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 microglia-mediated 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1180-1188 |
| Number of pages | 9 |
| Journal | Current Protein and Peptide Science |
| Volume | 19 |
| Issue number | 12 |
| DOIs | |
| State | Published - 2018 |
| Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2018 Bentham Science Publishers.
Keywords
- Alzheimer´s disease
- Amyloid-beta
- Microglia
- Neuroinflammation
- Neuroprotection
- Oligomers
- Smad signaling
- Transforming growth factor-β1