Of the neurodegenerative diseases presented in this book, Huntington's disease (HD) stands as the archetypal autosomal dominantly inherited neurodegenerative disorder. Its occurrence through generations of affected families was noted long before the basic genetic underpinnings of hereditary diseases was understood. The early classification of HD as a distinct hereditary neurodegenerative disorder allowed the study of this disease to lead the way in the development of our understanding of the mechanisms of human genetic disorders. Following its clinical and pathologic characterization, the causative genetic mutation in HD was subsequently identified as a trinucleotide (CAG) repeat expansion in the huntingtin (HTT) gene, and consequently, the HTT gene and huntingtin protein have been studied in great detail. Despite this concentrated effort, there is still much about the function of huntingtin that still remains unknown. Presented in this chapter is an overview of the current knowledge on the normal function of huntingtin and some of the potential neurobiologic mechanisms by which the mutant HTT gene may mediate neurodegeneration in HD.
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http://dx.doi.org/10.1007/7854_2014_353 | DOI Listing |
Heliyon
January 2025
Anhui Medical University School of Basic Medicine, Hefei, 230032, China.
The anxieties and concerns about health hazards caused by microwave has been growing recently. Previous studies have reported microwave induced structural and functional injuries to brain. However, the biological effects caused by compound microwave were largely unexplored.
View Article and Find Full Text PDFMethods Cell Biol
January 2025
State University of Minas Gerais, Department of Biomedical Sciences and Health, Passos, MG, Brazil. Electronic address:
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by a repeat of the cytosine-adenine-guanine trinucleotide (CAG) in the huntingtin gene (HTT). This results in the translation of a mutant huntingtin (mHTT) protein with an abnormally long polyglutamine (polyQ) repeat. The pathology of HD leads to neuronal cell loss, motor abnormalities, and dementia.
View Article and Find Full Text PDFMetabolites
January 2025
Department of Obstetrics and Gynecology, Oakland University-William Beaumont School of Medicine, Rochester, MI 48309, USA.
Background: Huntington's disease (HD) is a multifaceted neurological disorder characterized by the progressive deterioration of motor, cognitive, and psychiatric functions. Despite a limited understanding of its pathogenesis, research has implicated abnormal trinucleotide cytosine-adenine-guanine CAG repeat expansion in the huntingtin gene (HTT) as a critical factor. The development of innovative strategies is imperative for the early detection of predictive biomarkers, enabling timely intervention and mitigating irreversible cellular damage.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Neurobiology and Behavior, University of California Irvine, Irvine, CA, USA.
Fluid biomarkers play important roles in many aspects of neurodegenerative diseases, such as Huntington's disease (HD). However, a main question relates to how well levels of biomarkers measured in CSF are correlated with those measured in peripheral fluids, such as blood or saliva. In this study, we quantified levels of four neurodegenerative disease-related proteins, neurofilament light (NfL), total tau (t-tau), glial fibrillary acidic protein (GFAP) and YKL-40 in matched CSF, plasma and saliva samples from Huntingtin (HTT) gene-positive individuals (n = 21) using electrochemiluminescence assays.
View Article and Find Full Text PDFNat Genet
January 2025
Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
Huntington's disease, one of more than 50 inherited repeat expansion disorders, is a dominantly inherited neurodegenerative disease caused by a CAG expansion in HTT. Inherited CAG repeat length is the primary determinant of age of onset, with human genetic studies underscoring that the disease is driven by the CAG length-dependent propensity of the repeat to further expand in the brain. Routes to slowing somatic CAG expansion, therefore, hold promise for disease-modifying therapies.
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