The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index; 9 of the 11 sources its claims cite were checked for support.
Neurotoxic reactive astrocytes are induced by activated microglia
Open accessAbstract
Reactive astrocytes are strongly induced by central nervous system (CNS) injury and disease, but their role is poorly understood. Here we show that a subtype of reactive astrocytes, which we termed A1, is induced by classically activated neuroinflammatory microglia. We show that activated microglia induce A1 astrocytes by secreting Il-1α, TNF and C1q, and that these cytokines together are necessary and sufficient to induce A1 astrocytes. A1 astrocytes lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce the death of neurons and oligodendrocytes. Death of axotomized CNS neurons in vivo is prevented when the formation of A1 astrocytes is blocked. Finally, we show that A1 astrocytes are abundant in various human neurodegenerative diseases including Alzheimer's, Huntington's and Parkinson's disease, amyotrophic lateral sclerosis and multiple sclerosis. Taken together these findings help to explain why CNS neurons die after axotomy, strongly suggest that A1 astrocytes contribute to the death of neurons and oligodendrocytes in neurodegenerative disorders, and provide opportunities for the development of new treatments for these diseases.
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Claims the paper makes
9 of 11 cited sources checked · 4 supported · 1 flagged · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“All three of these cytokines are highly expressed specifically by microglia13,15, again suggesting a critical role for microglia in inducing A1 reactive astrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 1. Screen for cellular and molecular inducers of the A1 phenotype
What the sources say
- Disputedcites [13] Zhang, Y. et al. An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex. J. Neurosci. 34, 11929–11947 (2014) sourceExperimental — accuracy not yet measured
Table 2 (Additional information; page unavailable) lists C1qa, C1qb, and C1qc among microglia-enriched ligands, but places Tnf and Il1a in the myelinating-oligodendrocyte column. The source therefore contradicts the claim that all three are specifically highly expressed by microglia. (LLM, conf=0.87)
Checked by a reasoning model — may be wrong.
- Partly supportedcites [15] Bennett, M. L. et al. New tools for studying microglia in the mouse and human CNS. Proc. Natl Acad. Sci. USA 113, E1738–E1746 (2016) sourceExperimental — accuracy not yet measured
In “Tmem119 mRNA Expression Is Highly Enriched in the CNS and Specific,” Il1a is listed among highly expressed microglia-enriched candidates. The RNA-seq section reports much higher C1q gene expression in microglia than in other myeloid cells, but also identifies C1q-positive macrophages. The activation section reports Tnf upregulation after LPS, not that TNFα is highly expressed specifically by microglia. No page numbers are supplied for these passages. (LLM, conf=0.88)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Disputed
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“As expected, wild-type littermate controls had a normal response to LPS injection5,17, with robust induction of an A1 response (Fig. 1a)”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 1. Screen for cellular and molecular inducers of the A1 phenotype
What the sources say
- Supportedcites [5] Zamanian, J. L. et al. Genomic analysis of reactive astrogliosis. J. Neurosci. 32, 6391–6410 (2012) source
The citation is attached to the expected response to LPS injection, while the citing paper points to its own Fig. 1a for the littermate-control result. The cited paper’s Results section, “MCAO and systemic LPS-injection induce astrocyte reactive gliosis” (page unavailable), reports increased GFAP expression after LPS; its transcriptome results also report strong induction of complement-pathway genes in LPS-reactive astrocytes. It does not itself describe wild-type littermate controls or use the term “A1.” (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [17] Cartmell, T., Luheshi, G. N. & Rothwell, N. J. Brain sites of action of endogenous interleukin-1 in the febrile response to localized inflammation in the rat. J. Physiol. (Lond.) 518, 585–594 (1999) source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This phagocytic deficit corresponded with a 90% decrease in Mertk and 60% decrease in Megf10 mRNA, phagocytic receptors we have previously found mediate synaptic phagocytosis3 (Fig. 3f).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased phagocytic capacity
What the sources say
- Supportedcites [3] Chung, W.-S. S. et al. Astrocytes mediate synapse elimination through MEGF10 and MERTK pathways. Nature 504, 394–400 (2013) source
The citation is attached to the identification of Mertk and Megf10 as receptors previously found to mediate synaptic phagocytosis, not to the citing authors’ 90% and 60% mRNA decreases. In “Astrocytes phagocytose synapses in vitro and in vivo” (page not supplied), the source reports reduced synapse engulfment in Megf10- and Mertk-deficient astrocytes. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Death of axotomized CNS neurons in vivo is prevented when A1 formation is blocked.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A1s lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce death of neurons and oligodendrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, we show that A1s are highly present in human neurodegenerative diseases including Alzheimer’s, Huntington’s, Parkinson’s, ALS, and Multiple Sclerosis.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A1s lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce death of neurons and oligodendrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A1s lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce death of neurons and oligodendrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We show that activated microglia induce A1s by secreting Il-1α, TNFα, and C1q, and that these cytokines together are necessary and sufficient to induce A1s.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A1s lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce death of neurons and oligodendrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- Probably not a substantial claim. 16
- It may state two separate claims as one. 37
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“previous studies have provided evidence that reactive astrocytes induced by ischemia promote CNS recovery and repair1,10,11.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Introduction
What the sources say
- Supportedcites [1] Sofroniew, M. V. & Vinters, H. V. Astrocytes: biology and pathology. Acta Neuropathol. 119, 7–35 (2010) source
