Journal
CURRENT PROTEIN & PEPTIDE SCIENCE
Volume 19, Issue 12, Pages 1180-1188Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389203719666171129094937
Keywords
Transforming growth factor-beta 1; Alzheimer's disease; amyloid-beta; oligomers; Smad signaling; neuroprotection; neuroinflammation; microglia
Categories
Funding
- FONDECYT Initiation into Research Grant [11130561]
- CONICYT [PIA /BASAL PFB 12]
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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.
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