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Family functioning in Huntington's disease (HD) is known from previous studies to be adversely affected. However, which aspects of family functioning are disrupted is unknown, limiting the empirical basis around which to create supportive interventions.
In Huntington's disease (HD), it remains unclear how symptom severity and rate of symptomatic change relates to age and CAG repeat number (CAGn). It is often difficult for clinicians to assess whether an affected individual's symptoms are progressing at a similar rate to their affected peers, limiting their ability to intervene at the most appropriate time.
Huntington's disease (HD) is a fatal progressive neurodegenerative disease characterized by chorea, cognitive impairment and psychiatric symptoms. Retinal examination of HD patients as well as in HD animal models have shown evidence of retinal dysfunction. However, a detailed retinal study employing clinically available measurement tools has not been reported to date in HD.
A number of studies evaluating physical therapy and exercise interventions in Huntington's disease have been conducted over the past 15 years. However, an assessment of the quality and strength of the evidence in support of these interventions is lacking.
Blood biomarkers of neuronal damage could facilitate clinical management of and therapeutic development for Huntington's disease. We investigated whether neurofilament light protein NfL (also known as NF-L) in blood is a potential prognostic marker of neurodegeneration in patients with Huntington's disease.
Clinical Trials Corner of Journal of Huntington's Disease will regularly review ongoing and recently completed clinical trials in Huntington's disease. In this inaugural issue, we list all currently registered and ongoing clinical trials, expand on LEGATO-HD and IONIS-HTTRx, and cover two recently finished trials: Amaryllis and Pride-HD.
Huntington's disease (HD), is a neurodegenerative disorder that is associated with cognitive, behavioral, and motor impairments that diminish health related quality of life (HRQOL). The HD-PRO-TRIADTM is a quality of life measure that assesses health concerns specific to individuals with HD. Preliminary psychometric characterization was limited to a convenience sample of HD participants who completed measures at home so clinician-ratings were unavailable.
Huntington's disease (HD) is an autosomal dominant disorder caused by a CAG expansion in the huntingtin gene that results in expression of mutant huntingtin protein. Iron accumulates in HD brain neurons. Amyloid precursor protein (APP) promotes neuronal iron export. However, the role of APP in brain iron accumulation in HD is unclear.
Although the early and middle stages of Huntington's Disease (HD) and its complications have been well described, less is known about the course of late-stage illness. In particular, little is known about the population of patients who enroll in hospice.
R6/2 mice contain an N-terminal fragment of human huntingtin with an expanded polyQ and develop a neurological disease resembling Huntington disease. Although the brain of R6/2 mice contains numerous inclusions, there is very little neuronal death. In that respect, R6/2 mice differ from patients with Huntington disease whose striatum and cerebral cortex develop inclusions associated with extensive neuronal loss. We have previously demonstrated using synchrotron-based infrared microspectroscopy that the stri...
A consistent feature of predictive testing guidelines for Huntington's disease (HD) is the recommendation not to undertake predictive tests on those
Sleep disturbance occurs early in Huntington's disease (HD). Consumer- and research-grade activity monitors may enable routine assessment of sleep disturbances in HD. We compared Actiwatch Spectrum Pro, Jawbone UP2 and Fitbit One to the gold standard, polysomnography, in four late presymptomatic and three early HD participants. Compared to polysomnography, all ambulatory monitors overestimated total sleep time by >60 minutes and sleep efficiency by ∼15%. Thus, for assessment of specific sleep parameters i...
Motor disturbances are clinical hallmarks of Huntington's disease (HD) and involve chorea, dystonia, hypokinesia and visuomotor dysfunction. Investigating the association between specific motor signs and different regional volumes is important to understand the heterogeneity of HD.
The huntingtin gene has two mRNA isoforms that differ in their 3' UTR length. The relationship of these isoforms with Huntington's disease is not established. We provide evidence that the abundance of huntingtin 3' UTR isoforms differs between patient and control neural stem cells, fibroblasts, motor cortex, and cerebellum. Huntingtin 3' UTR isoforms, including a mid-3' UTR isoform, have different localizations, half-lives, polyA tail lengths, microRNA sites, and RNA-binding protein sites. Isoform shifts in...
Huntington's disease (HD) is an autosomal, dominantly inherited, neurodegenerative disease. The main clinical features are motor impairment, progressive cognitive deterioration and behavioral changes. The aim of our study was to find out whether patients with HD suffer from disorders of the auditory system.
Motor dysfunction is a major component of the Huntington's disease (HD) phenotype, both in patients and animal models. Motor function in mice is usually measured using tests that involve a novel environment, or require a degree of learning, which creates potential confounds in animals, such as anxiety and/or learning.
In this issue of Neuron, Gasset-Rosa et al. (2017) and Grima et al. (2017) describe defects in the nuclear pore complex and impaired nucleocytoplasmic transport in Huntington's disease (HD). The findings suggest that erosion of nuclear gatekeeping function, which is found in normal brain aging, may play an important role in the pathogenesis of multiple neurodegenerative disorders, including HD.
Huntington disease (HD) affects the nervous system and leads to mental and motor dysfunction. Previous studies have shown that HD is caused by the exon 1 region of the huntingtin (HTT) gene having expanded CAG trinucleotide repeats. However, few studies have focused on the relationship between HD and pain. The purpose of this study is to investigate the relationship between HD and pain response.
To present a case of Huntington's disease (HD) with severe neck infection.
Although Huntington's disease (HD) is primarily considered a rare neurodegenerative disorder, it has been linked to glucose metabolism alterations and diabetes, as has been described in other neuro syndromes such as Friedreich's ataxia or Alzheimer's disease. This review surveys the existing literature on HD and its potential relationship with diabetes, glucose metabolism-related indexes and pancreas morphology, in humans and in animal's models. The information is reported in chronological sequence. That is...
In Huntington's Disease (HD) cognitive decline can occur before unequivocal motor signs become apparent. As cognitive decline often starts early in the course of the disease and has a progressive nature over time, cognition can be regarded as a key target for symptomatic treatment. The specific progressive profile of cognitive decline over time is unknown.
Little is known about the importance of the Mediterranean Diet (MeDi) and dietary intake as environmental neuroprotective factors in Huntington's disease (HD); so, we evaluated and analyzed the prevalence and factors associated with MeDi adherence, and dietary intake in HD.
Huntington's disease is an inherited, degenerative brain disease, characterized by involuntary movements, cognitive disorder and neuropsychiatric change. Men and women are affected equally. Symptoms emerge at around 40 years, although there is wide variation. A rare juvenile form has onset in childhood or adolescence. The evolution of disease is insidious and structural and functional brain changes may be present more than a decade before symptoms and signs become manifest. The earliest site of pathology is...
Huntington's disease (HD) is an autosomal-dominant inherited neurodegenerative disorder, characterized by motor, psychiatric and cognitive symptoms for which as yet no causal treatment is available. It has a prevalence of 1 : 10 000 in Germany. Its cause is a mutation in the Huntington gene (CAG-repeat). The mutation induces a polyglutamine expansion in the huntingtin protein (HTT). Mutant HTT (mHTT) has cytotoxic properties, aggregates in the cell and leads to complex pathophysiological disturbances ...