The “Stroke and cerebrovascular disease” section (page unavailable) says studies suggest reactive astrocytes provide essential neuronal support during transient ischemia. It also reports that disrupting astroglial scar formation after stroke increases inflammation and lesion volume. The “Reactive astrogliosis, glial scar formation and CNS inflammation” section (page unavailable) identifies tissue repair among the beneficial functions of reactive astrogliosis, supporting the citing sentence’s characterization of the evidence. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [10] Bush, T. G. et al. Leukocyte infiltration, neuronal degeneration, and neurite outgrowth after ablation of scar-forming, reactive astrocytes in adult transgenic mice. Neuron 23, 297–308 (1999) source
- Could not verifycites [11] Zador, Z., Stiver, S., Wang, V. & Manley, G. T. Role of aquaporin-4 in cerebral edema and stroke. Handb. Exp. Pharmacol. 190, 159–170 (2009) sourceExperimental — accuracy not yet measured
Section 3.2 discusses ischemic edema and tissue damage, but does not say that reactive astrocytes promote recovery or repair. Searches for reactive astrocytes, recovery, repair, and glial scar formation found no passage making that claim; the glial-scar reference alone does not establish it. (LLM, conf=0.73)
Strength:hedged· 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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We previously purified and gene profiled reactive astrocytes from mice treated either with a systemic injection of lipopolysaccharide (LPS), or received middle cerebral artery occlusion to induce ischemia5. We found neuroinflammation and ischemia induced two different types of reactive astrocytes that we termed “A1” and “A2” respectively”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Introduction
What the sources say
- Partly supportedcites [5] Zamanian, J. L. et al. Genomic analysis of reactive astrogliosis. J. Neurosci. 32, 6391–6410 (2012) sourceExperimental — accuracy not yet measured
The Discussion section on stimulus-dependent phenotypes reports distinct LPS- and MCAO-induced reactive astrocyte subtypes, supporting the core finding. Our copy calls them the LPS and MCAO subtypes, but does not show that this paper termed them “A1” and “A2”; searches for those labels returned no matching passage. Page numbers were unavailable. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“they strongly induce A1s, which could drive neurodegeneration not only by secreting a neurotoxin but by releasing multiple complement components that help to drive synapse degeneration33.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
What the sources say
- Partly supportedcites [33] Stevens, B. et al. The classical complement cascade mediates CNS synapse elimination. Cell 131, 1164–1178 (2007) sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says activated microglia secrete most complement-cascade components, and the Introduction (page unavailable) reports that C1q and C3 are required for developmental synapse elimination. The paper does not establish that activated microglia strongly induce A1 astrocytes or that A1s secrete a neurotoxin or release those complement components. (LLM, conf=0.89)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Quantitative RT-PCR was conducted following the MIQE (minimum information for publication of quantitative real-time PCR experiments) guidelines38.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Microfluidic qPCR (pooled cell samples)
What the sources say
- Supportedcites [38] Bustin, S. A. et al. The MIQE guidelines: minimum information for publication of quantitative real-time PCR experiments. Clin. Chem. 55, 611–622 (2009) source
The Abstract identifies this paper as the MIQE guidelines for quantitative real-time PCR experiments. Sections 6 (Reverse Transcription) and 7 (qPCR) give requirements relevant to RT-qPCR, so the citation correctly identifies the guidelines the citing authors say they followed. (LLM, conf=0.91)
Strength:plain· 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.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We show that activated microglia induce A1s by secreting Il-1α, TNFα, and C1q, and that these cytokines together are necessary and sufficient to induce A1s.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Weekly injection of neutralizing antibodies to Il-1α, TNFα, and C1q together into the vitreous of the eye from the time of injury inhibited A1 formation and prevented death of RGCs at least as long as 14 days post-ONC (Fig. 4g–j).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 5. Death of CNS neurons after axotomy in vivo is prevented by inhibiting A1 reactive astrocyte formation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“LPS-activated MCM, but not resting MCM, strongly induced A1 reactive astrocytes (Fig. 1a).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 2. Reactive microglia induce A1 reactive astrocytes by secreting Il-1α, TNFα and C1q
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microglia from these same knock-out mice still upregulate inflammatory mediators in response to LPS injection, but simply fail to release A1 initiators (Extended Data Fig. 4).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 2. Reactive microglia induce A1 reactive astrocytes by secreting Il-1α, TNFα and C1q
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Levels of Il-1α, TNFα and C1q were all significantly elevated after microglial activation (Fig. 1b, c).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 2. Reactive microglia induce A1 reactive astrocytes by secreting Il-1α, TNFα and C1q
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Il-1β secretion also increased in LPS-activated MCM, but was unable to induce expression of A1 transcripts (Fig. 1a).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 2. Reactive microglia induce A1 reactive astrocytes by secreting Il-1α, TNFα and C1q
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although not toxic to oligodendrocyte precursor cells, A1s were able to slow their differentiation and division (Extended Data Fig. 8).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 4. A1 reactive astrocytes are powerfully neurotoxic
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ONC rapidly induced robust A1 generation that was temporally paired with death of RGCs (Fig. 4i–o).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 5. Death of CNS neurons after axotomy in vivo is prevented by inhibiting A1 reactive astrocyte formation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, we found control astrocytes are able to robustly phagocytose myelin debris, but upon conversion to an A1 reactive phenotype almost completely lose this capacity (Fig. 3a,c).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased phagocytic capacity
