHoon,
Jang YongChul,
Lee Jin,
Cho InHo,
Lee Youngil,
Cho JoonYong
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb766
Subject(s) - unfolded protein response , presenilin , downregulation and upregulation , endoplasmic reticulum , inflammation , amyloid beta , apoptosis , genetically modified mouse , programmed cell death , caspase 12 , p38 mitogen activated protein kinases , endocrinology , medicine , neuroprotection , microbiology and biotechnology , chemistry , transgene , caspase , biology , alzheimer's disease , signal transduction , mapk/erk pathway , biochemistry , disease , gene
Alzheimer's disease (AD) is characterized by the deposition of aggregated amyloid‐beta (Aβ) in the brain, which triggers endoplasmic reticulum (ER) stress and inflammation and leads to apoptotic cell death. Growing evidence has suggested that endurance exercise is protective against neurodegenerative diseases including AD. However, the cellular mechanisms responsible for endurance exercise‐mediated brain protection against AD remain to be determined. Here, we show that treadmill exercise (TE) prevented memory impairment and reduced Aβ‐42 deposition via the inhibition of β‐secretase 1 in the brain of aged presenilin‐2 (PS2) mutant transgenic (Tg) mouse. Moreover, we found that TE inhibited ER stress‐induced unfolded protein response such as GRP78/Bip, and JNK‐p38 as well as the apoptotic pathways of the UPR such as CHOP, caspase‐12, caspase‐3 with upregulation of Bcl‐2 and downregulation of Bax in the hippocampus. Finally, TE attenuated the generation of TNF‐α and IL‐1β and the number of TUNEL‐positive cells. Collectively, these results suggest that TE will lead to important clinical benefits in the management of patients with AD and provide new insight into the mechanisms by which exercise protects the brain against AD.

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