Transforming Growth Factor Beta Type I Role in Neurodegeneration: Implications for Alzheimer's Disease

被引：50

作者：

Estrada, Lisbell D. ^{[1
]}

Oliveira-Cruz, Luciana ^{[1
]}

Cabrera, Daniel ^{[2
,3
]}

机构：

[1] Univ Bernardo O Higgins, CIBQA, POB 0000-000, Santiago, Chile

[2] Univ Bernardo O Higgins, Fac Salud, Dept Ciencias Quim & Biol, Santiago, Chile

[3] Pontificia Univ Catolica Chile, Fac Med, Dept Gastroenterol, Santiago, Chile

来源：

CURRENT PROTEIN & PEPTIDE SCIENCE | 2018年 / 19卷 / 12期

关键词：

Transforming growth factor-beta 1; Alzheimer's disease; amyloid-beta; oligomers; Smad signaling; neuroprotection; neuroinflammation; microglia; TGF-BETA; AMYLOID-BETA; TRANSGENIC MICE; SYNAPTIC PLASTICITY; GENE-EXPRESSION; UP-REGULATION; DNA-BINDING; TGF-BETA-1; PROTEIN; GROWTH-FACTOR-BETA-1;

D O I：

10.2174/1389203719666171129094937

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alzheimer's disease is a neurodegenerative condition affecting millions of people worldwide. Alzheimer's symptoms include memory loss and cognitive decline. Pathologically, the hallmarks of Alzheimer's are the presence of Amyloid beta-plaques, neurofibrillary tangles, and neuronal loss. Unfortunately, no cure is presently available and current treatments are only symptomatic. Transforming growth factor beta type I (TGF-beta 1) is a trophic factor involved in neuronal development and synaptic plasticity. Impairment of TGF-beta 1 signaling is associated with exacerbated A beta deposition and neurofibrillary tangle formation, which increases neurodegeneration. Aging and chronic inflammation reduce the canonical TGF-beta 1/Smad signaling, facilitating cytotoxic activation of microglia and microgliamediated neurodegeneration This review gathers together evidence for a neuroprotective role of TGF-beta in Alzheimer's disease. Restoring TGF-beta 1 signaling impairment may be a new pharmacological strategy Alzheimer's treatment.

引用

页码：1180 / 1188

页数：9

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