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. 1990 Aug 20;525(2):209-14.
doi: 10.1016/0006-8993(90)90866-a.

Calbindin D28K as a marker for the degeneration of the striatonigral pathway in Huntington's disease

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Calbindin D28K as a marker for the degeneration of the striatonigral pathway in Huntington's disease

H Kiyama et al. Brain Res. .

Abstract

An antibody raised against the chick calcium-binding protein calbindin D28K was used in immunohistochemical studies of normal post mortem human brain and the brains of individuals with Huntington's disease. Calbindin D28K immunoreactivity in the caudate nucleus and putamen coincided with the distribution of areas of acetylcholinesterase staining termed the matrix. In the matrix, calbindin D28K immunoreactivity was present in medium-sized neurons, the major neuronal population, however a further minor population of more strongly stained large neurons was detected. In Huntington's disease there was a dramatic loss of the majority of matrix calbindin D28K immunoreactive neurons and a parallel loss of calbindin D28K immunoreactivity from the substantia nigra. In contrast to the medium-sized calbindin D28K immunoreactive neurons which degenerate in Huntington's disease, the larger immunoreactive neurons were relatively preserved.

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