Loss of DARPP-32 and calbindin in multiple system atrophy

Autor: Hideki Mochizuki, Jiro Takano, Makoto Saegusa, Yasuto Nakata, Masahiko Takada, Yoshikuni Mizuno, Takaomi C. Saido, Tetsuo Mikami, Tomoko Nihira, Aya Kawanami, Makiko Nagai, Hideki Hayakawa, Mieko Ogino, Junichi Hamada, Kazutoshi Nishiyama
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Zdroj: Journal of Neural Transmission
ISSN: 1435-1463
0300-9564
Popis: We evaluated the immunohistochemical intensities of α-synuclein, phosphorylated α-synuclein (p-syn), dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32), calbindin-D 28k, calpain-cleaved carboxy-terminal 150-kDa spectrin fragment, and tyrosine hydroxylase in multiple system atrophy (MSA). The caudate head, anterior putamen, posterior putamen, substantia nigra, pontine nucleus, and cerebellar cortex from six MSA brains, six age-matched disease control brains (amyotrophic lateral sclerosis), and five control brains were processed for immunostaining by standard methods. Immunostaining for α-synuclein, p-syn, or both was increased in all areas examined in oligodendrocytes in MSA. Immunostaining for DARPP-32 and calbindin-D 28k was most prominently decreased in the posterior putamen, where neuronal loss was most prominent. Immunostaining for DARPP-32 and calbindin-D 28k was also diminished in the anterior putamen and caudate head, where neuronal loss was less prominent or absent. Calbindin immunostaining was also decreased in the dorsal tier of the substantia nigra and cerebellar cortex. Loss of immunostaining for DARPP-32 and calbindin-D 28k compared with that of neurons indicates calcium toxicity and disturbance of the phosphorylated state of proteins as relatively early events in the pathogenesis of MSA.
Databáze: OpenAIRE