神经发生
齿状回
神经退行性变
瘦素
星形胶质增生
老年斑
神经干细胞
神经科学
室下区
海马体
亚颗粒带
小鼠苗条素受体
生物
阿尔茨海默病
内分泌学
病理
医学
干细胞
中枢神经系统
细胞生物学
疾病
肥胖
作者
Michele Longoni Calió,Amanda Cristina Mosini,Darci Souza Marinho,Geisa Nogueira Salles,Fernando Henrique Massinhani,Gui Mi Ko,Marimélia Porcionatto
标识
DOI:10.1016/j.nbd.2020.105219
摘要
Alzheimer's disease (AD) is the most common dementia worldwide and is characterized by the presence of senile plaques by amyloid-beta (Aβ) and neurofibrillary tangles of hyperphosphorylated Tau protein. These changes lead to progressive neuronal degeneration and dysfunction, resulting in severe brain atrophy and cognitive deficits. With the discovery that neurogenesis persists in the adult mammalian brain, including brain regions affected by AD, studies of the use of neural stem cells (NSCs) for the treatment of neurodegenerative diseases to repair or prevent neuronal cell loss have increased. Here we demonstrate that leptin administration increases the neurogenic process in the dentate gyrus of the hippocampus as well as in the subventricular zone of lateral ventricles of adult and aged mice. Chronic treatment with leptin increased NSCs proliferation with significant effects on proliferation and differentiation of newborn cells. The expression of the long form of the leptin receptor, LepRb, was detected in the neurogenic niches by reverse qPCR and immunohistochemistry. Moreover, leptin modulated astrogliosis, microglial cell number and the formation of senile plaques. Additionally, leptin led to attenuation of Aβ-induced neurodegeneration and superoxide anion production as revealed by Fluoro-Jade B and dihydroethidium staining. Our study contributes to the understanding of the effects of leptin in the brain that may lead to the development of new therapies to treat Alzheimer's disease.
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