The contribution of neuroinflammation to amyloid toxicity in Alzheimer's disease
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia. Deposition of amyloid-β (Aβ) remains a hallmark feature of the disease, yet the precise mechanism(s) by which this peptide induces neurotoxicity remain unknown. Neuroinflammation has long been implicated in AD pathology, yet its contribution to disease progression is still not understood. Recent evidence suggests that various Aβ complexes interact with microglial and astrocytic expressed pattern recognition receptors that initiate innate immunity. This process involves secretion of pro-inflammatory cytokines, chemokines and generation of reactive oxygen species that, in excess, drive a dysregulated immune response that contributes to neurodegeneration. The mechanisms by which a neuroinflammatory response can influence Aβ production, aggregation and eventual clearance are now becoming key areas where future therapeutic intervention may slow progression of AD. This review will focus on evidence supporting the combined neuroinflammatory-amyloid hypothesis for pathogenesis of AD, describing the key cell types, pathways and mediators involved. Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide. Deposition of intracellular plaques containing amyloid-beta (Aβ) is a hallmark proteinopathy of the disease yet the precise mechanisms by which this peptide induces neurotoxicity remains unknown. A neuroinflammatory response…
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Activated microglia and reactive astrocytes accumulate around senile plaques, contributing to disease severity by dysregulating the inflammatory response.
“Together, activated microglia and reactive astrocytes accumulate in the surrounding area of senile plaques, contributing to the severity of the disease by dysregulating the inflammatory response [18].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [18]
Microglia, monocytes, and astrocytes as well as inflammatory cytokines and chemokines are elevated in the AD brain.
“First, microglia, monocytes, and astrocytes as well as inflammatory cytokines and chemokines are elevated in the AD brain (108).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [108]
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“Together, activated microglia and reactive astrocytes accumulate in the surrounding area of senile plaques, contributing to the severity of the disease by dysregulating the inflammatory response [18].”
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- Authors
- Minter, M. R., Taylor, J. M., & Crack, P. J.
- Affiliations
- The University of Melbourne (AU)
- Corresponding author
- Crack, Peter J.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2015-11-18
- Volume
- 136
- Issue
- 3
- Pages
- 457-474
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1841772591
- Cited by
- 451
- References
- 47
- Citations by year
- 2026: 23 · 2025: 42 · 2024: 36 · 2023: 54 · 2022: 66 · 2021: 64 · 2020: 39 · 2019: 26 · 2018: 30 · 2017: 45 · 2016: 23 · 2015: 1 · 2012: 1
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Health and Medical Research Council (APP1044714)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- Alzheimer's disease, neuroinflammation, amyloid-beta, amyloid toxicity, microglia, astrocytes, pattern recognition receptors, innate immunity, inflammatory cytokines, chemokines, reactive oxygen species, neurodegeneration, amyloid fibril formation, amyloid clearance, immunomodulatory therapy
- MeSH terms
- Alzheimer Disease, Animals, Encephalitis, Humans, Immunity, Innate, Neuroglia, Cytokines, Amyloidogenic Proteins
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