ArticleBrain pathology (Zurich, Switzerland)2016
Mortalin is Expressed by Astrocytes and Decreased in the Midbrain of Parkinson's Disease Patients.
Article in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Whole organism and tissue-specific analysis of pexophagy inOpen biology · 2025Article
- Dynamin-like Protein 1 (DNML1) as a Molecular Target for Antibody-Based Immunotherapy to Treat Glaucoma.International journal of molecular sciences · 2022Article
- Mitochondrial chaperones in human health and disease.Free radical biology & medicine · 2022Review
- Insights Into the Role of Mortalin in Alzheimer's Disease, Parkinson's Disease, and HIV-1-Associated Neurocognitive Disorders.Frontiers in cell and developmental biology · 2022Review
- HSPA9/Mortalin mediates axo-protection and modulates mitochondrial dynamics in neurons.Scientific reports · 2021Article
- Mitochondrial HSP70 Chaperone System-The Influence of Post-Translational Modifications and Involvement in Human Diseases.International journal of molecular sciences · 2021Review
- Optimization of expression and purification of mitochondrial HSP 40 (Tid1-L) chaperone: Role of mortalin and tid1 in the reactivation and amyloid inhibition of proteins.Saudi journal of biological sciences · 2020Article
- Article
- Novel role of mortalin in attenuating HIV-1 Tat-mediated astrogliosis.Journal of neuroinflammation · 2020Article
- Anti-stress, Glial- and Neuro-differentiation Potential of Resveratrol: Characterization by Cellular, Biochemical and Imaging Assays.Nutrients · 2020Article
- Oxidative Stress in Parkinson's Disease: Potential Benefits of Antioxidant Supplementation.Oxidative medicine and cellular longevity · 2020Review
- Translation Imaging in Parkinson's Disease: Focus on Neuroinflammation.Frontiers in aging neuroscience · 2020Article
- Alterations in the E3 ligases Parkin and CHIP result in unique metabolic signaling defects and mitochondrial quality control issues.Neurochemistry international · 2018Review
- Serum Mortalin Correlated with α-Synuclein as Serum Markers in Parkinson's Disease: A Pilot Study.Neuromolecular medicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
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 (∼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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.