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Cited by 33Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

Parkinson’s Disease: Can Targeting Inflammation Be an Effective Neuroprotective Strategy?

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Gundersen, Vidar·2021·Frontiers in Neuroscience
DOI 10.3389/fnins.2020.580311PMC PMC7946840
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Abstract

The reason why dopamine neurons die in Parkinson’s disease remains largely unknown. Emerging evidence points to a role for brain inflammation in neurodegeneration. Essential questions are whether brain inflammation happens sufficiently early so that interfering with this process can be expected to slow down neuronal death and whether the contribution from inflammation is large enough so that anti-inflammatory agents can be expected to work. Here I discuss data from human PD studies indicating that brain inflammation is an early event in PD. I also discuss the role of T-lymphocytes and peripheral inflammation for neurodegeneration. I critically discuss the failure of clinical trials targeting inflammation in PD.

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  • At diagnosis, about 30% of dopamine neuronal cell bodies in substantia nigra and 50% of dopamine axon terminals in dorsal putamen have been lost in PD patients.

    “Analysis of postmortem tissues of PD patients has shown that about 30% of dopamine neuronal cell bodies in the substantia nigra and 50% of dopamine axon terminals in the dorsal putamen have been lost at the time of diagnosis.51”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [51]

  • At 4 years after initial PD diagnosis, almost all dopamine axon terminals are lost, while majority of neuronal cell bodies are lost 5 years after diagnosis.

    “At 4 years after the initial diagnosis, almost all of the dopamine axon terminals are lost, while the majority of the neuronal cell bodies are lost 5 years after diagnosis.”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [51]

  • In animal models of PD and in PD patients, misfolded α-synuclein is released from injured neurons into extracellular fluid.

    “In animal models of PD and in PD patients, misfolded α-synuclein was found to be released from injured neurons into the extracellular fluid.51,61,62”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [51]

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Cited by

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Authors
Gundersen, V.
Affiliations
Oslo University Hospital (NO)
Corresponding author
Gundersen, Vidar
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2021-02-25
Volume
14
Pages
580311-580311
ISSN
1662-453X (ISSN-L)
DOI
10.3389/fnins.2020.580311
PMC
PMC7946840
OpenAlex
W3135024069
Cited by
33
References
24
Citations by year
2026: 2 · 2025: 8 · 2024: 7 · 2023: 7 · 2022: 5 · 2021: 4
FWCI
0.74
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
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, neuroinflammation, neuroprotection, neurodegeneration, anti-inflammatory therapy, T cells, peripheral inflammation, clinical trial failure

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