ArticleMolecular neurodegeneration2022
Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits in a mouse model of DLB/PD.
Article in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Eight-week Flexi-bar vibration exercise enhances cognitive function via altering the circulating levels of BDNF, TNF-α, and microRNAs in middle-aged and elderly women.European journal of applied physiology · 2026Trial
- OAB-14 Attenuated Glymphatic System Disorder, Neuroinflammation and Dyskinesia in Parkinson's Disease Model Mice Induced by Rotenone.Neurochemical research · 2025Article
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Investigation in the cannabigerol derivative VCE-003.2 as a disease-modifying agent in a mouse model of experimental synucleinopathy.Behavioral and brain functions : BBF · 2024Article
- Immunity impacts cognitive deficits across neurological disorders.Journal of neurochemistry · 2024Review
- Umbilical cord blood-derived exosomes attenuate dopaminergic neuron damage of Parkinson's disease mouse model.Journal of nanobiotechnology · 2024Article
- Article
- The Synergistic Effect Study of Lipopolysaccharide (LPS) and A53T-α-Synuclein: Intranasal LPS Exposure on the A53T-α-Synuclein Transgenic Mouse Model of Parkinson's Disease.Molecular neurobiology · 2024Article
- Current insights and assumptions on α-synuclein in Lewy body disease.Acta neuropathologica · 2024Review
- Effect of host and strain factors on α-synuclein prion pathogenesis.Trends in neurosciences · 2024Review
- Integration of National Health Insurance claims data and animal models reveals fexofenadine as a promising repurposed drug for Parkinson's disease.Journal of neuroinflammation · 2024Article
- Tdrd3-null mice show post-transcriptional and behavioral impairments associated with neurogenesis and synaptic plasticity.Progress in neurobiology · 2024Article
- Article
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- Impaired neuronal activity as a potential factor contributing to the underdeveloped cerebrovasculature in a young Parkinson's disease mouse model.Scientific reports · 2023Article
- Investigation of Inflammation in Lewy Body Dementia: A Systematic Scoping Review.International journal of molecular sciences · 2023Article
- Tdrd3-null mice show post-transcriptional and behavioral impairments associated with neurogenesis and synaptic plasticity.Research square · 2023Article
- Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Synucleins: New Data on Misfolding, Aggregation and Role in Diseases.Biomedicines · 2022Review
Corrections and comments
- Retraction · 2024-10-16Concerns/Issues about Image · Duplication of/in Image · Error in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · Objections by Author(s) · Unreliable Data · · see also: https://pubpeer.com/publications/8C0194022EFF3652F36C2964A88C0B
- Retracted
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough ɑ-synuclein (ɑ-syn) spreading in age-related neurodegenerative diseases such as Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) has been extensively investigated, the role of aging in the manifestation of disease remains unclear.
methodsWe explored the role of aging and inflammation in the pathogenesis of synucleinopathies in a mouse model of DLB/PD initiated by intrastriatal injection of ɑ-syn preformed fibrils (pff).
resultsWe found that aged mice showed more extensive accumulation of ɑ-syn in selected brain regions and behavioral deficits that were associated with greater infiltration of T cells and microgliosis. Microglial inflammatory gene expression induced by ɑ-syn-pff injection in young mice had hallmarks of aged microglia, indicating that enhanced age-associated pathologies may result from inflammatory synergy between aging and the effects of ɑ-syn aggregation. Based on the transcriptomics analysis projected from Ingenuity Pathway Analysis, we found a network that included colony stimulating factor 2 (CSF2), LPS related genes, TNFɑ and poly rl:rC-RNA as common regulators.
conclusionsWe propose that aging related inflammation (eg: CSF2) influences outcomes of pathological spreading of ɑ-syn and suggest that targeting neuro-immune responses might be important in developing treatments for DLB/PD.
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What OpenQuestion holds
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.