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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 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.
Athetosis is a symptom primarily caused by the marbling, or degeneration of the basal ganglia. [citation needed] This degeneration is most commonly caused by complications at birth or by Huntington's disease, in addition to rare cases in which the damage may also arise later in life due to stroke or trauma.
The CBGTC loop has been implicated in many diseases. For example, in Parkinson's disease, degeneration of dopaminergic neurons leading to decreased activity of the excitatory pathway is thought to result in hypokinesia, [15] and in Huntington's disease, degeneration of GABAergic neurons driving the inhibitory pathway is thought to result in the jerky body movements. [2]
Caused by the Huntington gene, the disease eventually contributes to selective atrophy of the Caudate nucleus and Putamen, especially of GABAergic and acetylcholinergic neurons, with some additional degeneration of the frontal and temporal cortices of the brain. The disrupted signaling in the basal ganglia network is thought to cause the ...
It is caused by many different diseases and agents. It is a symptom of several diseases, including GLUT1 deficiency syndrome, Lesch–Nyhan syndrome, phenylketonuria, and Huntington disease and can be a feature of kernicterus (rapidly increasing unconjugated bilirubin that cross the blood-brain-barrier in infants).
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