Aspects of innate immunity and Parkinson's disease
Open accessAbstract
Genetic studies on PARK genes have identified dysfunction in proteasomal, lysosomal, and mitochondrial enzymes as pathogenic for Parkinson's disease (PD). We review the role of these and similar enzymes in mediating innate immune signaling. In particular, we have identified that a number of PARK gene products as well as other enzymes have roles in innate immune signaling as well as DNA repair and regulation, ubiquitination, mitochondrial functioning, and synaptic trafficking. PD enzymatic dysfunction is likely to contribute to inadequate innate immune responses to a variety of extra- and intra-cellular stimuli, with a number of the innate immunity related enzymes found in the characteristic Lewy body pathology of PD. The decrease in innate immunity in PD is associated with an increase in markers of adaptive immunity, and recent GWAS studies have identified variants in human leukocyte antigen region as associated with late-onset sporadic PD (Hamza et al., 2010; Hill-Burns et al., 2011). Intriguing new data also suggest that peripheral immune responses may be involved, giving some potential to alleviate such peripheral dysfunction more directly in patients with PD. It is now important to identify the cell type specific immune responses contributing to the initial changes that occur in PD, as well as to the propagating immune responses important for the progression of PD pathology between cells and within the brain. Overall, a complex interplay between different types of immunity appear to be involved in the underlying pathology of PD.
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In the context of exercise, IL-6 may play an anti-inflammatory role.
“In addition, the cytokine IL-6, while generally considered a pro-inflammatory marker in PD that correlates with functional impairment (decreased walking speed), may in the context of exercise, play an anti-inflammatory role.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [114]
IL-6 originates in skeletal muscle.
“Specifically, IL-6, which originates in skeletal muscle, has been shown with exercise to elicit an anti-inflammatory response that includes elevated expression of a number of factors including IL-10 and IL-1RA, and as well as inhibition of factors like tumor necrosis factor alpha (TNF-alpha).113–115”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [114]
Exercise-induced IL-6 elicits an anti-inflammatory response including elevated expression of IL-10 and IL-1RA and inhibition of TNF-alpha.
“Specifically, IL-6, which originates in skeletal muscle, has been shown with exercise to elicit an anti-inflammatory response that includes elevated expression of a number of factors including IL-10 and IL-1RA, and as well as inhibition of factors like tumor necrosis factor alpha (TNF-alpha).113–115”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [114]
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The role of mitochondria in pathological mechanisms of innate immunity in multiple
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- Authors
- Huang, Y., & Halliday, G. M.
- Affiliations
- UNSW Sydney (AU)
- Corresponding author
- Halliday, Glenda M.
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2012
- Volume
- 3
- Pages
- 33-33
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC3296959
- OpenAlex
- W2016385391
- Cited by
- 22
- References
- 121
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 4 · 2012: 2
- FWCI
- 1.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
- UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- University of New South Wales
- LG Display
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, innate immunity, PARK genes, proteasome dysfunction, lysosomal dysfunction, mitochondrial dysfunction, innate immune signaling, DNA repair, ubiquitination, Lewy bodies, adaptive immunity, human leukocyte antigen, peripheral immune response, neuroinflammation
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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