ArticleNeurobiology of disease2015
Low levels of astroglial markers in Parkinson's disease: relationship to α-synuclein accumulation.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 109 citations in OpenAlex.
- Current potential biomarkers for Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis: review of literature.Dialogues in clinical neuroscience · 2026Review
- Elevated levels of colonic interleukin-1beta and interleukin-8 in isolated REM sleep behavior disorder without associated changes in permeability.NPJ Parkinson's disease · 2026Article
- The Brain-Gut Axis in Parkinson's Disease Pathology.Comprehensive Physiology · 2026Review
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Comparative Analysis of T-Cell Signatures and Astroglial Reactivity in Parkinson's Pathology Across Animal Models with Distinct Regenerative Capacities.International journal of molecular sciences · 2026Article
- Interconnected roles of astrocytes and the blood-brain barrier in Parkinson's disease: pathological evidence, mechanistic insights, and knowledge gaps.Frontiers in aging neuroscience · 2026Review
- Innovative approach in Parkinson's targeting via berberine-loaded mucoadhesive surface-modified liposomes: a multi-faceted study.BMC pharmacology & toxicology · 2025Article
- Early α-Synuclein Pathology Induces Neuroinflammation and Decreases Topoisomerase IIβ Expression in A53T Mice.Inflammation · 2025Article
- The spatial landscape of glial pathology and T cell response in Parkinson's disease substantia nigra.Nature communications · 2025Article
- Caloric restriction mimetic 2-deoxyglucose alters metabolic and transcriptomic phenotype in association with changes in chromatin accessibility in human astrocytes.Scientific reports · 2025Article
- MIRO1 mutation leads to metabolic maladaptation resulting in Parkinson's disease-associated dopaminergic neuron loss.NPJ systems biology and applications · 2025Article
- Human Endogenous Retrovirus K in Astrocytes Is Altered in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- New perspectives on heterogeneity in astrocyte reactivity in neuroinflammation.Brain, behavior, & immunity - health · 2025Article
- Shared interactions of six neurotropic viruses with 38 human proteins: a computational and literature-based exploration of viral interactions and hijacking of human proteins in neuropsychiatric disorders.Discover mental health · 2025Article
- Revisiting astrocytic calcium signaling in the brain.Fundamental research · 2024Review
- GFAP and NfL as fluid biomarkers for clinical disease severity and disease progression in multiple system atrophy (MSA).Journal of neurology · 2024Article
- Disruption of lysosomal proteolysis in astrocytes facilitates midbrain organoid proteostasis failure in an early-onset Parkinson's disease model.Nature communications · 2024Article
- Brain-Biomarker Changes in Body Fluids of Patients with Parkinson's Disease.International journal of molecular sciences · 2023Review
- Identification of phosphorylated tau protein interactors in progressive supranuclear palsy (PSP) reveals networks involved in protein degradation, stress response, cytoskeletal dynamics, metabolic processes, and neurotransmission.Journal of neurochemistry · 2023Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Although gliosis is a normal response to brain injury, reports on the extent of astrogliosis in the degenerating substantia nigra in Parkinson's disease (PD) are conflicting. It has also been recently suggested that accumulation of nigral α-synuclein in this disorder might suppress astrocyte activation which in turn could exacerbate the degenerative process. This study examined brain protein levels (intact protein, fragments, and aggregates, if any) of astroglial markers and their relationship to α-synuclein in PD and in the positive control parkinson-plus conditions multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Autopsied brain homogenates of patients with PD (n=10), MSA (n=11), PSP (n=11) and matched controls (n=10) were examined for the astroglial markers glial fibrillary acidic protein (GFAP), vimentin, and heat shock protein-27 (Hsp27) by quantitative immunoblotting. As expected, both MSA (putamen>substantia nigra>caudate>frontal cortex) and PSP (substantia nigra>caudate>putamen, frontal cortex) showed widespread but regionally specific pattern of increased immunoreactivity of the markers, in particular for the partially proteolyzed fragments (all three) and aggregates (GFAP). In contrast, immunoreactivity of the three markers was largely normal in PD in brain regions examined with the exception of trends for variably increased levels of cleaved vimentin in substantia nigra and frontal cortex. In patients with PD, GFAP levels in the substantia nigra correlated inversely with α-synuclein accumulation whereas the opposite was true for MSA. Our biochemical findings of generally normal protein levels of astroglial markers in substantia nigra of PD, and negative correlation with α-synuclein concentration, are consistent with some recent neuropathology reports of mild astroglial response and with the speculation that astrogliosis might be suppressed in this disorder by excessive α-synuclein accumulation. Should astrogliosis protect, to some extent, the degenerating substantia nigra from damage, therapeutics aimed at normalization of astrocyte reaction in PD could be helpful.
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