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Calbindin‐D 28K in the basal ganglia of patients with parkinsonism
Author(s) -
Ito Hidefumi,
Goto Satoshi,
Sakamoto Shizuki,
Hirano Asao
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410320410
Subject(s) - globus pallidus , substantia nigra , progressive supranuclear palsy , calbindin , basal ganglia , pars reticulata , striatum , parkinsonism , pathology , parkinson's disease , neuroscience , biology , endocrinology , dopamine , medicine , central nervous system , immunohistochemistry , disease , atrophy
An immunohistochemical study was carried out to investigate the topographic distribution of calbindin‐D 28K in the human basal ganglia and substantia nigra and its alterations in patients with idiopathic Parkinson's disease (PD), parkinsonism‐dementia complex on Guam, progressive supranuclear palsy, and striatonigral degeneration. In normal control subjects, calbindin‐D 28K immunoreactivity was identified in the medium‐sized neurons and neuropil of the matrix compartment of the striatum, the woolly fiber arrangements of the globus pallidus, and the fiber structures of the pars reticulata of the substantia nigra. Calbindin‐D 28k expression in the basal ganglia of patients with PD and parkinsonism‐dementia on Guam was not different from that of control subjects, suggesting that the matrical output pathway is spared in these disorders. In contrast, its disruption is inferred from the observed disorganization of woolly fibers in the globus pallidus of patients with progressive supranuclear palsy and the reduced calbindin‐D 28k reactivity in the putaminal matrix and the pars reticulata of the substantia nigra of subjects with striatal degeneration. Thus, our results indicate that calbindin‐D 28k is a useful marker for the projection system from the matrix compartment and that its expression is modified in patients with progressive supranuclear palsy and striatal degeneration.

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