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Quantitative PCR showed decreased Gpc6 and Sparcl1, while simultaneously showing increased expression of Thbs1/2 (Fig. 2c).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased synaptic functions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, we looked at double (Il-1α−/−TNFα−/−) and triple knock-out mice (Il-1α−/−TNFα−/−C1q−/−) and saw decreases in A1 reactivity, with triple knock-out animals having no response following systemic LPS injection (Fig. 1e).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 2. Reactive microglia induce A1 reactive astrocytes by secreting Il-1α, TNFα and C1q
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This death could not be attributed to Il-1α, TNFα, and C1q alone, which did not cause death of cells in purified cultures.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 4. A1 reactive astrocytes are powerfully neurotoxic
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Death was blocked by caspase-2/-3 inhibitors but not by necrostatin or glutamate blockers and thus appeared to be due to apoptosis (Extended Data Fig. 9).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 4. A1 reactive astrocytes are powerfully neurotoxic
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“S100A10 positive, GFAP colabelled astrocytes (red arrows) were only faintly labelled, and total numbers were very low.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Strength:plain· 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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Note presence of A2-specific GFAP+ reactive astrocytes (S100A10; red arrows) in low CD68+ density areas (phagocytes; yellow arrowheads).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both CFB and MX1 co-localised 100% with C3, and were found in close association with CD68+ reactive microglia (yellow arrowheads).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
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.
- Rests on an assumption: CD68+ cells in MS lesions are reactive microglia.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Pexinartinib (PLX-3397)- treated adult mice have dramatic reduction in number of microglia and no increase in myeloid cell infiltration after LPS compared to vehicle control treatment”
- Also stated in: § Depletion of microglia using Pexidartinib (PLX-3397) · plain
“At this stage flow cytometry showed around 95% decrease in microglia cell number (Extended Data Fig. 1).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Depletion of microglia using Pexidartinib (PLX-3397) · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“f–h, Representative RT-PCR ethidium bromide gel showing no increase in mature OL marker Mbp transcript in OPCs treated with A1 ACM, with no change in OPC marker Pdgfra and Cspg4 expression – evidence of a lack of differentiation into mature oligodendrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Saline injected (control) mice had robust AQP4 protein localization to astrocytic endfeet on blood vessels (red stain, white arrows), while LPS injected mice had loss of polarization of AQP4 immunoreactivity, with bleeding of immunoreactivity away from endfeet (white arrows) and increased staining in other regions of the astrocyte (yellow arrowheads).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
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.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although A1s are not directly toxic to bacteria”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The expression levels of S100a10, determined by qPCR, was not significantly altered at different stages of MS.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Strength:plain· not yet calibratedn = 8Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“24 hours following LPS-induced systemic neuroinflammation, astrocytes were either non-reactive (no reactive genes upregulated), or fell into three forms of reactivity – all with A1 reactive cassette genes upregulated.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Conditioned media from control astrocytes contained less chondroitin sulphate proteoglycans Brevican, Ng2, Neurocan and Versican, while simultaneously having higher levels of heparan sulphate proteoglycans Syndecan and Glypican.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Cultured immunopanned astrocytes retain their non-activated in vivo gene profiles.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Triple knock-out mice (Il1α−/−TNFα−/−C1q−/−) did retained AQP4 immunoreactivity in endfeet following LPS-induced neuroinflammation (white arrows), though some low-level ectopic immunoreactivty was still seen (yellow arrowheads).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Individual knock-out animals had far less TUNEL+ cells in the dentate gyrus (no cells in Il1α−/− or TNFα−/− animals) than wild type animals, suggesting A1-induced toxicity may be apoptosis.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Number of C3+GFAP+ colabelled cells is quantified and was highest in acute active demyelinating lesions, however they were still present in chronic active and inactive lesions.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Extended Data
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.
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
“Thus A1 reactive astrocytes are harmful, contributing to neuron death after acute CNS injury.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Introduction
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
“Thus, A1s secrete a soluble toxin that rapidly kills a subset of CNS neurons and mature oligodendrocytes, but not other CNS cell types.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 4. A1 reactive astrocytes are powerfully neurotoxic
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
“suggesting that A1s are either unable to maintain these synapses or actively disassemble them.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased synaptic functions
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
“Taken together these results show A1 reactive astrocytes induce formation of fewer synapses, and the few synapses they do induce are significantly weaker when compared to those produced by healthy resting astrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased synaptic functions
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
“These data provide strong evidence that death of RGCs after axotomy is not due to trophic deprivation but is instead due to release of a toxic signal from nearby neurotoxic A1 reactive astrocytes.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 5. Death of CNS neurons after axotomy in vivo is prevented by inhibiting A1 reactive astrocyte formation
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
“and suggest that A1s may well lose the capacity to clear myelin debris in vivo, an important area for future investigation.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 3. A1 reactive astrocytes lose many normal astrocyte functions > A1 reactive astrocytes have decreased phagocytic capacity
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.
