{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T16:14:03Z","timestamp":1789834443580,"version":"4.0.1"},"reference-count":133,"publisher":"SAGE Publications","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2023,5,30]]},"abstract":"<jats:p>The pathogenesis of Alzheimer\u2019s disease (AD) is complicated and involves multiple contributing factors. Mounting evidence supports the concept that AD is an age-related metabolic neurodegenerative disease mediated in part by brain insulin resistance, and sharing similar metabolic dysfunctions and brain pathological characteristics that occur in type 2 diabetes mellitus (T2DM) and other insulin resistance disorders. Brain insulin signal pathway is a major regulator of branched-chain amino acid (BCAA) metabolism. In the past several years, impaired BCAA metabolism has been described in several insulin resistant states such as obesity, T2DM and cardiovascular disease. Disrupted BCAA metabolism leading to elevation in circulating BCAAs and related metabolites is an early metabolic phenotype of insulin resistance and correlated with future onset of T2DM. Brain is a major site for BCAA metabolism. BCAAs play pivotal roles in normal brain function, especially in signal transduction, nitrogen homeostasis, and neurotransmitter cycling. Evidence from animal models and patients support the involvement of BCAA dysmetabolism in neurodegenerative diseases including Huntington\u2019s disease, Parkinson\u2019s disease, and maple syrup urine disease. More recently, growing studies have revealed altered BCAA metabolism in AD, but the relationship between them is poorly understood. This review is focused on the recent findings regarding BCAA metabolism and its role in AD. Moreover, we will explore how impaired BCAA metabolism influences brain function and participates in the pathogenesis of AD.<\/jats:p>","DOI":"10.3233\/jad-221147","type":"journal-article","created":{"date-parts":[[2023,4,25]],"date-time":"2023-04-25T12:33:53Z","timestamp":1682426033000},"page":"847-862","source":"Crossref","is-referenced-by-count":21,"title":["Insulin Resistance and Impaired Branched-Chain Amino Acid Metabolism in Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"93","author":[{"given":"Rui","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Public Health and Preventive Medicine, School of Medicine, Jianghan University, Wuhan, Hubei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Chinese Medicine, School of Medicine, Jianghan University, Wuhan, Hubei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"You","sequence":"additional","affiliation":[{"name":"Department of Public Health and Preventive Medicine, School of Medicine, Jianghan University, Wuhan, Hubei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-221147_ref1","doi-asserted-by":"crossref","first-page":"1589","DOI":"10.1016\/S0140-6736(19)30851-7","article-title":"Alzheimer\u2019s disease","volume":"393","author":"Barnett","year":"2019","journal-title":"Lancet"},{"key":"10.3233\/JAD-221147_ref2","doi-asserted-by":"crossref","first-page":"391","DOI":"10.1002\/alz.12068","article-title":"2020 Alzheimer\u2019s disease facts and figures","volume":"16","author":"Alzheimer\u2019s Association","year":"2020","journal-title":"Alzheimers Dement"},{"key":"10.3233\/JAD-221147_ref3","doi-asserted-by":"crossref","unstructured":"(2022) 2022 Alzheimer\u2019s disease facts and figures. 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