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The area of the brain most damaged in early Huntington's disease is the dorsal striatum made up of the caudate nucleus and the putamen. Initially, damage to the brain is regionally specific with the dorsal striatum in the subcortical basal ganglia being primarily affected, followed later by cortical involvement in all areas.
Huntington's disease is a neurodegenerative disease caused by mutations in a single gene HTT, that encodes for huntingtin protein. Symptoms include cognitive impairment and this usually declines further into dementia. [83] The first main symptoms of Huntington's disease often include: difficulty concentrating; memory lapses
Huntingtin (Htt) is the protein coded for in humans by the HTT gene, also known as the IT15 ("interesting transcript 15") gene. [5] Mutated HTT is the cause of Huntington's disease (HD), and has been investigated for this role and also for its involvement in long-term memory storage.
This is a list of major and frequently observed neurological disorders (e.g., Alzheimer's disease), symptoms (e.g., back pain), signs (e.g., aphasia) and syndromes (e.g., Aicardi syndrome). There is disagreement over the definitions and criteria used to delineate various disorders and whether some of these conditions should be classified as ...
Although Alzheimer's disease accounts for the majority of cases of neurocognitive disorders, there are various medical conditions that affect mental functions such as memory, thinking, and the ability to reason, including frontotemporal degeneration, Huntington's disease, dementia with Lewy bodies, traumatic brain injury (TBI), Parkinson's ...
The Huntington's disease Outreach Project for Education at Stanford (HOPES) is a student-run project at Stanford University dedicated to making scientific information about Huntington's disease (HD) more readily accessible to patients and the public.
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Huntington's disease stems from a defect that consists of an expanded CAG repeat in the huntingtin gene (HTT) located on the short arm p of chromosome 4. [7] Evidence shows that the basal ganglia in patients with Huntington's disease show a decrease in activity of the mitochondrial pathway , complex II-III.
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