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
“they do secrete many classical complement cascade components that are expected to greatly enhance clearance of bacteria by the immune system.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Cell-type specific transcripts were also detected for microglia, oligodendrocyte lineage cells, and neurons, with any astrocyte samples containing measurable levels of other cell types removed from further analysis.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Microfluidic qPCR (pooled cell samples)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All Procedure were conducted in accordance with the animal care standards of the National Institute of Health and approved by Stanford University’s Administrative Panel on Laboratory Animal Care.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Methods Summary
Strength:plain· 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Negative control sections without primary antibodies were processed in parallel.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Immunohistochemistry – human
Strength:plain· 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All experiments with mutants were performed blindly without knowledge of their genotype.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Methods Summary
Strength:plain· 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Animals were randomly assigned numbers and evaluated thereafter blind (to both experimental condition and genotype).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Animals
Strength:plain· 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We purified retinal ganglion cells from postnatal day 5 rats by sequential immunopanning to greater than 99% purity and cultured them in serum-free medium as previously described41.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Synapse formation assay
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Group sizes were used to provide at least 80% calculable power with the following parameters: probability of Type I error (0.05), conservative effect size (0.25).”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Statistical analysis and power calculations
Strength:plain· 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“At least 6 independent experiments were conducted for each condition.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > Methods > Survival/cell toxicity assay
Strength:plain· 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.
- Rests on an assumption: Cultured immunopanned astrocytes retain their non-activated in vivo gene profiles.
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
“Here we have identified A1 neurotoxic reactive astrocyte formation as a fundamental pathological response of the CNS to LPS-induced neuroinflammation, acute CNS injury, and most or all neurodegenerative diseases.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
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
“A1s are also highly present in neurodegenerative diseases where their presence may well contribute to neurodegeneration and help to drive disease progression.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt 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
“A1s are rapidly induced after acute CNS injury and responsible for the death of axotomized RGCs.”
§ Neurotoxic reactive astrocytes are induced by activated microglia > 7. Concluding Remarks
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The role of reactive astrocytes in CNS injury and disease is poorly understood.
“Reactive astrocytes are strongly induced by central nervous system (CNS) injury and disease but their role is poorly understood.”
The paper relies on this without support.
It has been a longstanding mystery why CNS neurons die after axotomy.
“It has been a longstanding mystery why CNS neurons die after axotomy.”
The paper relies on this without support.
Reactive microglia are found in neurodegenerative diseases.
“because reactive microglia are found in neurodegenerative diseases”
The paper relies on this without support.
Cultured immunopanned astrocytes retain their non-activated in vivo gene profiles.
“These astrocytes retain their non-activated in vivo gene profiles.”
The paper relies on this without support.
CD68+ cells in MS lesions are reactive microglia.
“CD68+ reactive microglia (yellow arrowheads)”
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
“These aging-related cell states exhibit upregulation of genes (e.g., B2m and Trem2 in Micro-3, Xdh in Endo-3, and Gfap and C4b in Astro-2) (Figure 2C) that have been previously shown to be enriched in microglia, endothelial cells, and astrocytes activated by inflammation and/or aging.”
From Molecular and spatial signatures of mouse brain aging at single-cell resolution (2023) · cites this paper as [40]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For microglia and astrocytes, we observed that the genes highly upregulated with age overlapped substantially with genes that have been previously reported as being upregulated in the activated (or “reactive”) state of these cell types (e.g., Gfap and C4b for astrocytes; B2m and Lyz2 for microglia)”
From Molecular and spatial signatures of mouse brain aging at single-cell resolution (2023) · cites this paper as [40]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Two major astrocyte activation states have been described in neurodegenerative diseases: A1 neurotoxic astrocytes and A2 neuroprotective astrocytes 23 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [23]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“activated microglia secrete chemokines and cytokines that promote astrocyte activation [42]”
From The protective PLCγ2-P522R variant mitigates Alzheimer’s disease-associated pathologies by enhancing beneficial microglial functions (2025) · cites this paper as [42]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“It is thought that the “neurotoxic” reactive astrocytes associated with AD release pro-inflammatory cytokines and can no longer support neuronal synapse formation, facilitate synaptic pruning and clearance of myelin debris and may even induce cell death in neighboring neurons, thereby promoting further neurodegeneration and inflammation [17, 186].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [17]
Experimental — accuracy not yet measured
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
“However, recent data indicate that microglia and astrocytes coordinate their functions in many ways, both in the healthy and diseased brain [14–21].”
From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [16]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In humans, activated microglia are capable of producing neurotoxic, reactive astrocytes in multiple sclerosis lesions (Liddelow et al., 2017).”
From A quantitative neuropathological assessment of translocator protein expression in multiple sclerosis (2019) · cites this paper as Liddelow et al., 2017
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This sensitization intends to recapitulate that caused by microglial activation, a current condition in AD [70,71], reported to enhance GFAP protein levels and astrocyte neurotoxicity [44].”
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 [44]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“they induce oligodendrocyte death by secreting saturated lipids (Guttenplan et al. 2021).”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Liddelow et al. 2017
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the inflammation model mice, the number of C3-positive astrocytes were increased compared that in the control group treated with PBS, which was in accordance with previous findings (Liddelow et al. 2017) (Fig. S2A, B).”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Liddelow et al. 2017
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“reactive astrocytes induced by microglial activation induce cell toxicity via the secretion of saturated lipids (5, 8)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These transformations exacerbate neurodegeneration and reduce the ability of astrocytes to maintain synaptic plasticity36–38.”
