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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.
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.
Huntington's disease (HD) is an inherited disorder that causes progressive degeneration of neurons within the cerebral cortex and striatum of the brain [98] resulting in loss of motor functions (involuntary muscle contractions), decline in cognitive ability (eventually resulting in dementia), and changes in behavior.
Neurogenesis in the adult brain is often associated with diseases that deteriorate the CNS, like Huntington's disease, Alzheimer's disease, and Parkinson's disease. While adult neurogenesis is up-regulated in the hippocampus in patients with these diseases, whether its effects are regenerative or inconclusive remains to be seen. [7]
Huntington's disease is a degenerative neurological disorder that is inherited. Degeneration of neuronal cells occurs throughout the brain, especially in the striatum. There is a progressive decline that results in abnormal movements. [31] Statistics show that Huntington's disease may affect 10 per 100,000 people of Western European descent.
It is believed that accumulation of high levels of the free form of this protein (free as in dissociated from the huntingtin and free to bind other key protein(s)) in the cell is one of the mechanisms by which neuron cell death is caused in Huntington's disease (via the caspase-3 route). The role of Hip-1 in caspase mediated cell death remains ...
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These often are translated into polyglutamine-containing proteins that form inclusions and are toxic to neuronal cells. Examples of the disorders caused by this mechanism include Huntington's disease and Huntington disease-like 2, spinal-bulbar muscular atrophy, dentatorubral-pallidoluysian atrophy, and spinocerebellar ataxia 1–3, 6–8, and 17.
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