Mitochondrial SIRT3 may protect neurons against Aβ pathology and excitotoxicity скачать в хорошем качестве

Mitochondrial SIRT3 may protect neurons against Aβ pathology and excitotoxicity

Mark Mattson, PhD, Johns Hopkins University School of Medicine, Baltimore, MD, discusses recent findings on the role of mitochondrial protein deacetylase sirtuin-3 (SIRT3) in protecting neurons against amyloid beta (Aβ) pathology and excitotoxicity. Significant reductions in SIRT3 levels have been shown in brain cells during aging. To investigate the impact of SIRT3 deficiency and the consequential increase in mitochondria protein acetylation, SIRT3-deficient mice were generated. These animal models showed mitochondrial protein hyperacetylation, neuronal network hyperexcitability, and increased sensitivity to kainic acid-induced seizures. When crossbred with APP/PS1 double mutant transgenic mice, SIRT3 deficiency caused a significant increase in amyloid pathology and cognitive deficits. Prof. Mattson explains that these findings implicate mitochondrial SIRT3 in regulating excitability and neuronal vulnerability to aging. This interview took place at the Alzheimer's Association International Conference (AAIC) 2022 in San Diego, CA.