{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:18:00Z","timestamp":1792034280467,"version":"4.4.0"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","license":[{"start":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T00:00:00Z","timestamp":1773446400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0 http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Huntington\u2019s disease is an autosomal dominant neurodegenerative disorder marked by progressive motor, cognitive, and psychiatric decline. Huntington\u2019s disease arises from the expansion of particular DNA sequences (cytosine\/ adenosine\/guanine repeats that encode glutamine) within the huntingtin (HTT) gene. This expansion leads to the synthesis of a mutant huntingtin protein (mhtt) featuring an excessively long polyglutamine segment, which is harmful and prone to form aggregates or clusters within cells. A range of abnormalities has been observed in both the central nervous system and peripheral tissues as a consequence of mhtt. These include inhibition in autophagy, mitochondrial dysfunction leading to metabolic deficiencies, immune system dysregulation, metabolic alterations, skeletal muscle deterioration, heart failure, testicular shrinkage, and bone density loss. Additionally, mhtt has been implicated in altering lipid metabolism pathways, leading to an increase in lipid accumulation, especially within neuronal cells. This lipid accumulation contributes significantly to cellular toxicity and dysfunction, further exacerbating the neurodegeneration seen in Huntington\u2019s disease. Although most studies have focused on neurological, behavioral, motor, and cognitive changes associated with Huntington\u2019s disease, several studies have reported changes in proteins, nucleic acids, lipids, and carbohydrate metabolism, which may lead to an anomalous molecular energy profile in individuals with Huntington\u2019s disease. This review will focus on understanding how metabolic changes may contribute to central alterations in Huntington\u2019s disease by analyzing preclinical and clinical evidence. Additionally, it will explore potential pathways that could be targeted to develop more effective treatments for Huntington\u2019s disease.<\/jats:p>","DOI":"10.4103\/nrr.nrr-d-25-01573","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T12:00:39Z","timestamp":1773662439000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Metabolic-based therapeutic strategies to treat Huntington\u2019s disease"],"prefix":"10.4103","author":[{"given":"Mariana Coelho","family":"Moraes","sequence":"first","affiliation":[{"name":"Department of Pharmacology, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muhammad Olanrewaju","family":"Buhari","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"},{"name":"PPG Neurosciences, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3496-6749","authenticated-orcid":false,"given":"Luciene Bruno","family":"Vieira","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7042-9433","authenticated-orcid":false,"given":"Fabiola Mara","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2026,3,14]]},"container-title":["Neural Regeneration Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ovid.com\/10.4103\/NRR.NRR-D-25-01573","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T13:25:49Z","timestamp":1787837149000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ovid.com\/10.4103\/NRR.NRR-D-25-01573"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,3,14]]},"references-count":0,"URL":"https:\/\/doi.org\/10.4103\/nrr.nrr-d-25-01573","relation":{},"ISSN":["1673-5374","1876-7958"],"issn-type":[{"value":"1673-5374","type":"print"},{"value":"1876-7958","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,3,14]]},"assertion":[{"value":"2025-10-17","name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-02-10","name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}}]}}