From Cholesterol-driven pathological astrocytic responses in diabetes-associated cognitive impairment through astrocytic SCAP accumulation and NF-κB–C3 signaling modulation (2025) · cites this paper as [36]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Complement proteins, including C1q and C3, are upregulated in AD brain tissues36 and cerebrospinal fluid87,91, where they are pivotal in neuroinflammation and synapse elimination88,92.”
From Cholesterol-driven pathological astrocytic responses in diabetes-associated cognitive impairment through astrocytic SCAP accumulation and NF-κB–C3 signaling modulation (2025) · cites this paper as [36]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Activated microglia propagate the inflammatory response to astrocytes, which become reactive and neurotoxic (Liddelow et al., 2017).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Liddelow et al., 2017
The cited source says what the claim attributes to it.
In the citing paper
“Microglial activation or inflammatory insults induce astrocytes into a reactive state, which can have both neuroprotective and neurotoxic effects [17, 183–185].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“While it has been shown that microglia-derived factors (e.g., IL-1α, TNF, and C1q) can induce astrocytes into an inflammatory phenotype10”
From Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer’s disease (2024) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“Moreover, sc-8 astrocytes displayed an enrichment for gene signatures of Disease-associated astrocytes (DAA) identified in an AD mouse model42, reactive astrocytes linked to inflammatory state10, as well as EAE astrocytes43 (Fig. 4G).”
From Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer’s disease (2024) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“known to induce neurotoxic reactive astrocytosis [44]”
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 [44]
The cited source says what the claim attributes to it.
In the citing paper
“They can also induce highly reactive A1 astrocytes that secrete a soluble toxin that directly kills neurons and OLs [347].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [347]
The cited source says what the claim attributes to it.
In the citing paper
“Instead, upon damage detection, microglia secretion of IL-1α, TNF, and complement component 1q (C1q) stimulates astrocytes to acquire a more reactive, inflammatory phenotype [347].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [347]
The cited source says what the claim attributes to it.
In the citing paper
“For example, the now widely-used cocktail of factors released by LPS-treated neonatal microglia72 cannot be simply assumed to model reactive astrocytes in diseases other than neonatal septic shock due to infection by gram-negative bacteria.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [72]
The cited source says what the claim attributes to it.
In the citing paper
“Activated microglia, via C1q release, have been implicated as potential mediators of neurotoxic effects, resulting in reactive astrocyte-mediated neuronal and oligodendrocyte death [87].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [87]
The cited source says what the claim attributes to it.
In the citing paper
“Astrocytes are another major immune-competent cell population in the brain, and have long been proposed to play a role in neurodegeneration (Ben Haim et al., 2015; Liddelow et al., 2017).”
From Overexpressing low‐density lipoprotein receptor reduces tau‐associated neurodegeneration in relation to apoE‐linked mechanisms (2021) · cites this paper as Liddelow et al., 2017
The cited source says what the claim attributes to it.
In the citing paper
“a subtype that exerts neurotoxic effects, known as C3-positive reactive astrocytes (A1 astrocytes), has been identified (Liddelow et al. 2017).”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Liddelow et al. 2017
The cited source says what the claim attributes to it.
In the citing paper
“The differentiation of C3-positive reactive astrocytes is induced by three cytokines secreted by microglia, namely, IL-1α, TNF-α, and C1q.”
From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Liddelow et al. 2017
The cited source says what the claim attributes to it.
In the citing paper
“astrocyte activity is an executing factor (5)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“and A1 astrocyte (p < 0.05 relative to TG-Abi3-Gngt2+/+) [38] gene profile signatures”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [38]
The cited source says what the claim attributes to it.
In the citing paper
“We did not detect any selective induction of either the ARM [26] or A2 astrocyte [38] phenotypes in the three TG-Abi3-Gngt2 genotypes”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [38]
The cited source says what the claim attributes to it.
In the citing paper
“C1q expression in microglia is also an important component of astrocyte activation, with implications for microglia/astrocyte crosstalk in AD (Liddelow, Guttenplan et al. 2017).”
From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Liddelow, Guttenplan et al. 2017
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Astrocytes use ELOVL1 to elongate FAs into VLCFAs [347].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [347]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Astrocytes transfer their VLCFAs to OLs or microglia [347].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [347]
Experimental — accuracy not yet measuredIn the citing paper
“Recent investigations on astrocyte dysregulation in neurodegenerative diseases have provided substantial evidence that a proinflammatory microglial cytokine cocktail containing TNF α, IL 1α, and C1qa reprograms a subset of astrocytes to change their expression profile and phenotype, thus becoming neurotoxic (designated A1 astrocytes) [108].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [108]
In the citing paper
“Overall, the AD astrocyte profile was quite different from that of A1 astrocytes induced by inflammatory mediators released by microglia33, reiterating a lack of bona fide inflammation in the AD brain.”
From Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease (2020) · cites this paper as [33]
In the citing paper
“Interestingly, the mechanism of synapse elimination involves complement tagging of synapses for phagocytosis by microglia, showing a potential for cross-talk between different glial cell types in aging, which may be bidirectional (Liddelow et al., 2017; Schafer et al., 2012).”
