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Rhes as a Potential Modulator of PINK1/Parkin-Dependent Mitophagy in Huntington's Disease
J Integr Neurosci. 2026 Oct 26;25(10):53852. doi: 10.31083/JIN53852.ABSTRACTHuntington's disease (HD) is an inherited neurodegenerative disorder caused by cytosine-adenine-guanine (CAG) repeat expansion in the huntingtin (HTT) gene, resulting in progressive motor, cognitive, and psychiatric impairment. Despite the widespread expression of mutant huntingtin (mHTT), disease progression is characterized by the selective degeneration...Read more
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The postsynaptic scaffolding protein SAPAP3 shapes mitochondrial activity: the case of Huntington's disease
Cell Death Dis. 2026 Aug 7;17(1):936. doi: 10.1038/s41419-026-09156-4.ABSTRACTPostsynaptic scaffolding protein SAP90/PSD95-associated protein 3 (SAPAP3) modulates cortico-striatal signalling and regulates the maintenance of synaptic structure. Notably, SAPAP3 defects have been reported in several human psychiatric disorders that share pathophysiological features with Huntington's disease (HD), a neurodegenerative disorder characterized by the expression...Read more
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Bioinformatics Analysis to Reveal Potential Targets of Huntington's Disease
IET Syst Biol. 2026 Jan-Dec;20(1):e70088. doi: 10.1049/syb2.70088.ABSTRACTHuntington's disease (HD) is a progressive neurodegenerative disease resulted from the expansion of CAG repeats in huntingtin (HTT) gene and characterised by motor impairment, psychiatric disorders and cognitive decline. Currently, there are no available disease-modifying treatments. In this study, we performed an integrative analysis...Read more
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Computational modeling and preclinical evaluation support targeting somatic instability for Huntington's disease treatment
Nat Commun. 2026 Oct 28;17(1):11036. doi: 10.1038/s41467-026-78769-2.ABSTRACTGenetic modifiers of Huntington's disease (HD) disease onset and progression implicate somatic instability (SI) of the expanded CAG repeat as a key pathogenic driver, with MSH3 emerging as a therapeutic target. Here, we generated a computational model that uses HD patient data to infer...Read more
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Quantifying multidisciplinary collaboration in Huntington's disease before and after service redesign: a social network analysis
BMC Health Serv Res. 2026 Jul 28;26(1):1475. doi: 10.1186/s12913-026-15212-8.ABSTRACTBACKGROUND: Effective multidisciplinary collaboration underpins integrated care for people living with Huntington's disease (HD). Traditional evaluations focus on patient outcomes or self-reported collaboration, which may not capture the underlying structure of team interactions. Social network analysis (SNA) provides an objective method to...Read more
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Emotion regulation difficulties are selectively associated with executive and behavioural apathy in Huntington's disease
J Neurol. 2026 Oct 23;273(11):683. doi: 10.1007/s00415-026-14214-0.ABSTRACTOBJECTIVE: Apathy occurs frequently in psychiatric and neurological disorders and is associated with functional impairment, reduced quality of life, and caregiver burden. Its underlying mechanisms are incompletely understood, but recent studies indicate that apathy is multidimensional and has heterogeneous manifestations across disorders. Self-regulatory processes,...Read more
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Antidopaminergic Medications and Clinical Outcomes in Huntington Disease: Evidence From the PROOF-HD Placebo-Controlled Trial
Neurology. 2026 Nov 24;107(10):e218627. doi: 10.1212/WNL.0000000000218627. Epub 2026 Oct 22.ABSTRACTBACKGROUND AND OBJECTIVES: Antidopaminergic medications (ADMs), including vesicular monoamine transporter-2 (VMAT2) inhibitors and antipsychotics, are widely used to manage motor and psychiatric symptoms in Huntington disease (HD). Observational evidence suggests that ADM use may be associated with accelerated worsening of clinical...Read more
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Cas9 nickase-mediated contraction of CAG/CTG repeats is associated with phenotypic improvements in a Huntington's disease mouse model
