The DOI matches its Crossref record; 161 of the 162 references it cites were found in a registry or an index; none of the 112 sources its claims cite is checked for support yet.
Microglia in Alzheimer's disease
Open accessAbstract
Microglia are brain-resident myeloid cells that mediate key functions to support the CNS. Microglia express a wide range of receptors that act as molecular sensors, which recognize exogenous or endogenous CNS insults and initiate an immune response. In addition to their classical immune cell function, microglia act as guardians of the brain by promoting phagocytic clearance and providing trophic support to ensure tissue repair and maintain cerebral homeostasis. Conditions associated with loss of homeostasis or tissue changes induce several dynamic microglial processes, including changes of cellular morphology, surface phenotype, secretory mediators, and proliferative responses (referred to as an "activated state"). Activated microglia represent a common pathological feature of several neurodegenerative diseases, including Alzheimer's disease (AD). Cumulative evidence suggests that microglial inflammatory activity in AD is increased while microglial-mediated clearance mechanisms are compromised. Microglia are perpetually engaged in a mutual interaction with the surrounding environment in CNS; thus, diverse microglial reactions at different disease stages may open new avenues for therapeutic intervention and modification of inflammatory activities. In this Review, the role of microglia in the pathogenesis of AD and the modulation of microglia activity as a therapeutic modality will be discussed.
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In the paper
“PRRs bind to different species of Aβ with various affinities (71).”
§ Microglia in Alzheimer's disease > Alzheimer's disease
What the sources say
- Not checked yetcites [71] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Microglial-derived immune factors can induce a so-called A1 astrocyte phenotype that contributes to neuronal death through reduced trophic support, impaired clearance capacity, and release of toxins (69).”
§ Microglia in Alzheimer's disease > Microglia activation in AD
What the sources say
- Not checked yetcites [69] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Activated microglia along with immunoglobulins and complement components are closely associated with Aβ deposits in brains from AD patients and AD mouse models (58)(59)(60)(61)(62).”
§ Microglia in Alzheimer's disease > Microglia activation in AD
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“microglia also were implicated in spreading tau aggregates through endocytosis (via phagocytosis) and exocytosis (via exosomes) in a nonsynaptic transmission pathway (68).”
§ Microglia in Alzheimer's disease > Microglia activation in AD
What the sources say
- Not checked yetcites [68] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Stewart and colleagues demonstrated that Aβ-mediated release of proinflammatory factors and neurotoxicity partially involved signaling through the CD36/ TLR4/TRL6 complex (108).”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [108] source
Strength:boosted· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“TLRs bind both fibrillar and oligomeric forms of Aβ (74).”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [74] Landreth, 2009, Toll-like receptors in Alzheimer’s disease, Curr Top Microbiol Immunol
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“recent GWAS link several immune genes, particularly complement receptor-1 (CR1), CD33, and triggering receptor expressed on myeloid cells-2 (TREM2), with increased AD risk (55).”
§ Microglia in Alzheimer's disease > Loss of inhibitory signals
What the sources say
- Not checked yetcites [55] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“These findings raise the possibility that innate immune activation may actively contribute to AD pathogenesis, rather than arising as a pure bystander reaction to amyloid deposition, as previously assumed (57).”
§ Microglia in Alzheimer's disease > Loss of inhibitory signals
What the sources say
- Not checked yetcites [57] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“a network-based integrative analysis of AD-related genes revealed that an immune/microglial gene network had the strongest association with AD neuropathology (56).”
§ Microglia in Alzheimer's disease > Loss of inhibitory signals
What the sources say
- Not checked yetcites [56] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“APOE4 expression was associated with enhanced Aβ production, driven by increasing APP expression in neurons (54).”
§ Microglia in Alzheimer's disease > Loss of inhibitory signals
What the sources say
- Not checked yetcites [54] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 35
- Probably not a substantial claim. 4
In the paper
“Increased expression of Tlr2, Tlr4, Tlr5, Tlr7, and Tlr9 mRNAs was found in Aβ plaques, and expression of Tlr2/5 was elevated in plaque-associated tissue in comparison with plaquefree tissue (107)”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [107] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Depletion of microglia suppressed tau propagation (68), suggesting that microglia actively contribute to tau pathology during AD pathogenesis.”
