BDNF trafficking and signaling impairment during early neurodegeneration is prevented by moderate physical activity

被引:12
作者
Almeida, Michael F. [1 ]
Chaves, Rodrigo S. [1 ]
Silva, Carolliny M. [1 ]
Chaves, Juliana C. S. [1 ]
Melo, Karla P. [1 ]
Ferrari, Merari F. R. [1 ]
机构
[1] Univ Sao Paulo, Inst Biosci, Dept Genet & Evolutionary Biol, Rua Matao 277,Cidade Univ, BR-05508090 Sao Paulo, SP, Brazil
来源
IBRO REPORTS | 2016年 / 1卷
基金
巴西圣保罗研究基金会;
关键词
TrkB receptor; Treadmill running; Hyperphosphorylated Tau; Early neurodegeneration; Aging; Hippocampus;
D O I
10.1016/j.ibror.2016.08.001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Physical exercise can attenuate the effects of aging on the central nervous system by increasing the expression of neurotrophins such as brain-derived neurotrophic factor (BDNF), which promotes dendritic branching and enhances synaptic machinery, through interaction with its receptor TrkB. TrkB receptors are synthesized in the cell body and are transported to the axonal terminals and anchored to plasma membrane, through SLP1, CRMP2 and Rab27B, associated with KIF1B. Retrograde trafficking is made by EDH-4 together with dynactin and dynein molecular motors. In the present study it was found that early neurodegeneration is accompanied by decrease in BDNF signaling, in the absence of hyperphosphorylated tau aggregation, in hippocampus of 11 months old Lewis rats exposed to rotenone. It was also demonstrated that moderate physical activity (treadmill running, during 6 weeks, concomitant to rotenone exposure) prevents the impairment of BDNF system in aged rats, which may contribute to delay neurodegeneration. In conclusion, decrease in BDNF and TrkB vesicles occurs before large aggregate-like p-Tau are formed and physical activity applied during early neurodegeneration may be of relevance to prevent BDNF system decay. (C) 2016 The Authors. Published by Elsevier Ltd on behalf of International Brain Research Organization.
引用
收藏
页码:19 / 31
页数:13
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