Sci Transl Med. 2026 Oct 21;18(872):eaef9466. doi: 10.1126/scitranslmed.aef9466. Epub 2026 Oct 21.ABSTRACTExpanded CAG/CTG repeats cause more than 15 different diseases that all remain without a disease-modifying treatment. Because repeat length accounts for most of the variation in disease severity, contracting CAG/CTG repeats presents an attractive therapeutic avenue. Here, we show...Read more
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Neuroprotective Role of Withaferin A in Huntington's Disease: Current Evidence and Future Perspectives
Mol Neurobiol. 2026 Oct 17;63(1):975. doi: 10.1007/s12035-026-06274-0.ABSTRACTHuntington's disease (HD) is an inherited neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. Its pathogenesis involves mutant huntingtin aggregation, impaired proteostasis and autophagy, transcriptional dysregulation, mitochondrial dysfunction, oxidative stress, neuroinflammation and progressive neuronal loss. Withaferin A (WA), a...Read more
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Huntington's disease vasculopathy is barrier-type-selective and arteriolar-dominant with spatially-coupled astrogliosis and reversible by S1pr1 stimulation
Nat Commun. 2026 Sep 12;17(1):10775. doi: 10.1038/s41467-026-77474-4.ABSTRACTBrain vascular barriers are dysfunctional in many neurological disorders, including Huntington's disease (HD), but which vessels are affected and how remains unclear. Using in vivo two-photon microscopy in R6/2 HD-model mice, we reveal a striking divergence in barrier dysfunction. Surface vessels of the blood-cerebrospinal...Read more
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Extracellular Vesicles and Exosomes as Biomarkers in Huntington's Disease: Uncovering Pathogenic Insights and Pioneering Therapies
Mol Neurobiol. 2026 Oct 7;63(1):951. doi: 10.1007/s12035-026-06205-z.ABSTRACTHuntington's disease (HD) is a neurodegenerative disorder caused by the expression of the mutant huntingtin protein (mHTT), characterized by a progressive decline in motor function, cognitive abilities, and psychiatric symptoms. Exosomes, a distinct class of small extracellular vesicles, have emerged as promising diagnostic biomarkers...Read more
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Monitoring huntingtin aggregation in Huntington's disease: methods, challenges and future opportunities
Expert Rev Proteomics. 2026 Oct;23(10):283-299. doi: 10.1080/14789450.2026.2741175. Epub 2026 Oct 29.ABSTRACTINTRODUCTION: Huntington's disease is characterized by the progressive misfolding and aggregation of mutant huntingtin, a dynamic process generating a heterogeneous spectrum of soluble oligomers, fibrillar assemblies and inclusion bodies. Increasing evidence suggests that distinct aggregation intermediates differ in their toxicity...Read more
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Chaperone-mediated remodelling of mutant huntingtin
Philos Trans R Soc Lond B Biol Sci. 2026 Oct 1;381(1960):20250269. doi: 10.1098/rstb.2025.0269.ABSTRACTHuntington's disease is caused by the trinucleotide repeat CAG expansion in the huntingtin gene, resulting in an N-terminal polyglutamine (polyQ) tract that renders the huntingtin protein (HTT) prone to misfolding and aggregation. Although polyQ expansion is an intrinsic...Read more
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Zebrafish as an Alternative Animal Model of Huntington's Disease: Challenges and Future Directions
J Integr Neurosci. 2026 Sep 22;25(9):49403. doi: 10.31083/JIN49403.ABSTRACTHuntington's disease (HD) is a lethal autosomal dominant neurodegenerative disorder characterized by progressing cognitive, motor, and other behavioral deficits. Animal models, especially rodent-based, are a valuable tool to study brain disorders, including HD. Given the existence of multiple valid and predictive models of...Read more
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Sex-dependent mild cardiac dysfunction and neurometabolic abnormalities in a model of Huntington's disease
Dis Model Mech. 2026 Sep 1;19(9):dmm052922. doi: 10.1242/dmm.052922. Epub 2026 Sep 30.ABSTRACTHuntington's disease (HD) is a neurodegenerative disease with progressive decline in psychiatric, motor and cognitive symptoms. Hallmarks of HD include brain volume loss and abnormal metabolism. However, HD is a multi-system disorder, and the impact on other organ systems...Read more
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