§ Microglia in Alzheimer's disease > Microglia activation in AD
What the sources say
- Not checked yetcites [68] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In AD pathogenesis, microglia activation may play a dual role: on one side, acute microglial activation in some experimental paradigms leads to decreased Aβ accumulation by increasing phagocytosis or clearance.”
- Also stated in: § Alzheimer's disease · plain
“chronic activation of microglia contributes to neurotoxicity and synapse loss by triggering several proinflammatory cascades.”
§ Microglia in Alzheimer's disease > Microglia activation in AD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Alzheimer's disease · plain
None of the sources cited for this claim have been checked yet.
In the paper
“activated microglia in AD show increased proliferation (63,64) and increased expression of inflammatory markers such as CD36, CD14, CD11c, MHC-II, and iNOS (65,66)”
§ Microglia in Alzheimer's disease > Microglia activation in AD
What the sources say
- Not checked yetcites [63] source
- Not checked yetcites [64] Olmos-Alonso, 2016, Pharmacological targeting of CSF1R inhibits microglial proliferation and prevents the progression of Alzheimer’s-like pathology, Brain source
- Not checked yetcites [65] Kamphuis, 2016, Transcriptional profiling of CD11c-positive microglia accumulating around amyloid plaques in a mouse model for Alzheimer’s disease, Biochim Biophys Acta source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In vivo imaging shows that microglia activation precedes the onset of AD (100) and is paralleled by increased levels of inflammatory markers in the cerebrospinal fluid (101)”
§ Microglia in Alzheimer's disease > Multifaceted immune activation
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“the COX-1 inhibitor naproxen was beneficial in fast decliners only; in contrast, the selective COX-2 inhibitor celecoxib was beneficial in slow decliners but harmful in the fast-progressing group.”
§ Microglia in Alzheimer's disease > Multifaceted immune activation
What the sources say
- Not checked yetcites [105] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“repeated monthly injections of CpG-ODNs reduced amyloid deposition and cerebral amyloid angiopathy, and prevented cognitive deficits.”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [116] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“These findings suggested that CD14 deletion shifts microglia activation to an immunomodulatory state, possibly by blocking TLR2 signaling, which contributes to inflammation and AD pathology (115).”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [115] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In contrast to TLR4 stimulation, TLR9 stimulation decreased tau-related pathology (116).”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [116] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“COX-2 expression peaks in neurons in Braak phases 0-II (an early stage characterized by neurofibrillary changes beginning at transentorhinal regions), probably representing an adaptive response that subsequently declines (105).”
§ Microglia in Alzheimer's disease > Multifaceted immune activation
What the sources say
- Not checked yetcites [105] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“microglial activation correlated with glucose hypometabolism in AD patients (103), suggesting a link between microglial activation and synaptic dysfunction.”
§ Microglia in Alzheimer's disease > Multifaceted immune activation
What the sources say
- Not checked yetcites [103] Fan, 2015, Longitudinal influence of microglial activation and amyloid on neuronal function in Alzheimer’s disease, Brain source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hence, it seems that TLR9 stimulation activates an innate immune response that benefits AD pathology without provoking inflammation.”
§ Microglia in Alzheimer's disease > Microglia proliferation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“APP/PS1dE9 mice lacking functional TRL4 showed an increase in Aβ load associated with decreased expression of IL-1β, CCL3, and CCL4 and decreased cognitive function (110), suggesting a protective role of TRL4 in amyloid clearance.”
§ Microglia in Alzheimer's disease > Toll-like receptors
What the sources say
- Not checked yetcites [110] Song, 2011, TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer’s disease, J Neuroinflammation source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“other studies have reported that inhibition of different components of complement impaired Aβ phagocytosis, resulting in elevated synapse loss.”
§ Microglia in Alzheimer's disease > Complement system
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Inhibition of microglial C3aR reduced microglial activation and augmented Aβ clearance in the brain (125), suggesting a detrimental role for complement.”