From The aging astrocyte transcriptome from multiple regions of the mouse brain. (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“Senescent microglia actively secrete proinflammatory cytokines, which further leads to activation of astrocyte and neuronal apoptosis.145”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [145]
In the citing 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).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [69]
In the citing paper
“Neurons directly reprogrammed from fibroblasts maintain some features reflecting the age of the donor and mirroring some properties of aged neurons120,121; however they are not readily obtained in quantities required for large-scale screens.”
From CRISPR-based functional genomics for neurological disease (2020) · cites this paper as [121]
In the citing paper
“The release of C1q from microglia is necessary to induce neurotoxic, inflammatory astrocytes (A1) (Liddelow et al. , 2017), which also strongly upregulate genes involved in classical complement activation such as C4 (Figure 4I and S4B) (Zamanian et al. , 2012).”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Liddelow et al., 2017
In the citing paper
“Moreover, activated microglia can secrete toxic factors to directly or indirectly injure neurons (Colonna and Butovsky, 2017; Liddelow et al., 2017).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“A triad of factors released by activated microglia (IL-1α, TNFα, and C1q) is necessary and sufficient to induce astrocytes into a neurotoxic state termed “A1” that causes neuronal death (Liddelow et al., 2017).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“and are reportedly found in CNS tissue from patients with various neurodegenerative diseases, including AD (Liddelow et al., 2017).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“For example, previous studies using transgenic mouse models of AD have identified various mechanisms that lead to synaptic impairment in AD, including the accumulation of soluble amyloid-beta, Tau hyperphosphorylation, loss of VGF signaling, and glial state dysregulation (e.g., the induction of disease-associated microglia and disease-associated astrocytes) (9, 23–30).”
From Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer’s disease (2020) · cites this paper as [9]
In the citing paper
“A1 astrocytes lost their ability to promote neuronal survival, growth, synaptogenesis, and phagocytosis and were also highly toxic to neurons, though the exact mechanism of toxicity is still unknown [122, 123].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [122]
In the citing paper
“Importantly, this group has demonstrated that A1 astrocytes are upregulated in AD and other neurodegenerative disorders, though additional tauopathies were not tested.”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [122]
In the citing paper
“These studies illustrated activated microglia induce what was termed an “A1” astrocytic subtype by secretion of IL-1α, TNF, and C1q.”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [122]
In the citing paper
“Interacting with astrocytes is another important microglial function involved in homeostasis, inflammation, and possibly neurodegeneration26.”
From Microglia in neurodegeneration (2018) · cites this paper as [26]
In the citing paper
“Reactive microglia produce IL-1α, TNFα, and C1q, which induce the neurotoxic A1 astrocytes phenotype conversion.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [112]
In the citing paper
“microglia have been shown to regulate astrocytic expression of the receptor”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Liddelow et al., 2017
In the citing paper
“These data suggest that microglia regulate astrocyte reactivity in disease, fully consistent with previous reports19,20.”
From Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model (2019) · cites this paper as [19]
In the citing paper
“The disease-associated microglial transcriptional phenotype in EAE also contributes to the inflammatory cascade by activating astrocytes150.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [150]
In the citing paper
“This study shows that classically activated neuroinflammatory microglia induce toxic astrocytes, which contribute to the death of neurons and oligodendrocytes in neurodegenerative disorders.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [150]
In the citing paper
“This study shows that classically activated neuroinflammatory microglia induce toxic astrocytes, which contribute to the death of neurons and oligodendrocytes in neurodegenerative disorders.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [150]
In the citing paper
“Notably, activated microglia is recognized to cause the activation of astrocytes, which in turn can also liberate signaling molecules that act on microglia [77].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [77]
In the citing paper
“suggest that BG astrocytes are well positioned to participate in shaping baseline microglial phenotypes.”
From Local cues establish and maintain region-specific phenotypes of basal ganglia microglia (2017) · cites this paper as Liddelow et al., 2017
In the citing paper
“Similar analysis of gene expression in purified astrocytes of the four groups of animals showed increased expression of Gfap and pan astrocyte markers Aspg, Osmr, Serpina3n, and Cxcl10, complement genes, and the recently described neurotoxic A1 astrocyte genes in PS19 mice (Liddelow et al., 2017).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“Complement C3 is highly expressed in reactive astrocytes where it marks the A1 neurotoxic sub-type implicated in AD and other neurodegenerative disorders (Lian et al., 2016; Liddelow et al., 2017).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Liddelow et al., 2017
In the citing paper
“activated microglia can crosstalk with astrocytes, inducing reactive astrocytes to rapidly kill neurons via secreted neurotoxic factors and loss of neurotrophic function9”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [9]
In the citing paper
“A1 astrocytes demonstrate strong neurotoxicity by secreting toxic factors that can rapidly induce neuronal death, and by losing normal functions to support neuronal survival, growth or functionality and to maintain environmental homeostasis9.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [9]
In the citing paper
“However, astrocytes are immune-competent. They respond to a wide range of brain insults and are activated in a wide range of neurodegenerative diseases including Alzheimer’s disease9,69–71.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [9]
In the citing paper
“LPS-induced inflammatory microglia are found to activate A1 astrocytes by producing a collection of molecules: TNF, IL-1α and complement 1q (C1Q)9.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [9]
In the citing paper
“Activated microglia can induce A1 astrocytes by secreting IL-1α, TNF, and C1q, and this type of astrocyte contribute to the death of neurons in the neurodegenerative disorders and could be analog to the M1-like phenotype microglia (Liddelow et al., 2017).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Liddelow et al., 2017
In the citing paper
“Our findings may reflect the two types of astrocytes as described in the literature—reactive astrocytes that lose the ability to promote neuronal survival, outgrowth, and synaptogenesis, and induce death of neurons and oligodendrocytes, and homeostatic astrocytes that promote neural functioning54.”
