Description
Here is a rephrased overview of recent SS‑31 research highlighting its effects on cognition and age‑related mitochondrial decline:
* **Neuroprotective effects in inflammation‑induced memory loss:** In a 2019 mouse study, researchers induced neuroinflammation and mitochondrial damage using lipopolysaccharide. Animals exposed to LPS showed mitochondrial dysfunction, oxidative stress, neuronal apoptosis and loss of dendritic spines, which impaired hippocampus‑dependent learning and memory. Administration of elamipretide (SS‑31) ameliorated these effects—treated mice performed better in behavioral tests, showed reduced oxidative stress and neuroinflammation, and demonstrated restoration of brain‑derived neurotrophic factor (BDNF) signalling and synaptic protein expression. The authors concluded that the mitochondrion‑targeted peptide could counteract LPS‑induced cognitive deficits and may offer a therapeutic avenue for perioperative neurocognitive disorders.
* **Reversal of age‑related redox stress and muscle fatigue:** Another investigation evaluated whether SS‑31 could address age‑associated declines in mitochondrial function and exercise tolerance. Female mice aged 26 months received 3 mg/kg/day SS‑31 for eight weeks. Treatment reversed the age‑related drop in maximal mitochondrial ATP production and improved coupling of oxidative phosphorylation. Interestingly, these functional improvements occurred without increased mitochondrial protein expression or respiration in permeabilized muscle fibers. SS‑31 restored redox balance (more reduced glutathione state and reversal of cysteine S‑glutathionylation), increased gastrocnemius muscle mass and fatigue resistance, and significantly enhanced treadmill endurance. The study suggests that targeting mitochondrial oxidant production can address energetic defects and exercise intolerance, making elamipretide a promising candidate for improving mobility and quality of life in the elderly.
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Taken together, these studies show SS‑31’s potential to mitigate neuroinflammation‑driven cognitive deficits and to restore mitochondrial redox homeostasis, thereby enhancing both brain function and physical endurance in preclinical models.
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