Lisbell D. Estrada*, Luciana Oliveira-Cruz and Daniel Cabrera Pages 1180 - 1188 ( 9 )
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.
Transforming growth factor-β1, Alzheimer´s disease, amyloid-beta, oligomers, Smad signaling, neuroprotection, neuroinflammation, microglia.
Centro Integrativo de Biologia y Quimica Aplicada (CIBQA), Universidad Bernardo O Higgins, Santiago, Centro Integrativo de Biologia y Quimica Aplicada (CIBQA), Universidad Bernardo O Higgins, Santiago, Departamento de Ciencias Quimicas y Biologicas, Facultad de Salud, Universidad Bernardo O Higgins, Santiago