Results 61 to 70 of about 2,427 (143)
Brain and Behavior, Volume 16, Issue 4, April 2026.This study examined lifetime stressor exposure in adolescents at genetic risk for Huntington disease (HD) compared to community controls. At‐risk participants reported significantly greater lifetime stressor exposure than controls and were more likely to report externalizing problems such as rule‐breaking behavior when exposed to stress.
Katherine E. McDonell +7 more
wiley +1 more source
4472 Plasma Neurofilament Light as a Biomarker for Pediatric Patients with Huntington’s Disease
Journal of Clinical and Translational Science, 2020 OBJECTIVES/GOALS: The goal of this study is to compare plasma neurofilament light (NfL) concentrations in asymptomatic children and young adults that carry the gene expansion (GE group) that causes Huntington’s Disease to similar subjects that do not ...
Jordan L Schultz
doaj +1 more source
Biological Reviews, Volume 101, Issue 2, Page 911-925, April 2026.ABSTRACT Three categories of explanations exist for why we age: mechanistic theories, which omit reference to evolutionary forces; weakening force of selection theories, which posit that barriers exist that prevent evolutionary forces from optimising fitness in ageing; and optimisation theories, which posit that evolutionary forces actually select for ...
Michael S. Ringel
wiley +1 more source
Neurobiology of Disease, 2009 The R6/2 mouse is the most common mouse model used for Huntington's disease (HD), a fatal, inherited neurodegenerative CAG disorder characterized by marked brain atrophy. We scanned 47 R6/2 transgenic and 42 wildtype (WT) ex vivo mouse brains at 18 weeks
S.J. Sawiak +4 more
doaj +1 more source
The Clinical Manifestation of Homozygous Huntington's Disease
Clinical Case Reports, Volume 14, Issue 4, April 2026.ABSTRACT Huntington's disease is an incurable neurodegenerative disease with deficits in many areas including cognitive, psychiatric, and most notably, motor. It is autosomal dominant, meaning one affected allele is enough to express the condition.
Brishti Sengupta, Pritha Dasgupta
wiley +1 more source
Neurobiology of Disease, 2014 Spinocerebellar ataxias (SCAs) are hereditary diseases leading to Purkinje cell degeneration and cerebellar dysfunction. Most forms of SCA are caused by expansion of CAG repeats similar to other polyglutamine disorders such as Huntington's disease.
Jingmin Ji +5 more
doaj +1 more source
Neurobiology of Disease, 2016 Ataxin-2 (ATXN2) polyglutamine domain expansions of large size result in an autosomal dominantly inherited multi-system-atrophy of the nervous system named spinocerebellar ataxia type 2 (SCA2), while expansions of intermediate size act as polygenic risk ...
Nesli Ece Sen +10 more
doaj +1 more source
Juvenile Huntington's Disease: A Case Report and a Review of Diagnostic Challenges. [PDF]
Cureus, 2023 Yu SY, Gough S, Niyibizi A, Sheikh M.
europepmc +1 more source
Neuropathology in juvenile Huntington disease
Journal of Neuropathology and Experimental Neurology, 2007 Juvenile onset Huntington disease (HD) often has variant clinical and neuropathological features: Case 1 (CAG repeat length 140): Onset age 3 with so‐called cerebral palsy. By age 5 marked dysarthria, bradykinesia and extensor plantar responses.
openaire +1 more source
Clinical and genetic analysis of juvenile-onset Huntington's disease: 10 cases report
Chinese Journal of Contemporary Neurology and Neurosurgery, 2017 Objective To investigate the clinical features and dynamic mutation of 10 cases with juvenile-onset Huntington's disease (HD). Methods The cytosine-adenine-guanine (CAG) repeats of IT15 gene were detected by polymerase chain reaction (PCR) and capillary
Ying HAO +4 more
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