| First Author | Castello NA | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 8 | Pages | e39566 |
| PubMed ID | 22870188 | Mgi Jnum | J:189666 |
| Mgi Id | MGI:5446830 | Doi | 10.1371/journal.pone.0039566 |
| Citation | Castello NA, et al. (2012) Genetic knockdown of brain-derived neurotrophic factor in 3xTg-AD mice does not alter Abeta or tau pathology. PLoS One 7(8):e39566 |
| abstractText | Brain-derived neurotrophic factor (BDNF) is a neurotrophin critically involved in cell survival, synaptic plasticity, and memory. BDNF has recently garnered significant attention as a potential therapeutic target for neurodegenerative diseases such as Alzheimer disease (AD), but emerging evidence suggests that BDNF may also be mechanistically involved in the pathogenesis of AD. AD patients have substantially reduced BDNF levels, which may be a result of Abeta and tau pathology. Recent evidence, however, indicates reduced BDNF levels may also serve to drive pathology in neuronal cultures, although this has not yet been established in vivo. To further investigate the mechanistic role of BDNF in AD, we generated 3xTg-AD mice with a heterozygous BDNF knockout (BDNF(+/-)) and analyzed Abeta and tau pathology. Aged 3xTg-AD/BDNF(+/-) mice have significantly reduced levels of brain BDNF, but have comparable levels of Abeta and tau pathology to 3xTg-AD/BDNF(+/+) mice. These findings indicate that chronic reduction of BDNF does not exacerbate the development of Abeta and tau pathology, and instead suggests the reduced BDNF levels found in AD patients are a consequence of these pathologies. |
