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Huntington’s disease and Alzheimer’s disease are neurodegenerative disorders associated with the aggregation of misfolded polypeptides, leading to amyloids and neuronal damage.1
Huntington’s disease is caused by expanded glutamine repeats that encode polyglutamine tracts of the gene encoding the huntingtin protein, and is associated with dementia. Polyglutamine tracts in Huntington’s disease form amyloid structures in the cerebral cortex and in the striatum.2
In Alzheimer’s disease, extracellular amyloid β (Aβ) peptides form amyloid plaques in the brain, and lower levels of Aβ1–42 in the cerebrospinal fluid (CSF) may reflect neuropathological processes in amyloid-related disorders. A quantitative urea-based Aβ-sodium dodecylsulphate–polyacrylamide gel electrophoresis with western immunoblot (Aβ-SDS–PAGE/immunoblot) recently showed the regular abundance of Ct-truncated Aβ peptides in the CSF and displayed disease-specific variations.3,4
The morphological substrate of dementia in Huntington’s disease is controversial, and concomitant Alzheimer’s disease pathology has been discussed.5 Thus, Alzheimer’s disease and Huntington’s disease share pathological similarities and may even culminate in a common mechanism of pathogenesis or concomitance in which these protein aggregates affect cellular functions and cause neuronal death.
Of the 69 patients in the study, 16 had Huntington’s disease, 16 had Alzheimer’s disease, 20 had other choreatic diseases and 17 were neurological controls without dementia. Mean age did not differ significantly between diagnostic groups, except between those with Alzheimer’s disease and those with Huntington’s disease (p = 0.002). The Mini-Mental Status Examination (MMSE) score was significantly different between the group with other choreatic diseases and that with Alzheimer’s disease (p = 0.002).
Clinical diagnosis in patients with Huntington’s disease (6 men and 10 women) was confirmed by DNA analysis. Their median age …
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