Mitochondrial antioxidant elamipretide improves learning and memory impairment induced by chronic sleep deprivation in mice

Brain Behav. 2024 May;14(5):e3508. doi: 10.1002/brb3.3508.

Abstract

Background: The inflammation and synaptic dysfunction induced by mitochondrial dysfunction play essential roles in the learning and memory impairment associated with sleep dysfunction. Elamipretide (SS-31), a novel mitochondrion-targeted antioxidant, was proven to improve mitochondrial dysfunction, the inflammatory response, synaptic dysfunction, and cognitive impairment in models of cerebral ischemia, sepsis, and type 2 diabetes. However, the potential for SS-31 to improve the cognitive impairment induced by chronic sleep deprivation (CSD) and its underlying mechanisms is unknown.

Methods: Adult c57BL/6J mice were subjected to CSD for 21 days using an activity wheel accompanied by daily intraperitoneal injection of SS-31 (5 mg/kg). The novel object recognition and Morris water maze test were used to evaluate hippocampus-dependent cognitive function. Western blotting and reverse transcription-quantitative polymerase chain reaction assays were used to determine the effects of CSD and SS-31 on markers of mitochondria, inflammation response, and synaptic function. Enzyme-linked immunosorbent assays were used to examine the levels of proinflammatory cytokines.

Results: SS-31 could improve the cognitive impairment induced by CSD. In particular, SS-31 treatment restored the CSD-induced decrease in sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator alpha levels and the increase in levels nuclear factor kappa-B and inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha. Furthermore, SS-31 significantly increased the levels of brain-derived neurotrophic factor, postsynaptic density protein-95, and synaptophysin in CSD mice.

Conclusion: Taken together, these results suggest that SS-31 could improve CSD-induced mitochondrial biogenesis dysfunction, inflammatory response, synaptic dysfunction, and cognitive impairment by increasing SIRT1 expression levels.

Keywords: SIRT1; SS‐31; inflammatory; learning and memory; mitochondrial dysfunction; synaptic proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants* / pharmacology
  • Cognitive Dysfunction / drug therapy
  • Cognitive Dysfunction / etiology
  • Disease Models, Animal
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Male
  • Memory Disorders / drug therapy
  • Memory Disorders / etiology
  • Mice
  • Mice, Inbred C57BL*
  • Mitochondria* / drug effects
  • Mitochondria* / metabolism
  • Oligopeptides* / administration & dosage
  • Oligopeptides* / pharmacology
  • Sirtuin 1 / metabolism
  • Sleep Deprivation* / complications
  • Sleep Deprivation* / drug therapy
  • Sleep Deprivation* / metabolism

Substances

  • arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide
  • Oligopeptides
  • Antioxidants
  • Sirtuin 1