From Large-scale proteomic analysis of human brain identifies proteins associated with cognitive trajectory in advanced age (2019) · cites this paper as [54]
In the citing paper
“In addition to these direct effects of inflammatory mediators on cellular plasticity in the brain, microglia also induce neurotoxic astrocyte reactivity through cytokine signaling (Liddelow et al., 2017).”
From Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation (2022) · cites this paper as Liddelow et al., 2017
In the citing paper
“Astrocytes can assume a range of reactive states (Hasel et al., 2021; Sadick et al., 2022) that can induce further pathophysiology, with certain states of reactive astrocytes inducing oligodendrocyte and neuronal cell death (Liddelow et al., 2017; Guttenplan et al., 2021).”
From Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation (2022) · cites this paper as Liddelow et al., 2017
In the citing paper
“Additionally, this sub-state of reactive astrocytes are poor supporters of synaptic connections—further adding to network dysfunction (Liddelow et al., 2017).”
From Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation (2022) · cites this paper as Liddelow et al., 2017
In the citing paper
“As occurs after cancer therapies and in other disease states, the microglial reactivity present after mild respiratory SARS-CoV-2 infection may also induce neurotoxic astrocyte reactivity (Liddelow et al., 2017; Gibson et al., 2019; Guttenplan et al., 2021), as well as aberrant microglial pruning of synapses (Hinkle et al., 2019; Hosseini et al., 2018; Vasek et al., 2016).”
From Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation (2022) · cites this paper as Liddelow et al., 2017
In the citing paper
“The oligodendrocyte loss observed here could be caused reactive astrocyte toxic lipids, which is known to cause oligodendrocyte cell death (Liddelow et al., 2017; Guttenplan et al., 2021).”
From Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation (2022) · cites this paper as Liddelow et al., 2017
In the citing paper
“These results are consistent with a newly emerging literature which indicates that different types of glia may contribute to the disease via different regulatory mechanisms55–57.”
From Neuronal and glial 3D chromatin architecture informs the cellular etiology of brain disorders (2021) · cites this paper as [56]
In the citing paper
“We previously characterized astrocytes following systemic inflammation, finding that microglial-derived interleukin 1 alpha (IL-1α), tumor necrosis factor (TNF), and complement component 1q (C1q) are necessary and sufficient to induce astrocyte reactivity in neuroinflammatory contexts2.”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“Astrocytes activated by these cytokines in vitro secrete factors that are toxic to neurons and oligodendrocytes, but not to other CNS cells2.”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“Previous data showed that Ferrostatin-1, an inhibitor of lipid peroxidation, does not affect reactive ACM-mediated toxicity2.”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“most of these changes correspond to known reactivity signature genes, with the inflammatory astrocyte protein complement component C3 showing the largest increase (Extended Data Figure 1d)2.”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“Sample sizes were determined by reference to previous literature, with samples sizes for optic nerve crush and in vitro experiments determined according to Liddelow et al.2”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“While Elovl1 cKO mice still showed neuronal death following ONC (unlike in Il1a−/−Tnf−/−C1qa−/− mice, which show no RGC death following axon crush2,3,20), the amount of death was reduced”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
In the citing paper
“This data, in addition to the data that Ferrostatin-1 has no effect on astrocyte toxicity2, suggests that lipid peroxidation may not mediate the ACM toxicity.”
From Neurotoxic reactive astrocytes induce cell death via saturated lipids (2021) · cites this paper as [2]
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.
C3 marker evidence cites the OPC figure
MinorThe cited Extended Data Figure 10 addresses OPC proliferation and differentiation. The caption reporting that A2-cassette-expressing cells were not C3-positive is Extended Data Figure 12.
“Because complement component C3 is one of the most characteristic and highly upregulated genes in A1s and is not expressed by ischemic A2 reactive astrocytes (Extended Data Fig. 10),”
“Figure: EXTENDED DATA FIG 12 Single cell analysis of C3 expression following neuroinflammatory and ischemic injury”
LGN experiment cites the synapse-formation figure
MinorThe cited Extended Data Figure 6 is captioned as a synapse-formation and neurite-outgrowth experiment. The legend describing LGN astrocytes after LPS injection is numbered Figure 7.
“To determine whether A1s also display decreased phagocytic ability in vivo, we used Aldh1l1-eGFP transgenic mice and LPS injection (Extended Data Fig. 6) to visualize phagocytosis of Alexa594-conjugated cholera toxin-β, CTB-594, labelled synapses by control and A1 astrocytes.”
“Figure: EXTENDED DATA FIGURE 7 P4 lateral geniculate nucleus astrocytes become A1 reactive following systemic LPS injection”
Motor-neuron subtype result cites the LGN figure
MinorThe motor-neuron subtype analysis is identified as panel m of Extended Data Figure 8, not Figure 7; the Figure 7 caption concerns LGN astrocytes.
