Aging causes morphological alterations in astrocytes and microglia in human substantia nigra pars compacta

Abstract Age being a risk factor for Parkinson's disease, assessment of age-related changes in the human substantia nigra may elucidate its pathogenesis. Increase in Marinesco bodies, α-synuclein, free radicals and so forth in the aging nigral neurons are clear indicators of neurodegeneration....

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Published inNeurobiology of aging Vol. 36; no. 12; pp. 3321 - 3333
Main Authors Jyothi, H.J, Vidyadhara, D.J, Mahadevan, Anita, Philip, Mariamma, Parmar, Suresh Kumar, Manohari, S. Gowri, Shankar, S.K, Raju, Trichur R, Alladi, Phalguni Anand
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2015
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Summary:Abstract Age being a risk factor for Parkinson's disease, assessment of age-related changes in the human substantia nigra may elucidate its pathogenesis. Increase in Marinesco bodies, α-synuclein, free radicals and so forth in the aging nigral neurons are clear indicators of neurodegeneration. Here, we report the glial responses in aging human nigra. The glial numbers were determined on Nissl-stained sections. The expression of glial fibrillary acidic protein, S100β, 2′, 3′-cyclic nucleotide 3′ phosphodiesterase, and Iba1 was assessed on cryosections of autopsied midbrains by immunohistochemistry and densitometry. The glial counts showed a biphasic increase, of which, the first prominent phase from fetal age to birth could be physiological gliogenesis whereas the second one after middle age may reflect mild age-related gliosis. Astrocytic morphology was altered, but glial fibrillary acidic protein expression increased only mildly. Presence of type-4 microglia suggests possibility of neuroinflammation. Mild reduction in 2′, 3′-cyclic nucleotide 3′ phosphodiesterase–labeled area denotes subtle demyelination. Stable age-related S100β expression indicates absence of calcium overload. Against the expected prominent gliosis, subtle age-related morphological alterations in human nigral glia attribute them a participatory role in aging.
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ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2015.08.024