§ Microglia in Alzheimer's disease > Complement system
What the sources say
- Not checked yetcites [125] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“in the clinical phase of AD, the strong association between microglial activation and AD pathology was observed in young AD patients, but activation waned in AD patients older than 80 years (106)”
§ Microglia in Alzheimer's disease > Multifaceted immune activation
What the sources say
- Not checked yetcites [106] Hoozemans, 2011, Neuroinflammation in Alzheimer’s disease wanes with age, J Neuroinflammation source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Lian and colleagues demonstrated that Aβ induced release of C3 from astrocytes and impaired microglial Aβ phagocytosis (125).”
§ Microglia in Alzheimer's disease > Complement system
What the sources say
- Not checked yetcites [125] source
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“IL-1β, a key cytokine of the innate immune response, was shown to enhance Aβ pathology (126), as well as increase tau pathology (109).”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The NLRP3 inflammasome is critical for maturation of IL-1β, and loss of NLRP3 in APP/PS1 decreased amyloid burden (131).”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
- Not checked yetcites [131] Heneka, 2013, NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice, Nature source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Increased microglial proliferation was observed in several murine AD models (63), appearing with plaque onset and persisting for 18 months (63).”
§ Microglia in Alzheimer's disease > Microglia proliferation
What the sources say
- Not checked yetcites [63] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Lawson and colleagues reported a microglial turnover rate of 0.05% at any given time in healthy brain (141), but recent data from the same group indicated a turnover rate of 0.69% (7).”
§ Microglia in Alzheimer's disease > Complement system
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“IL-10 levels are elevated in AD brain, and IL-10 overexpression in mice increased APOE expression in addition to worsening AD-related pathology and cognitive impairment (132).”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
- Not checked yetcites [132] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“microglia from TNFR-deficient 3xTgAD mice showed defective phagocytosis, highlighting the protective role of TNF-α in facilitating clearance mechanisms.”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
- Not checked yetcites [129] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Il10 deletion led to increased Aβ phagocytosis and increased CD68 reactivity in Aβ depositassociated microglia (133).”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
- Not checked yetcites [133] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased microglial proliferation has been described in the brains of AD patients (135), and in the prodromal stage of Parkinson disease (136), suggesting that microglial proliferation is an early event in the course of neurodegenerative diseases.”
§ Microglia in Alzheimer's disease > Microglia proliferation
What the sources say
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“TNF receptor (TNFR) deficiency in 3xTgAD mice was associated with increased amyloid deposition and enhanced tau phosphorylation (129).”
§ Microglia in Alzheimer's disease > Cytokines
What the sources say
- Not checked yetcites [129] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“TREM2 deficiency impairs microglial phagocytosis of plaques opsonized with anti-Aβ antibodies, suggesting a critical role for TREM2 in the efficacy of antibody-based therapeutics (152).”
§ Microglia in Alzheimer's disease > TREM2
What the sources say
- Not checked yetcites [152] source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TREM2 promotes phagocytosis of apoptotic neurons, proliferation, and survival of microglia, and has been implicated in dampening TLR-induced inflammatory responses (147-151).”
§ Microglia in Alzheimer's disease > TREM2
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the CEBP/α/PU.1 pathway is involved in the regulation of monopoiesis and granulopoiesis (143, 144) and serves as a candidate for regulating proliferation in microglia.”
§ Microglia in Alzheimer's disease > Complement system
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Pharmacological inhibition of CSF1R in mice upregulated antiinflammatory mediators, including IL-4, IL-5, IL-13, and CCL9, and increased synapse and spine densities while reducing proinflammatory cytokine levels (64).”
§ Microglia in Alzheimer's disease > Complement system
What the sources say
- Not checked yetcites [64] Olmos-Alonso, 2016, Pharmacological targeting of CSF1R inhibits microglial proliferation and prevents the progression of Alzheimer’s-like pathology, Brain source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Although targeting CSF1R has therapeutic potential, caution should be taken, as CSF1R haploinsufficiency was linked to adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (145).”
§ Microglia in Alzheimer's disease > Complement system
What the sources say
- Not checked yetcites [145] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“TREM2 was upregulated in CD45 hi LyC + myeloid cells surrounding the amyloid plaques, but not in parenchymal P2Y12 + microglia (155).”
