Authors
Jie Jiao, Hui Chen, Alexei Verkhratsky, Yixun Su, Chenju Yi
Published in
Molecular neurodegeneration. Volume 21. Issue 1. May 21, 2026. Epub May 21, 2026.
Abstract
Mitochondria transfer has emerged as a distinctive mechanism for intercellular communication and neuronal homeostasis. Neurones, owing to their unique bioenergetic demands, are particularly vulnerable to mitochondrial dysfunction, a shared pathogenetic feature across many neurological conditions, including neurodegenerative disorders, cerebrovascular diseases, and brain injuries. Intercellular transfer of mitochondria represents a potential adaptive mechanism rectifying compromised mitochondrial function. Neuroglial cells, especially astrocytes and microglia, frequently act as mitochondrial donors, supplying functional mitochondria to stressed neurones to restore bioenergetic capacity and influence disease trajectories. However, mitochondria transfer is intrinsically context dependent and can exert opposing effects. In addition to providing metabolic support, damaged mitochondria may also be transferred, propagating pathological signals, and exacerbating tissue injury. Moreover, in advanced disease states, mitochondrial malfunction often affects all cell types in the nervous system, including neuroglia, limiting the availability of healthy endogenous mitochondrial donors. This review critically examines mitochondria transfer in neurological diseases, with a focus on glial contribution and underlying mechanisms, and outlines key challenges and opportunities for advancing both mechanistic understanding and therapeutic translation.
PMID:
42169139
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.
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