Neuroinflammation in Alzheimer's disease
Open accessAbstract
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.
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Chronic low-grade inflammation contributes to both the onset and progression of Alzheimer's disease and Parkinson's disease through microglial activation and pro-inflammatory cytokine release, accelerating neuronal injury.
“Chronic low-grade inflammation contributes to both the onset and progression of AD and PD through microglial activation and pro-inflammatory cytokine release, accelerating neuronal injury [4].”
From What Are the Key Biological Pathways Through Which Lifestyle Factors Influence Neurodegeneration? (2025) · cites this paper as [4]
The Introduction describes an early role for inflammation in Alzheimer's disease, and the Cytokines section links microglial activation and pro-inflammatory cytokines to neuronal injury. The Modulating innate immunity section also describes chronic, non-resolving inflammation in AD. These passages support the AD portion, but the paper does not establish the same claim for Parkinson's disease; searches for Parkinson's disease with inflammation, microglia, and progression did not find a supporting passage. Page numbers were not available in our copy. (LLM, conf=0.89)
Experimental — accuracy not yet measuredThe survey finding that diet type and sleep duration were associated with belief in preventability aligns with biological evidence on diet and circadian regulation in modulating neuroinflammation and glymphatic clearance.
“This aligns with biological evidence highlighting the roles of diet and circadian regulation in modulating neuroinflammation and glymphatic clearance [4,5].”
From What Are the Key Biological Pathways Through Which Lifestyle Factors Influence Neurodegeneration? (2025) · cites this paper as [4]
The Obesity section links a high-cholesterol diet to an Alzheimer’s risk factor and discusses obesity-related inflammation. The Astroglia section describes paravenous clearance of soluble amyloid-β, but the paper does not connect that clearance—or neuroinflammation—to sleep duration or circadian regulation. It therefore supports parts of the biological background, not the full claim attributed to it. (LLM, conf=0.83)
Experimental — accuracy not yet measuredDuring early stages of AD, microglia contribute to Aβ clearance.
“During early stages of AD, microglia contribute to Αβ clearance15”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [15]
The ‘Microglial Aβ clearance mechanisms’ subsection says microglia engulf Aβ fibrils by phagocytosis, supporting their contribution to clearance. ‘Modulating innate immunity’ says microglial roles vary by disease stage, but the passages do not establish that this clearance specifically occurs during the early stages of AD. Page numbers are unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMicroglia are major contributors to molecular and phenotypic changes, including synaptic loss and Aβ clearance, in the Alzheimer's disease brain.
“Converging lines of evidence from human genetics, neuroimaging and post-mortem brain tissue studies suggest that microglia are major contributors to molecular and phenotypic changes, including synaptic loss and Aβ clearance, in the AD brain [4].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [4]
The Cellular Players > Microglia section links microglial function to Aβ clearance and discusses AD-associated TREM2 and CD33 genetic findings, including a PET observation. It also describes microglial protection and remodeling of synapses, but does not establish that microglia cause synaptic loss in the AD brain; that specific part of the claim is unsupported by the passages found. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMicroglia recognize Aβ oligomers via receptors such as CD36, TLR4, TLR6 and TREM2, acquiring specific AD-associated phenotypes.
“Likewise, microglia, the brain-resident immunocompetent macrophages, also recognize Aβ oligomers via receptors such as CD36, toll-like receptor 4 (TLR4) and TLR6 and triggering receptor expressed on myeloid cells 2 (TREM2), acquiring specific AD-associated phenotypes [14,15,16].”
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 [14]
The Cellular Players > Microglia section says microglia bind Aβ oligomers through CD36 and TLRs including TLR4 and TLR6, and that Aβ binding through these receptors activates microglia. It also describes diverse microglial phenotypes. But it calls TREM2 an orphan receptor and does not identify it as a receptor for Aβ oligomers. (LLM, conf=0.90)
Experimental — accuracy not yet measured
In AD, intercellular networks become maladaptive, leading to sustained inflammation, impaired synaptic support, defective myelination, and breakdown of the blood-brain barrier, ultimately amplifying neurodegeneration.
“In AD, these networks become maladaptive, leading to sustained inflammation, impaired synaptic support, defective myelination (Nasrabady et al.; 2018, Zhou et al., 2022), and breakdown of the blood-brain barrier (BBB), ultimately amplifying neurodegeneration (Heneka et al., 2015; Sweeney et al., 2018).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
The sections on microglia and the neurovascular unit describe persistent inflammation, impaired synaptic maintenance, vascular alterations, and processes that amplify neurodegeneration in AD. The neurovascular-unit passage discusses Aβ transport across the blood-brain barrier, but does not establish BBB breakdown. Defective myelination has separate citations in the sentence and is not assessed against Heneka et al. (LLM, conf=0.84)
Experimental — accuracy not yet measuredReceptors on microglia can bind Aβ fibrils, driving an inflammatory response similar to the M1 proinflammatory phenotype.
“Receptors on microglia can bind Aβ fibrils, driving an inflammatory response similar to the M1 (proinflammatory) phenotype observed outside the central nervous system [84].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [84]
Reactive gliosis, encompassing microgliosis and astrogliosis, are prevalent neuropathological hallmarks in the brains of both human AD and mouse models of Aβ amyloidosis.
“The reactive gliosis, encompassing microgliosis and astrogliosis, are prevalent neuropathological hallmarks observed in the brains of both human AD and mouse models of Aβ amyloidosis8,15,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [15]
Amyloid-associated gliosis is consistently observed in the brains of AD patients and amyloidosis mouse models.
“Amyloid-associated gliosis is consistently observed in the brains of AD patients15 and amyloidosis mouse models8,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [15]
Neuroinflammation functions as a vital factor in AD pathogenesis.
“Increasing clinical evidence suggests that neuroinflammation functions as a vital factor in AD pathogenesis (2)”
From Understanding monocyte-driven neuroinflammation in Alzheimer’s disease using human cortical organoid microphysiological systems (2025) · cites this paper as [2]
Altered microglial function has been implicated in the progression of Alzheimer's disease.
“altered microglial function has been implicated in the progression of AD”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [4]
Aβ may initiate microglial activation, resulting in microglial migration to plaques, phagocytosis, and enzymatic degradation of Aβ.
“Furthermore, Aβ may initiate microglial activation, resulting in microglial migration to plaques, phagocytosis, and enzymatic degradation of Aβ [37].”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [37]
Astrocytes become reactive and inflammatory, while microglia transition into chronically activated states that can amplify neuroinflammation.
“Astrocytes become reactive and inflammatory, while microglia transition into chronically activated states that can amplify neuroinflammation (Heneka et al., 2015; Sofroniew and Vinters, 2010).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
Galectin-3 is a key neuroinflammation protein and is strongly upregulated in neurodegenerative conditions.
“Galectin-3 (Gal-3) is a key protein involved in neuroinflammation and is strongly upregulated in neurodegenerative conditions16.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [16]
The Microglia and Summary and outlook sections discuss neuroinflammation in neurodegenerative disease, but do not identify galectin-3 as a key protein or report that it is strongly upregulated. Searches for galectin-3, Gal-3, galectin, and LGALS3 found no passage addressing those claims; no page numbers were available in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measuredNeuroinflammation is a common feature of Alzheimer's disease, and GWAS have associated several immune-related genes with AD, including ABCA7, CD33, CLU, CR1, MS4A, and TREM2.
“Neuroinflammation is a common feature of AD9 and GWAS have associated several immune-related genes with AD including ABCA7, CD33, CLU, CR1, MS4A10, 11 and recently TREM2.12, 13”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [9]
TauO and brain inflammation appear in preclinical or prodromal AD stage, many decades prior to onset of dementia.
“Clinical evidence shows that TauO and brain inflammation also appear in the preclinical or prodromal AD stage, many decades prior to the onset of dementia. 100”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [100]
The immune response exists throughout the pathological progress of AD, suggesting that it may also participate in and aggravate disease development.
“Furthermore, since the immune response exists throughout the pathological progress of AD [104, 105], suggesting that it may also participate in and aggravate the disease development.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [104]
Plaques were evident in multiple brain regions by 4 months in male and female 5xFAD mice, concomitant with activation and gliosis of plaque-associated and non-plaque-associated microglia.
“Plaques were evident in multiple brain regions by 4mo in male and female 5xFAD mice, concomitant with the stereotypical activation and gliosis of plaque- and non-plaque-associated microglia (PAM and NPAM, respectively; Fig. 1A-C) [52, 53].”
From Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain (2020) · cites this paper as [52]
Microglial neurotoxicity may be related to their expression of tau, which is triggered by Aβ deposition and is neurotoxic.
“The neurotoxicity of microglial cells may also be related to their expression of tau, which is triggered by the deposition of Aβ in the brain and is known to be neurotoxic149.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [149]
In AD brains, reactive microglia have been found colocalized with amyloid plaques; reactive astrocytes accumulate around senile plaques next to activated microglia.
“In AD brains reactive microglia has been found colocalized with amyloid plaques. In addition, the reactive astrocytes accumulate around senile plaques next to the activated microglia (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
The sustained exposure to cytokines, chemokines and Aβ could be responsible for the functional impairment of microglial cells located around Aβ deposits.
“The sustained exposure to cytokines, chemokines and Aβ, could be responsible for the functional impairment of microglial cells located around Aβ− deposits (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
Microglial senescence can enhance the sensitivity of microglia to inflammatory stimuli; this phenomenon is called "priming."
“Microglial senescence can enhance the sensitivity of microglia to inflammatory stimuli; this phenomenon is called “priming” (Heneka et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2015
Popular neuroprotective strategies for Alzheimer's disease management include discovering small molecules that block amyloid-beta interactions with intracellular and extracellular targets to avoid caspase activation and proapoptotic protein expression, reduce stress kinase signaling cascades, inhibit tau protein phosphorylation, counterbalance cholinergic functional loss, and boost neuronalplastic
“Popular neuroprotective strategies for AD management consist of discovering small molecules with the ability to block these Aβ interactions with intracellular and extracellular targets to avoid caspase activation and the expression of proapoptotic proteins, to reduce the stress kinase signaling cascades, to inhibit tau protein phosphorylation, to counterpoise cholinergic functional loss, and to bo”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [37]
The FDA has approved two drugs, aducanemab and lecanemab, for mild cognitive impairment to early mild stages of Alzheimer's disease after years of failed clinical trials, with aducanemab receiving accelerated approval.
“The FDA has approved two drugs for mild cognitive impairment (MCI) to early, mild stages of AD after years of failed clinical trials. They are aducanemab, and lecanemab, among which aducanemab received accelerated approval [14, 15].”
From Current therapeutics for Alzheimer’s disease and clinical trials (2024) · cites this paper as [15]
There is a strong correlation between immune activation and oxidative damage in neurodegenerative disease.
“since there is a strong correlation between immune activation and oxidative damage in neurodegenerative disease [42,43,44]”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [42]
Neuroinflammation and oxidative stress are hallmarks of neurodegeneration and contribute to disease progression.
“Neuroinflammation and oxidative stress (OS) are undoubtedly hallmarks of neurodegeneration, contributing to disease progression.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [42]
Aberrantly activated microglia are commonly observed in pathologically relevant AD brain regions, including within and surrounding Aβ plaques.
“These genetic findings are further supported by the common observation of aberrantly activated microglia in pathologically relevant AD brain regions, including within and surrounding Aβ plaques [59, 60].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [60]
Many risk genes associated with AD mediate their effects through microglia.
“Indeed, many of the risk genes associated with AD mediate their effects through microglia, the brain‐resident macrophages (Glass et al, 2010; Heneka et al, 2015; Nott et al, 2019).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Heneka et al, 2015
Neuroinflammation is a key contributor to the pathobiology of Alzheimer's disease.
“Neuroinflammation has been identified as a key contributor to the pathobiology of AD [2–4]”
Neuroinflammation occurs at early disease stages of Alzheimer's disease.
“and occurs at early disease stages [2, 5–7]”
Peripheral inflammation may exacerbate neuroinflammation.
“Peripheral inflammation may exacerbate neuroinflammation [2].”
In AD, a subset of astrocytes undergoes reactive transformation, adopting inflammatory and metabolically altered states that compromise synaptic support and promote neurotoxicity.
“In AD, however, a subset of astrocytes undergoes reactive transformation, adopting inflammatory and metabolically altered states that compromise synaptic support and promote neurotoxicity (Heneka et al., 2015; Nassar et al., 2022).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
Microglia play a dual and stage-dependent role in AD, initially contributing to Aβ clearance but transitioning into a chronically reactive, pro-inflammatory state under persistent pathological stress.
