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

Autor(es)

Almeida, Michael F. ; Chaves, Rodrigo S. ; Silva, Carolliny M. ; Chaves, Juliana C. S. ; Melo, Karla P. ; Ferrari, Merari F. R.

• Tipo de documento: Artigo Científico
• Fonte: IBRO REPORTS; v. 1, p. 13-pg., 2016-12-01.

Resumo

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. (AU)

• Processo FAPESP: 11/15281-0 - Efeitos do exercício físico moderado sobre o tráfego de neurotrofinas e seus receptores no sistema nervoso central de ratos idosos
• Beneficiário: Michael Fernandes de Almeida
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 11/00478-2 - Influência do cálcio e das proteínas MIRO na mobilidade mitocondrial anteriormente e durante a agregação de proteínas envolvidas em neurodegeneração
• Beneficiário: Rodrigo dos Santos Chaves
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 12/15495-2 - Tráfego mitocondrial e autofagocitose em neurônios dopaminérgicos humanos derivados de células-tronco embrionárias e de pluripotência induzida
• Beneficiário: Merari de Fátima Ramires Ferrari
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 11/15283-2 - Autofagocitose e estresse oxidativo no sistema nervoso central de ratos idosos submetidos ao exercício físico moderado
• Beneficiário: Carolliny Moura da Silva
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 13/08028-1 - CEGH-CEL - Centro de Estudos do Genoma Humano e de Células-Tronco
• Beneficiário: Mayana Zatz
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs