Linking Neuroinflammation and Neurodegeneration in Parkinson's Disease
Open accessAbstract
Neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD) impose a pressing burden on our developed and consequently aging society. Misfolded protein aggregates are a critical aspect of several neurodegenerative diseases. Nevertheless, several questions remain unanswered regarding the role of misfolded protein aggregates and the cause of neuronal cell death. Recently, it has been postulated that neuroinflammatory processes might play a crucial role in the pathogenesis of PD. Numerous postmortem, brain imaging, epidemiological, and animal studies have documented the involvement of the innate and adaptive immunity in neurodegeneration. Whether these inflammatory processes are directly involved in the etiology of PD or represent secondary consequences of nigrostriatal pathway injury is the subject of intensive research. Immune alterations in response to extracellularα-synuclein may play a critical role in modulating Parkinson’s disease progression. In this review, we address the current concept of neuroinflammation and its involvement in PD-associated neurodegeneration.
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Persistent neuroinflammation can weaken the BBB, damage neurons, and contribute to neurodegenerative diseases, like Alzheimer's.
“Persistent neuroinflammation can weaken the BBB, damage neurons, and contribute to neurodegenerative diseases, like Alzheimer’s (Gelders et al., 2018).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Gelders et al., 2018
Section 2 links neuroinflammation to neuronal degeneration, while noting that whether it causes or follows degeneration remains unanswered. Section 4 reports evidence that inflammatory processes contribute to neuronal loss in Parkinson’s disease. The paper does not say persistent neuroinflammation weakens the BBB or establish the claimed contribution to Alzheimer’s; section 3 mentions BBB disruption only as an effect of neurotoxin injection in a model. (LLM, conf=0.87)
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- Authors
- Gelders, G., Baekelandt, V., & Van der Perren, A.
- Affiliations
- KU Leuven (BE)
- Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Leuven, Belgium
- Venue
- Journal of Immunology Research
- Publisher
- Wiley
- Published
- 2018
- Volume
- 2018
- Pages
- 1-12
- ISSN
- 2314-7156 (ISSN-L)
- 2314-8861
- PMC
- PMC5926497
- OpenAlex
- W2801720268
- Cited by
- 430
- References
- 108
- Citations by year
- 2026: 23 · 2025: 25 · 2024: 37 · 2023: 61 · 2022: 66 · 2021: 89 · 2020: 74 · 2019: 46 · 2018: 8
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Immunology Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- FWO Flanders
- KU Leuven
- ERA-NET JPco-fuND 2015 SYNACTION
- Queen Elisabeth Medical Foundation for Neurosciences
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, neuroinflammation, neurodegeneration, alpha-synuclein, innate immunity, adaptive immunity, nigrostriatal pathway, neuronal cell death, neurodegeneration pathogenesis
- MeSH terms
- Animals, Humans, Inflammation, Neurons, Parkinson Disease, Apoptosis, Neurodegenerative Diseases, Neurogenic Inflammation, alpha-Synuclein, Proteostasis Deficiencies
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