“Microglia, the brain's primary immune cells, play a dual and stage-dependent role in AD, initially contributing to Aβ clearance but transitioning into a chronically reactive, pro-inflammatory state under persistent pathological stress (Hansen et al., 2017; Heneka et al., 2015).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Heneka et al., 2015
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- Authors
- Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., Herrup, K., Frautschy, S. A., Finsen, B., Brown, G. C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A., Petzold, G. C., Town, T., Morgan, D., Shinohara, M. L., Perry, V. H., Holmes, C., Bazan, N. G., Brooks, D. J., Hunot, S., Joseph, B., Deigendesch, N., Garaschuk, O., Boddeke, E., Dinarello, C. A., Breitner, J. C., Cole, G. M., Golenbock, D. T., & Kummer, M. P.
- Affiliations
- University of Bonn (DE)
- University of California, Riverside (US)
- Case Western Reserve University (US)
- German Center for Neurodegenerative Diseases (DE)
- University of Illinois Chicago (US)
- University of Münster (DE)
- Cleveland Clinic (US)
- Hong Kong University of Science and Technology (HK)
- University of California, Los Angeles (US)
- University of Southern Denmark (DK)
- University of Cambridge (GB)
- Ikerbasque (ES)
- RIKEN (JP)
- Center of Advanced European Studies and Research (DE)
- University of Southern California (US)
- Duke Medical Center (US)
- Southampton General Hospital (GB)
- Southern Health NHS Foundation Trust (GB)
- Louisiana State University (US)
- Hammersmith Hospital (GB)
- Centre National de la Recherche Scientifique (FR)
- Karolinska Institutet (SE)
- Max Planck Institute for Infection Biology (DE)
- University of Tübingen (DE)
- University Medical Center Groningen (NL)
- University of Colorado Denver (US)
- Douglas Mental Health University Institute (CA)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Heneka, Michael T
- ORCID
- Heneka, Michael T
- Carson, Monica J
- Landreth, Gary E
- Brosseron, Frederic
- Feinstein, Douglas L
- Jacobs, Andreas H
- Ransohoff, Richard M
- Herrup, Karl
- Frautschy, Sally A
- Finsen, Bente
- Brown, Guy C
- Verkhratsky, Alexei
- Yamanaka, Koji
- Latz, Eicke
- Halle, Annett
- Petzold, Gabor C
- Shinohara, Mari L
- Perry, V Hugh
- Holmes, Clive
- Bazan, Nicolas G
- Brooks, David J
- Hunot, Stéphane
- Joseph, Bertrand
- Deigendesch, Nikolaus
- Garaschuk, Olga
- Boddeke, Erik
- Dinarello, Charles A
- Breitner, John C
- Golenbock, Douglas T
- Kummer, Markus P
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 14
- Issue
- 4
- Pages
- 388-405
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC5909703
- OpenAlex
- W2087243986
- Cited by
- 6,226
- References
- 244
- Citations by year
- 2026: 686 · 2025: 708 · 2024: 713 · 2023: 640 · 2022: 665 · 2021: 620 · 2020: 554 · 2019: 506 · 2018: 406 · 2017: 342 · 2016: 259 · 2015: 110 · 2014: 7
- FWCI
- 29.69
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- eScholarship (California Digital Library) (submittedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- HAL (submittedVersion, other-oa)
- Max Planck Digital Library (submittedVersion)
- Deposito de Investigacion Universidad de Sevilla (University of Seville) (submittedVersion, cc-by-nc-nd)
- DZNE Pub (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Medical Research Council (MR/L010593/1)
- Japan Society for the Promotion of Science (26293208)
- National Institute on Aging (R21AG053884)
- National Institute of Neurological Disorders and Stroke (R01NS059005, R01NS076794)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neuroinflammation, innate immunity, microglia, astrocytes, pattern recognition receptors, protein aggregation, misfolded proteins, inflammatory mediators, systemic inflammation, obesity, genetic risk factors, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Brain Injuries, Clinical Trials as Topic, Disease Models, Animal, Humans, Immunity, Innate, Immunization, Inflammation, Locus Coeruleus, Obesity, Phagocytosis, Risk Factors, Severity of Illness Index, Biomarkers, Protein Folding, Microglia, Disease Progression, Nootropic Agents, Inflammation Mediators
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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