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Although these disorders differ in clinical presentation and etiology, accumulating evidence points to a shared cellular vulnerability at the intersection of mitochondrial dynamics and actin cytoskeletal regulation. In this review, we examine the emerging role of actin\u2013mitochondria crosstalk as a convergent mechanism in neurodegeneration. We discuss how disruptions in actin filament remodeling, mitochondrial fission and fusion, organelle transport, and mitophagy contribute to neuronal dysfunction and loss across these diseases. Particular attention is given to disease\u2010specific pathways, including cofilin\u2010actin rod formation in AD, \u03b1\u2010synuclein\u2013driven actin disruption in PD, mutant huntingtin's effects on mitochondrial fragmentation in HD, and profilin\u20101\u2013associated mitochondrial defects in ALS. By synthesizing findings from diverse models, we highlight how perturbations in the cytoskeleton\u2013mitochondria interface may act as an upstream trigger and amplifier of neurodegenerative cascades. We also outline key knowledge gaps and propose future directions for research, with an emphasis on targeting actin\u2013mitochondrial interactions as a potential therapeutic strategy across multiple neurodegenerative conditions.<\/jats:p>","DOI":"10.1002\/cm.70095","type":"journal-article","created":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T10:32:59Z","timestamp":1767868379000},"page":"200-210","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Mitochondria and the Actin Cytoskeleton in Neurodegeneration"],"prefix":"10.1002","volume":"83","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-2045-2466","authenticated-orcid":false,"given":"Shivani","family":"Tuli","sequence":"first","affiliation":[{"name":"Department of Bioengineering University of Pittsburgh  Pittsburgh Pennsylvania 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