Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1020823 | ENA |
REPOSITORIES: ENA
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Project description:Lithium treatment and human hippocampal neurogenesis
| PRJNA767056 | ENA
Project description:Mediator Med23 regulates adult hippocampal neurogenesis
| PRJNA638362 | ENA
Project description:<p><strong>BACKGROUND:</strong> Ochratoxin A (OTA) have made it a serious hazard to food safety worldwide that poses a serious health risk to humans. Our previous research showed that Walnut green husk polysaccharides (WGP) can effectively alleviate intestinal inflammation and intestinal microbiota disturbances caused by OTA. The present study further explored whether WGP can prevents OTA-induced cognitive impairments and elucidate its neuroprotective mechanism. Here, we established fecal microbiota transplantation, Lactobacillus johnsonii (L.john) and Akkermansia muciniphila (AKK) colonization, L.john and AKK-derived extracellular vesicles (EVs), as well as 5-HT and short-chain fatty acid (SCFA) supplementation tests to evaluate the role of the intestinal microbiota and its metabolites in WGP in alleviating OTA-induced cognitive impairment. </p><p><strong>RESULTS:</strong> OTA exposure induced cognitive impairments and inhibition of hippocampal neurogenesis, which was reversed by WGP supplementation. Meanwhile, WGP supplementation significantly reversed OTA-induced gut dysbacteriosis and low abundance of L.john and AKK, high proinflammation factor levels and low neurotransmitter levels in serum, intestine and hippocampus, as well as low SCFA levels in fecal. Antibiotic cocktail treatment eliminates the neuroprotective effect of WGP on OTA-treated mice. In addition, transplantation of the OTA-gut microbiota into normal mice causing similar results to OTA treatment, and these changes were alleviated with the transplantation of OTA+WGP-gut microbiota. Furthermore, colonization with L.john and AKK markedly reversed OTA-induced cognitive impairments and inhibition of hippocampal neurogenesis, as well as increased 5-HT and SCFA levels. EVs derived from L.john and AKK exhibit consistent performance with colonized L.john and AKK, and also have superior abilities in alleviating OTA-induced cognitive impairment and inhibiting hippocampal neurogenesis. Moreover, as a key regulatory factor of microbiota-gut-brain axis, 5-HT and SCFA supplementation significantly alleviated OTA-induced cognitive impairment and inhibition of hippocampal neurogenesis. </p><p><strong>CONCLUSIONS:</strong> Taken together, this work provides new evidence for microbiota-gut-brain axis involved in the neuroprotective effects of WGP on OTA-induced cognitive dysfunction. L.john, AKK and its derived EVs mediate the ameliorative effects of WGP on OTA-induced cognitive impairment. A feasible mechanism is that WGP increased the content of L.john, AKK and its derived EVs, which improve 5-HT and SCFA production in colon to ameliorate cognitive impairment and enhance hippocampal neurogenesis.</p>
2024-10-10 | MTBLS10673 | MetaboLights
Project description:<p>Anxiety is an aggravating comorbidity of many psychiatric disorders that is often underdiagnosed and undertreated, and little is known on the mechanisms underlying its regulation. Here, we find that serum LPA16:0 abundance increases with trait anxiety in both humans and mice; while high LPA16:0 levels are sufficient to reduce the in vitro proliferation of adult hippocampal neural stem/progenitor cells. In humans, the main LPA receptor LPA1, bears single nucleotide polymorphism variants associated with anxiety. In mice, LPA16:0 decreases hippocampal neurogenesis and stress resilience, whereas LPA1 antagonism or the reduction of platelets, the main source of circulating LPA16:0, increases adult neurogenesis and resilience to acute stress. Conditional knockdown of LPA1 receptor in neural stem cells is sufficient to enhance cell proliferation in the dentate gyrus. Finally, the inhibition of adult neurogenesis abolishes the beneficial effect of LPA1 antagonism on resilience against both acute and chronic stress. Together, these findings identify circulating LPA16:0 as a biomarker of trait anxiety and LPA16:0-LPA1 signaling as a regulation mechanism of mood-related behavior through the decrease of adult neurogenesis.</p>
2026-02-05 | MTBLS13589 | MetaboLights
Project description:Electromagnetized gold nanopartilces can facilitate hippocampal neurogenesis.
