Journal
BRAIN PATHOLOGY
Volume 26, Issue 1, Pages 75-81Publisher
WILEY
DOI: 10.1111/bpa.12274
Keywords
astrocytes; fluorescence microscopy; human brain tissue; mortalin; Parkinson's disease
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Funding
- UW NIEHS-sponsored Biostatistics, Epidemiologic and Bioinformatics Training in Environmental Health (BEBTEH) Training Grant [NIEHS TSES015459]
- NIEHS [T32ES007032, ES016873, ES019277]
- Alzheimer's Disease Research Center [AG05136]
- Adult Changes in Thought Study [AG006781]
- Morris K Udall Center of Excellence for Parkinson's Disease Research [NS062684]
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [T32ES015459, R01ES019277, T32ES007032, R01ES016873] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS062684] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P50AG005136, U01AG006781, R01AG033398, R01AG025327] Funding Source: NIH RePORTER
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Mortalin, an essential mitochondrial chaperone protein, has previously been implicated in the pathogenesis of a wide array of diseases, including neurodegenerative conditions such as Parkinson's disease (PD) and Alzheimer's disease. Previous reports have consistently described mortalin protein levels to be lower in the brain tissue of patients with neurodegenerative disease, with expression demonstrated to be lower in neurons of post-mortem PD brain specimens. However, to date, mortalin expression has not yet been evaluated in astrocytes of post-mortem brain tissue from either normal or PD subjects. Mortalin expression was demonstrated in mouse primary astrocyte cultures by Western blot and quantitative polymerase chain reaction (PCR). Furthermore, confocal microscopy studies in human post-mortem tissue indicated co-localization of mortalin within astrocytes. Utilizing a quantitative immunofluorescence staining approach, the protein was found to be moderately reduced (approximate to 35%) in this cell type in the substantia nigra pars compacta, but not structures of the corpus striatum, in PD subjects as compared to age-/gender-matched controls. These findings highlight the potential contribution of disrupted astroglial function in the pathogenesis of PD.
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