§ Microglia in Alzheimer's disease > TREM2
What the sources say
- Not checked yetcites [155] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“AD risk variants in TREM2 impair the cell surface transport and expression of TREM2; some variants either impair or markedly enhance the binding of TREM2 to phospholipids, suggesting that balanced TREM2 function in AD is important to counteract disease progression (147).”
§ Microglia in Alzheimer's disease > TREM2
What the sources say
- Not checked yetcites [147] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“TREM2 deficiency eliminated plaque-associated CD45 hi LyC + myeloid cells, leading to reduced inflammation and AD-like pathology in these mice (155); however, TREM2-expressing myeloid cells were enriched in microglia processes contacting amyloid deposits in AD mice, and TREM2 deletion resulted in less compact plaques and increased dystrophic neurites.”
§ Microglia in Alzheimer's disease > TREM2
What the sources say
- Not checked yetcites [155] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Gamma oscillations arise from the activation of local circuits of excitatory and fast-spiking inhibitory neurons resonating at 20-50 Hz, and changes in gamma oscillation have been observed in neurological diseases (158).”
§ Microglia in Alzheimer's disease > Optogenics in activation of microglia
What the sources say
- Not checked yetcites [158] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Interestingly, entraining gamma oscillation at 40 Hz in 5xFAD mice induced amyloid reductions that were associated with an increase in microglial numbers and morphological changes such as soma enlargement and shortening of processes loaded with Aβ.”
§ Microglia in Alzheimer's disease > Optogenics in activation of microglia
What the sources say
- Not checked yetcites [158] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Gamma oscillations arise from the activation of local circuits of excitatory and fast-spiking inhibitory neurons resonating at 20-50 Hz, and changes in gamma oscillation have been observed in neurological diseases (158).”
§ Microglia in Alzheimer's disease > Optogenics in activation of microglia
What the sources say
- Not checked yetcites [158] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“It seems that combining human induced pluripotent stem cell (iPSC) technology (159) with recent advances in gene editing will provide new opportunities to model disease pathology that more closely resembles human AD.”
§ Microglia in Alzheimer's disease > Concluding remarks
What the sources say
- Not checked yetcites [159] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- The authors state this as an assumption: Existing mouse models do not show clear neurodegeneration or human-like tau pathology unless a tau mutation is used to induce the disease.
The authors state this as an assumption.
Aging strongly affects innate immunity and is a major risk factor for Alzheimer's disease.
“Given that age has a dramatic impact on innate immunity and represents a major risk factor for AD, more longitudinal studies need to be performed and the overall outcome of immune modulation needs to be tested in aged animals.”
The authors state this as an assumption.
Existing mouse models do not show clear neurodegeneration or human-like tau pathology unless a tau mutation is used to induce the disease.
“One limitation of current mouse models is the absence of clear neurodegeneration and human-like tau pathology unless the disease is induced by a tau mutation.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Neuroinflammation is a key contributor to AD progression. While early immune responses may aid in the clearance of Aβ and tau aggregates, prolonged activation of microglia and astrocytes leads to chronic inflammation and the release of pro-inflammatory cytokines such as IL-1β and TNF-α, promoting neuronal damage in vulnerable brain regions like the neocortex and hippocampus [34–36].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [34]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“For example, they facilitate the clearance of Aβ through phagocytosis42, yet they can also exacerbate neurodegeneration by driving persistent neuroinflammation43.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [43]
The cited source says what the claim attributes to it.
In the citing paper
“Microglia are brain-resident innate immune effector cells and are widely thought to be the key mediators of amyloid beta clearance [14–16].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [15]
The cited source says what the claim attributes to it.