“we found that preganglionic and gamma motor neurons were not susceptible to A1-induced toxicity (Extended Data Fig. 7m).”
“Figure: EXTENDED DATA FIGURE 8 Astrocyte-derived toxic factor promoting cell death a, Quantification of dose-responsive cell death in retinal ganglion cells (RGCs) treated with astrocyte conditioned media from cells treated with Il-1α, TNFα, or C1q alone, or combination of all three (A1 astrocyte conditioned media, ACM) for 24 h.”
LPS response in cultured astrocytes points to an unrelated extended-data figure
MinorThe cited Extended Data Figure 2 concerns microglia depletion in PLX-3397-treated mice, not the response of cultured astrocytes to LPS.
“As a control, we first investigated if astrocytes in culture can respond to LPS and found they do not (Extended Data Fig. 2).”
“Figure: EXTENDED DATA FIGURE 2 Pexinartinib (PLX-3397)- treated adult mice have dramatic reduction in number of microglia and no increase in myeloid cell infiltration after LPS compared to vehicle control treatment”
Synapse assay cites the astrocyte-morphology figure
MinorThe RGC synapse assay cites Extended Data Figure 5, whose caption concerns astrocyte morphology. Synapse formation is the subject of Extended Data Figure 6.
“We cultured purified retinal ganglion cells (RGCs) with resting or A1 reactive astrocytes and quantified synapse number by double immunostaining for pre- and post-synaptic proteins (Fig. 2a, Extended Data Fig. 5).”
“Figure: EXTENDED DATA FIGURE 5 A1 astrocytes are morphologically simple”
Knockout microglial-response citation points to a different experiment
MinorThe text cites Extended Data Figure 4 for microglial activation in knockout mice, but that experiment is captioned Extended Data Figure 11. Figure 4 instead describes astrocyte treatments with candidate mediators.
“Using qPCR we saw microglia from these animals still had many reactive transcripts15 highly upregulated 24 h following LPS injection (Extended Data Fig. 4).”
“Figure: EXTENDED DATA FIGURE 11 Activation of microglia following lipopolysaccharide injection in knockout mice Mice from single global knock-outs of Il-1α (a), TNFα (b), and C1q (c) were treated with lipopolysaccharide (5 mg/kg, i.p.) and microglia collected 24 h later.”
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Metadata
- Authors
- Liddelow, S. A., Guttenplan, K. A., Clarke, L. E., Bennett, F. C., Bohlen, C. J., Schirmer, L., Bennett, M. L., Münch, A. E., Chung, W.-S., Peterson, T. C., Wilton, D. K., Frouin, A., Napier, B. A., Panicker, N., Kumar, M., Buckwalter, M. S., Rowitch, D. H., Dawson, V. L., Dawson, T. M., Stevens, B., & Barres, B. A.
- Affiliations
- The University of Melbourne (AU)
- Stanford Medicine (US)
- University of California, San Francisco (US)
- Korea Advanced Institute of Science and Technology (KR)
- Boston Children's Hospital (US)
- Johns Hopkins University (US)
- Corresponding author
- Liddelow, Shane A.
- ORCID
- Liddelow, Shane A.
- Guttenplan, Kevin A.
- Bennett, Frederick C.
- Bohlen, Christopher J.
- Schirmer, Lucas
- Bennett, Mariko L.
- Münch, Alexandra E.
- Chung, Won-Suk
- Peterson, Todd C.
- Wilton, Daniel K.
- Napier, Brooke A.
- Panicker, Nikhil
- Kumar, Manoj
- Buckwalter, Marion S.
- Rowitch, David H.
- Dawson, Valina L.
- Dawson, Ted M.
- Stevens, Beth
- Barres, Ben A.
- Venue
- Nature
- Published
- 2017-01
- Volume
- 541
- Issue
- 7638
- Pages
- 481-487
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5404890
- OpenAlex
- W2572710398
- Cited by
- 7,971
- References
- 48
- Citations by year
- 2026: 917 · 2025: 978 · 2024: 1067 · 2023: 1007 · 2022: 1043 · 2021: 1015 · 2020: 754 · 2019: 553 · 2018: 428 · 2017: 194
- FWCI
- 261.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- Parkinson's UK (J-1402)
- National Institute on Aging (R01AG048814)
- National Institute on Drug Abuse (R01DA015043, R37DA015043)
- National Institute of Neurological Disorders and Stroke (R01NS084298, R37NS067525, P50NS038377)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD090255)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- reactive astrocytes, microglial activation, neuroinflammation, interleukin-1 alpha, TNF-α, C1q, neuronal cell death, oligodendrocyte death, axotomy, neurodegenerative diseases, Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, synaptogenesis, phagocytosis
- MeSH terms
- Animals, Astrocytes, Cell Survival, Central Nervous System, Humans, Inflammation, Mice, Inbred C57BL, Neurons, Oligodendroglia, Phagocytosis, Phenotype, Synapses, Toxins, Biological, Tumor Necrosis Factor-alpha, Complement C1q, Cell Death, Rats, Sprague-Dawley, Microglia, Disease Progression, Cell Culture Techniques, Neurodegenerative Diseases, Axotomy, Mice, Rats, Interleukin-1alpha
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.
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