Inflammation in neurodegenerative diseases—An update
Open accessAbstract
Neurodegeneration, the progressive dysfunction and loss of neurons in the central nervous system (CNS), is the major cause of cognitive and motor dysfunction. While neuronal degeneration is well-known in Alzheimer's and Parkinson's diseases, it is also observed in neurotrophic infections, traumatic brain and spinal cord injury, stroke, neoplastic disorders, prion diseases, multiple sclerosis and amyotrophic lateral sclerosis, as well as neuropsychiatric disorders and genetic disorders. A common link between these diseases is chronic activation of innate immune responses including those mediated by microglia, the resident CNS macrophages. Such activation can trigger neurotoxic pathways leading to progressive degeneration. Yet, microglia are also crucial for controlling inflammatory processes, and repair and regeneration. The adaptive immune response is implicated in neurodegenerative diseases contributing to tissue damage, but also plays important roles in resolving inflammation and mediating neuroprotection and repair. The growing awareness that the immune system is inextricably involved in mediating damage as well as regeneration and repair in neurodegenerative disorders, has prompted novel approaches to modulate the immune system, although it remains whether these approaches can be used in humans. Additional factors in humans include ageing and exposure to environmental factors such as systemic infections that provide additional clues that may be human specific and therefore difficult to translate from animal models. Nevertheless, a better understanding of how immune responses are involved in neuronal damage and regeneration, as reviewed here, will be essential to develop effective therapies to improve quality of life, and mitigate the personal, economic and social impact of these diseases.
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Peripheral insults that cause a systemic inflammatory response might affect ongoing inflammation in the central nervous system mainly by microglial activation, production of inflammatory molecules, and recruitment of peripheral immune cells into the brain, shaping a cerebral inflammatory milieu that may affect neuronal function.
“peripheral insults that cause a systemic inflammatory response might affect ongoing inflammation in the CNS mainly by microglial activation, production of inflammatory molecules, as well as recruitment of peripheral immune cells into the brain, thus shaping a cerebral inflammatory milieu that may seriously affect neuronal function (50, 52, 53).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [52]
Protein encrustations in Alzheimer's disease cause decreased brain glucose metabolism.
“Due to the protein encrustations, there is a persistent inflammatory process, brain decrease in glucose metabolism, and progressive neuronal death [1,2].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [2]
Protein encrustations in Alzheimer's disease cause a persistent inflammatory process.
“Due to the protein encrustations, there is a persistent inflammatory process, brain decrease in glucose metabolism, and progressive neuronal death [1,2].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [2]
Protein encrustations in Alzheimer's disease cause progressive neuronal death.
“Due to the protein encrustations, there is a persistent inflammatory process, brain decrease in glucose metabolism, and progressive neuronal death [1,2].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [2]
Alzheimer's disease is characterized by accumulation of beta-amyloid protein fragments in plaques outside brain neurons and twisted strands of tau protein in tangles inside neurons.
“AD is characterized by the accumulation of the protein fragment beta-amyloid in plaques outside the brain neurons and twisted strands of the protein tau in the form of tangles inside neurons.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [2]
Half of IBD patients reported sleep disturbances as assessed by the PSQI, with strongest associations in patients with active disease.
“In a recent study, half of the IBD patients reported sleep disturbances as assessed by the PSQI (550), with strongest associations in patients with active disease (10, 209).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [10]
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- Authors
- Amor, S., Peferoen, L. A. N., Vogel, D. Y. S., Breur, M., van der Valk, P., Baker, D., & van Noort, J. M.
- Affiliations
- Queen Mary University of London (GB)
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Department of Pathology VU University Medical Centre Amsterdam the Netherlands
- Delta Crystallon BV Leiden the Netherlands
- Corresponding author
- Amor, Sandra
- Venue
- Immunology
- Publisher
- Wiley
- Published
- 2014-04-24
- Volume
- 142
- Issue
- 2
- Pages
- 151-166
- ISSN
- 0019-2805 (ISSN-L)
- 1365-2567
- PMC
- PMC4008224
- OpenAlex
- W2063858768
- Cited by
- 550
- References
- 111
- Citations by year
- 2026: 18 · 2025: 30 · 2024: 34 · 2023: 45 · 2022: 38 · 2021: 72 · 2020: 54 · 2019: 68 · 2018: 50 · 2017: 52 · 2016: 37 · 2015: 38 · 2014: 13
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Multiple Sclerosis Society
- Stichting MS Research
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- neurodegeneration, neuroinflammation, microglia, innate immune response, adaptive immune response, neuroprotection, Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, prion disease, traumatic brain injury, stroke, nerve regeneration, immunomodulatory therapy, aging, systemic infection
- MeSH terms
- Humans, Inflammation, Neurodegenerative Diseases
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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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