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2000
Volume 19, Issue 12
  • ISSN: 1389-2037
  • E-ISSN: 1875-5550

Abstract

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-β1) is a trophic factor involved in neuronal development and synaptic plasticity. Impairment of TGF-β1 signaling is associated with exacerbated Aβ deposition and neurofibrillary tangle formation, which increases neurodegeneration. Aging and chronic inflammation reduce the canonical TGF-β1/Smad signaling, facilitating cytotoxic activation of microglia and microgliamediated neurodegeneration This review gathers together evidence for a neuroprotective role of TGF-β in Alzheimer's disease. Restoring TGF-β1 signaling impairment may be a new pharmacological strategy Alzheimer's treatment.

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/content/journals/cpps/10.2174/1389203719666171129094937
2018-12-01
2025-05-17
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