Alzheimer’s disease as an inflammatory disease
Open accessAbstract
Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia. In this short review, we focus on neuroinflammation in AD. Specifically, we describe the participation of microglia, as well as other factors that may contribute to inflammation, in neurodegeneration.
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Persistent activation of microglia and astrocytes elevates inflammatory mediators like chemokines and cytokines, and ROS and RNS release, with neurotoxic effects and responsible for chronic neurological/neurodegenerative disorders.
“Persistent activation of microglia and astrocytes elevates inflammatory mediators like chemokines and cytokines [79], the ROS and RNS release, with neurotoxic effects and responsible for chronic neurological/neurodegenerative disorders [80,81,82].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [79]
In Alzheimer's disease, the increase in soluble Aβ oligomeric species, aggregated Aβ plaques and neurofibrillary tangles of hyperphosphorylated Tau proteins leads to activation of microglia and thus to neuroinflammation.
“In AD, the increase in soluble Aβ oligomeric species, aggregated Aβ plaques and neurofibrillary tangles of hyperphosphorylated Tau proteins leads to activation of microglia and thus to neuroinflammation [79,139,140].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [79]
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- Authors
- Bolós, M., Perea, J. R., & Avila, J.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED) , Valderrebollo 5 , - Madrid , Spain
- Venue
- BioMolecular Concepts
- Publisher
- Walter de Gruyter GmbH
- Published
- 2017-02-23
- Volume
- 8
- Issue
- 1
- Pages
- 37-43
- ISSN
- 1868-5021 (ISSN-L)
- 1868-503X
- OpenAlex
- W2589440020
- Cited by
- 216
- References
- 90
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 11 · 2023: 18 · 2022: 20 · 2021: 44 · 2020: 23 · 2019: 27 · 2018: 34 · 2017: 15
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- BioMolecular Concepts (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, neuroinflammation, microglia, amyloid plaques, tau hyperphosphorylation, neurodegeneration, dementia, neuronal cell death
- MeSH terms
- Alzheimer Disease, Animals, Humans, Inflammation, tau Proteins, Microglia, Neurodegenerative Diseases
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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