| First Author | Comerota MM | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 15012 |
| PubMed ID | 29118388 | Mgi Jnum | J:256940 |
| Mgi Id | MGI:6110354 | Doi | 10.1038/s41598-017-15357-x |
| Citation | Comerota MM, et al. (2017) Near infrared light decreases synaptic vulnerability to amyloid beta oligomers. Sci Rep 7(1):15012 |
| abstractText | Synaptic dysfunction due to the disrupting binding of amyloid beta (Abeta) and tau oligomers is one of the earliest impairments in Alzheimer''s Disease (AD), driving initial cognitive deficits and clinical manifestation. Consequently, there is ample consensus that preventing early synaptic dysfunction would be an effective therapeutic strategy for AD. With this goal in mind, we investigated the effect of a treatment of mice with near infrared (NIR) light on synaptic vulnerability to Abeta oligomers. We found that Abeta oligomer binding to CNS synaptosomes isolated from wild type (wt) mice treated with NIR light was significantly reduced and the resulting suppression of long term potentiation (LTP) by Abeta oligomers was prevented. Similarly, APP transgenic mice treated with NIR showed a significant reduction of endogenous Abeta at CNS synapses. We further found that these phenomena were accompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 mice. This study provides evidence that NIR light can effectively reduce synaptic vulnerability to damaging Abeta oligomers, thus furthering NIR light therapy as a viable treatment for AD. |
