Therapeutic Potential of P110 Peptide: New Insights into Treatment of Alzheimer's Disease

Mitochondrial degeneration in various neurodegenerative diseases, specifically in Alzheimer's disease, involves excessive mitochondrial fission and reduced fusion, leading to cell damage. P110 is a seven-amino acid peptide that restores mitochondrial dynamics by acting as an inhibitor of mitochondrial fission. However, the role of P110 as a neuroprotective agent in AD remains unclear. Therefore, we performed cell culture studies to evaluate the neuroprotective effect of P110 on amyloid-beta accumulation and mitochondrial functioning. Human SH-SY5Y neuronal cells were incubated with 1 mu M and 10 mu M of P110, and Real-Time PCR and Western blot analysis were done to quantify the expression of genes pertaining to AD and neuronal health. Exposure of SH-SY5Y cells to P110 significantly increased APP mRNA levels at 1 mu M, while BACE1 mRNA levels were increased at both 1 mu M and 10 mu M. However, protein levels of both APP and BACE1 were significantly reduced at 10 mu M of P110. Further, P110 treatment significantly increased ADAM10 and Klotho protein levels at 10 mu M. In addition, P110 exposure significantly increased active mitochondria and reduced ROS in live SH-SY5Y cells at both 1 mu M and 10 mu M concentrations. Taken together, our results indicate that P110 might be useful in attenuating amyloid-beta generation and improving neuronal health by maintaining mitochondrial function in neurons.

Automated summary

P110, a peptide that inhibits mitochondrial fission, has shown neuroprotective effects in Alzheimer's disease by maintaining mitochondrial function and attenuating amyloid-beta generation. Cell culture studies revealed that P110 increased the expression of genes related to AD, while reducing the protein levels of APP and BACE1.