{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T20:41:34Z","timestamp":1780778494139,"version":"3.54.1"},"reference-count":195,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2013,11,15]],"date-time":"2013-11-15T00:00:00Z","timestamp":1384473600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Psychotropics (antipsychotics, mood stabilizers, antidepressants, anxiolytics, etc.) are commonly prescribed to treat Huntington\u2019s disease (HD). In HD preclinical models, while no psychotropic has convincingly affected huntingtin gene, HD modifying gene, or huntingtin protein expression, psychotropic neuroprotective effects include upregulated huntingtin autophagy (lithium), histone acetylation (lithium, valproate, lamotrigine), miR-222 (lithium-plus-valproate), mitochondrial protection (haloperidol, trifluoperazine, imipramine, desipramine, nortriptyline, maprotiline, trazodone, sertraline, venlafaxine, melatonin), neurogenesis (lithium, valproate, fluoxetine, sertraline), and BDNF (lithium, valproate, sertraline) and downregulated AP-1 DNA binding (lithium), p53 (lithium), huntingtin aggregation (antipsychotics, lithium), and apoptosis (trifluoperazine, loxapine, lithium, desipramine, nortriptyline, maprotiline, cyproheptadine, melatonin). In HD live mouse models, delayed disease onset (nortriptyline, melatonin), striatal preservation (haloperidol, tetrabenazine, lithium, sertraline), memory preservation (imipramine, trazodone, fluoxetine, sertraline, venlafaxine), motor improvement (tetrabenazine, lithium, valproate, imipramine, nortriptyline, trazodone, sertraline, venlafaxine), and extended survival (lithium, valproate, sertraline, melatonin) have been documented. Upregulated CREB binding protein (CBP; valproate, dextromethorphan) and downregulated histone deacetylase (HDAC; valproate) await demonstration in HD models. Most preclinical findings await replication and their limitations are reviewed. The most promising findings involve replicated striatal neuroprotection and phenotypic disease modification in transgenic mice for tetrabenazine and for sertraline. Clinical data consist of an uncontrolled lithium case series (n = 3) suggesting non-progression and a primarily negative double-blind, placebo-controlled clinical trial of lamotrigine. <\/jats:p>","DOI":"10.3390\/ijms141122558","type":"journal-article","created":{"date-parts":[[2013,11,15]],"date-time":"2013-11-15T11:50:00Z","timestamp":1384516200000},"page":"22558-22603","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Neuroprotective Effects of Psychotropic Drugs in  Huntington\u2019s Disease"],"prefix":"10.3390","volume":"14","author":[{"given":"Edward","family":"Lauterbach","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Behavioral Sciences, Mercer University School of Medicine,  655 First Street, Macon, GA 31201, USA"},{"name":"Department of Internal Medicine, Neurology Section, Mercer University School of Medicine,  707 Pine Street, Macon, GA 31201, USA"},{"name":"Center for Translational Studies In Neurodegenerative Disease, Mercer University,  1400 Coleman Avenue, Macon, GA 31207, USA\u00a0"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2013,11,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"218","DOI":"10.1016\/S0140-6736(07)60111-1","article-title":"Huntington\u2019s disease","volume":"369","author":"Walker","year":"2007","journal-title":"Lancet"},{"key":"ref_2","first-page":"135","article-title":"Mitochondrial dysfunction, metabolic deficits, and increased oxidative stress in Huntington\u2019s disease","volume":"34","author":"Chen","year":"2011","journal-title":"Chang. 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