{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:55:30Z","timestamp":1791291330659,"version":"4.3.0"},"reference-count":178,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:00:00Z","timestamp":1783468800000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Alzheimer's disease (AD) is a complex neurodegenerative disorder whose pathogenesis involves multi\u2010level pathological alterations. This review aims to systematically elucidate the central role and multifaceted molecular mechanisms of mitochondrial dysfunction in the progression of AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A comprehensive analysis of the existing literature was conducted, synthesizing findings from studies investigating mitochondrial involvement in AD pathology. The review focused on key mechanistic pathways, including energy metabolism deficits, oxidative stress, synaptic damage, mitochondrial dynamics, mitochondria\u2010associated membranes (MAMs), mitophagy, and the gut\u2013brain axis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The analysis revealed several critical mechanisms linking mitochondrial dysfunction to AD progression: (i) impaired mitochondrial energy metabolism, which establishes a causal relationship with oxidative stress and synaptic injury; (ii) dysregulation of mitochondrial fusion\/fission dynamics, particularly the aberrant interactions of amyloid\u2010beta (A\u03b2) and p\u2010Tau with the fission protein Drp1 and the channel protein VDAC1; (iii) dysfunction of mitochondria\u2010associated membranes (MAMs); (iv) defective mitophagy involving both the PINK1\/Parkin pathway and receptor\u2010mediated pathways; and (v) bidirectional crosstalk between mitochondria and the gut\u2013brain axis. These interconnected pathways converge to amplify neuroinflammation and neuronal death.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Accumulated evidence positions mitochondrial dysfunction as a critical hub that integrates A\u03b2\/Tau pathology, neuroinflammation, and neuronal loss, thereby perpetuating a self\u2010sustaining vicious cycle in AD. Targeting mitochondrial bioenergetics, dynamics, quality control, and the mitochondria\u2013inflammation axis offers substantial therapeutic promise. Emerging small molecules such as SS31 and DDQ have demonstrated protective effects in preclinical models. Future investigations should prioritize mechanistic dissection and translational research to facilitate the clinical development of mitochondria\u2010targeted therapies for AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.71418","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T16:06:04Z","timestamp":1783526764000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease"],"prefix":"10.1002","volume":"16","author":[{"given":"Tianyi","family":"Gu","sequence":"first","affiliation":[{"name":"College of Traditional Chinese Medicine Tianjin University of Traditional Chinese Medicine  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hangyan","family":"Guo","sequence":"additional","affiliation":[{"name":"College of Traditional Chinese Medicine Tianjin 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