Study summary · research use only
Mitochondrial-Derived Peptides: Implication in the Therapy of Neurodegenerative Diseases
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review examines literature on mitochondrial-derived peptides (MDPs) — humanin, MOTS-c, and small humanin-like peptides (SHLPs) — in neurodegenerative disease models, drawing on studies retrieved from PubMed, Scopus, and Web of Science. The authors describe MDPs' reported roles in Amyloid-beta (Aβ) toxicity in Alzheimer's disease, dopaminergic neuron loss in Parkinson's disease, and mutant huntingtin aggregation in Huntington's disease models, and their reported association with reduced oxidative stress and neuroinflammation. The review states current research remains limited in defining the precise molecular pathways involved and identifies gaps in understanding MDP mechanisms, targeted delivery, and clinical translation as areas for future study.
Abstract
Mitochondrial-derived peptides (MDPs), including humanin, MOTS-c, and small humanin-like peptides (SHLPs), have emerged as promising therapeutic candidates for neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). This review systematically evaluates current literature retrieved from databases including PubMed, Scopus, and Web of Science using keywords such as "mitochondrial-derived peptides," "neurodegeneration," "humanin," "MOTS-c," and "SHLPs." Studies were included based on their relevance to mitochondrial function, oxidative stress, neuroprotection, and anti-inflammatory mechanisms in AD, PD, and HD models. Despite growing interest, current research remains limited in understanding the precise molecular pathways. Our review highlights their role in mitigating disease-specific pathologies such as Amyloid-beta (Aβ) toxicity in AD, dopaminergic neuron loss in PD, and mutant huntingtin aggregation in HD while also emphasizing their potential to attenuate oxidative stress and neuroinflammation. By identifying critical knowledge gaps, particularly in the areas of molecular mechanisms of MDPs in neuroprotection, targeted delivery, and clinical translation, this review provides a comprehensive framework to guide future investigations.
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