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Restoring miR-132 expression rescues adult hippocampal neurogenesis and memory deficits in Alzheimer’s disease
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“Pathway enrichment analysis confirmed that the identified AD-specific targets are functionally involved in AD-relevant pathways reported previously or in the current study, like Ras, NF-kB and TLR4 signaling [31, 80] (Fig. 5H).”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
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 aligns with previous findings in mouse hippocampus, where miR-132 overexpression in neural stem cells modulated inflammatory signaling pathways, suggesting a prominent role for miR-132 in microglia-neuron crosstalk [31].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
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“Such an approach could also be envisioned for miR-132, considering the numerous neuroprotective and neurotrophic regulatory effects it has in AD [20, 24, 30–32, 34, 92–95].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
In the citing paper
“Increasing miR-132 levels beyond a certain context-dependent dose threshold may induce cellular toxicity that could eventually also impact functional output, as we have previously observed in mouse hippocampus [31].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
In the citing paper
“miR-132 overexpression led to the enrichment of many pathways involved in cell cycle when analysing GO biological processes among upregulated DEGs (Fig. 4D), similar to what has been previously reported [31].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
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“Lastly, miR-132 has been identified as a potent regulator of neural stem cell proliferation in the mouse dentate gyrus [31], and our data suggest a similar role in microglia, with miR-132 overexpression inducing several cell cycle-related pathways in healthy control iMGs.”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
In the citing paper
“Lastly, miR-132 has been identified as a potent regulator of neural stem cell proliferation in the mouse dentate gyrus [31], and our data suggest a similar role in microglia, with miR-132 overexpression inducing several cell cycle-related pathways in healthy control iMGs.”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
In the citing paper
“This aligns with previous findings in mouse hippocampus, where miR-132 overexpression in neural stem cells modulated inflammatory signaling pathways, suggesting a prominent role for miR-132 in microglia-neuron crosstalk [31].”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
In the citing paper
“Previous studies have reported potentially harmful consequences of supra-physiological miR-132 levels on physiological functions [31, 92], which emphasize the need to establish a safe therapeutic window for miR-132.”
From microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer’s disease patients (2026) · cites this paper as [31]
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“We used the DNA-alkylating agent temozolomide (TMZ), which has been previously shown to repress AHN and context discrimination (Egeland et al., 2017; Garthe et al., 2009; McAvoy et al., 2016; Niibori et al., 2012), to block cell proliferation in control- and miR-132-injected App mice (Figure 7F).”
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Self-citationDepression in Alzheimer’s Disease: Epidemiology, Mechanisms, and Treatment
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Metadata
- Authors
- Walgrave, H., Balusu, S., Snoeck, S., Vanden Eynden, E., Craessaerts, K., Thrupp, N., Wolfs, L., Horré, K., Fourne, Y., Ronisz, A., Silajdžić, E., Penning, A., Tosoni, G., Callaerts-Vegh, Z., D’Hooge, R., Thal, D. R., Zetterberg, H., Thuret, S., Fiers, M., Frigerio, C. S., De Strooper, B., & Salta, E.
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2021-10
- Volume
- 28
- Issue
- 10
- Pages
- 1805-1821.e8
- ISSN
- 1934-5909
- Cited by
- 175
- References
- 29
- Language
- en
- Licence
- Funders
- KU Leuven
- Horizon 2020
- Alzheimer's Association
- Vlaamse regering
- Medical Research Council (MR/N030087/1, MR/S00484X/1)
- European Research Council (ERC-2010-AG_268675)
- European External Action Service
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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