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Article Abstract
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764483 | PMC |
| http://dx.doi.org/10.1016/j.ymthe.2024.12.005 | DOI Listing |
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A small TAT-TrkB peptide prevents BDNF receptor cleavage and restores synaptic physiology in Alzheimer's disease.
Mol Ther
October 2024
Instituto de Farmacologia e Neurociências, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal. Electronic address:
Article Synopsis
- In Alzheimer's disease, amyloid beta (Aβ) triggers the cleavage of the TrkB-FL receptor, disrupting essential BDNF signaling that is crucial for neuron health and function.
- Researchers found that TrkB-FL cleavage occurs early in the disease and worsens with increased pathology, using human samples and cerebrospinal fluid for their studies.
- They developed a TAT-TrkB peptide that successfully prevents TrkB-FL cleavage, showing potential in improving cognitive function and synaptic issues in a mouse model of Alzheimer's, indicating it could be a safe and effective treatment option.