In the citing paper
“Alzheimer's disease (AD) is characterized by the hallmark pathology comprised of widespread amyloid-β (Aβ) deposition, neurofibrillary tangle (NFT) formation, extensive neurodegeneration, and profound activation of microglia in the brain (6).”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [6]
In the citing paper
“In the early stages of AD, activated microglia cause phagocytosis and clearance of pathologic Aβ and/or tau, positively affecting AD pathologies in animal models [89, 90].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [89]
In the citing paper
“Microglia both exert protective function by phagocytosing and clearing pathological protein aggregates”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [2]
In the citing paper
“Microglia phagocytose misfolded proteins, cellular debris, and dying cells to maintain homeostasis.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [2]
In the citing paper
“Reactive gliosis and neural inflammation are hallmarks of AD4,122–125.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [4]
In the citing paper
“Microglia represent innate immune cells of the CNS that play important disease-modifying roles in neurodegeneration including Alzheimer’s disease (AD) [1–4].”
From Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease (2018) · cites this paper as [3]
In the citing paper
“Data from mouse models have suggested dual roles for microglia in AD: pro-inflammatory functions that promote neurotoxicity and amyloid β (Aβ) accumulation, opposed by amyloid-clearing and neuroprotective functions [3, 4].”
From Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease (2018) · cites this paper as [3]
In the citing paper
“Aβ accumulation activates the microglia and promotes pro-inflammatory mediators’ production and impairment of their phagocytic function (232, 233).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [232]
In the citing paper
“Colocalization of reactive microglia with Aβ deposits is a hallmark of AD pathology and has been reported also in brains from AD mouse models [102,103].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [102]
In the citing paper
“Proliferation and activation of microglia in the brain, around amyloid plaques, is a prominent characteristic of AD [102].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [102]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
COX-2 treatment result conflicts with the proposed disease-stage effect
MinorThe paper places slow decliners earlier in the disease trajectory and says the selective COX-2 inhibitor celecoxib benefited them. It later suggests that blocking COX-2 in early phases may be harmful.
“the selective COX-2 inhibitor celecoxib was beneficial in slow decliners but harmful in the fast-progressing group.”
“Thus, COX-2 blockade in early phases may be harmful, whereas COX-1 inhibition (in addition to COX-2 inhibition) may be beneficial”
C5a blockade effect conflicts with the cited reference title
MinorThe text says blocking C5a increased Aβ levels and associates complement blockade with increased neurodegeneration, citing reference 124. That reference's title instead reports decreased pathology after antagonizing the C5a receptor.
“blocking of C5a (124), a downstream component of the complement cascade, increased Aβ levels in the absence of increased Aβ production, reflecting the role of complement in microglial phagocytosis.In the same studies, complement blockade was associated with increased neurodegeneration.”
“124. Fonseca MI, et al. Treatment with a C5aR antago- nist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease.”
Citations
Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
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Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
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Microglial P2Y12 Receptor Regulates Seizure-Induced Neurogenesis and Immature Neuronal Projections
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TREM2 in Alzheimer’s Disease: Microglial Survival and Energy Metabolism
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Mechanism of Enhanced MerTK-Dependent Macrophage Efferocytosis by Extracellular Vesicles
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The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease
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Metadata
- Authors
- Sarlus, H., & Heneka, M. T.
- Affiliations
- University of Bonn (DE)
- Corresponding author
- Heneka, Michael T.
- Venue
- Journal of Clinical Investigation
- Published
- 2017-09-01
- Volume
- 127
- Issue
- 9
- Pages
- 3240-3249
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5669553
- OpenAlex
- W2750718695
- Semantic Scholar
- ef022dba477c27d3e9b6fce59a1f5267296be580
- Cited by
- 911
- References
- 162
- Citations by year
- 2026: 64 · 2025: 98 · 2024: 109 · 2023: 105 · 2022: 134 · 2021: 127 · 2020: 148 · 2019: 66 · 2018: 52 · 2017: 7
- FWCI
- 7.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- DZNE Pub (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, Alzheimer's disease, microglial activation, neuroinflammation, phagocytosis, neuroprotection, microglial receptors, neurodegeneration, brain homeostasis
- MeSH terms
- Alzheimer Disease, Animals, Brain, Central Nervous System, Complement System Proteins, Humans, Immune System, Inflammation, Macrophages, Phagocytosis, Cytokines, Microglia, Neurodegenerative Diseases, Cell Proliferation, Toll-Like Receptors, Mice
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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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