2021-02-19 | GSE167006 | GEO
Project description:We performed snRNA-seq of macaque hippocampal formation sample to investigate whether there is the existence of adult neural stem cells and adult hippocampal neurogenesis.
2022-06-29 | GSE163737 | GEO
Project description:N6-methyladenine (6mA), the most prevalent DNA modification in mammals and other eukaryotes, regulates DNA mismatch repair, chromosome replication, and transcription. However, its role in adult hippocampal neurogenesis remains unkown. Here we showed that the methyltransferase N6amt1 and 6mA modification were highly enriched in hippocampal neurons both in vitro and in vivo. Functionally, knockdown of N6amt1 in neural stem cells (NSCs) significantly reduced 6mA levels, neuronal genesis, and proliferation while promoting glial differentiation. Conversely, N6amt1 overexpression enhanced neuronal differentiation and proliferation. Mechanistically, N6amt1-mediated 6mA modification of Txnrd3 DNA increased its transcription, thereby promoting hippocampal neurogenesis. Furthermore, exogenous Txnrd3 overexpression rescued the defects in cell differentiation and proliferation induced by N6amt1 depletion. Notably, N6amt1 deficiency impaired hippocampal neurogenesis and spatial memory in adult mice. Our findings highlight the critical role of DNA 6mA in N6amt1-mediated neurogenesis and suggest that targeting N6amt1 may offer a novel therapeutic strategy for neurological disorders associated with cognitive impairment.
2026-01-14 | GSE307093 | GEO
Project description:Dynamic DNA methylation controls gene-regulatory networks underlying cell fate specification. How DNA methylation patterns change during adult hippocampal neurogenesis and their relevance for the generation of new neurons from adult neural stem cells has, however, remained unknown. Here, we show that neurogenesis-associated de novo DNA methylation is critical for maturation and functional integration of adult-born hippocampal neurons. Cell stage-specific bisulfite sequencing revealed a pronounced gain of DNA methylation at neuronal enhancers, gene bodies and binding sites of pro-neuronal transcription factors during adult neurogenesis, which mostly correlated with transcriptional up-regulation of the associated loci. Inducible deletion of both de novo DNA methyltransferases Dnmt3a and Dnmt3b in adult neural stem cells specifically impaired dendritic outgrowth and synaptogenesis of new neurons, resulting in impaired hippocampal excitability and specific deficits in hippocampus-dependent learning and memory. Our results highlight that, during adult neurogenesis, remodeling of neuronal methylomes is fundamental for proper hippocampal function.
2021-03-02 | GSE167952 | GEO
Project description:Dynamic DNA methylation controls gene-regulatory networks underlying cell fate specification. How DNA methylation patterns change during adult hippocampal neurogenesis and their relevance for the generation of new neurons from adult neural stem cells has, however, remained unknown. Here, we show that neurogenesis-associated de novo DNA methylation is critical for maturation and functional integration of adult-born hippocampal neurons. Cell stage-specific bisulfite sequencing revealed a pronounced gain of DNA methylation at neuronal enhancers, gene bodies and binding sites of pro-neuronal transcription factors during adult neurogenesis, which mostly correlated with transcriptional up-regulation of the associated loci. Inducible deletion of both de novo DNA methyltransferases Dnmt3a and Dnmt3b in adult neural stem cells specifically impaired dendritic outgrowth and synaptogenesis of new neurons, resulting in impaired hippocampal excitability and specific deficits in hippocampus-dependent learning and memory. Our results highlight that, during adult neurogenesis, remodeling of neuronal methylomes is fundamental for proper hippocampal function.
2021-03-02 | GSE167953 | GEO
Project description:Dynamic DNA methylation controls gene-regulatory networks underlying cell fate specification. How DNA methylation patterns change during adult hippocampal neurogenesis and their relevance for the generation of new neurons from adult neural stem cells has, however, remained unknown. Here, we show that neurogenesis-associated de novo DNA methylation is critical for maturation and functional integration of adult-born hippocampal neurons. Cell stage-specific bisulfite sequencing revealed a pronounced gain of DNA methylation at neuronal enhancers, gene bodies and binding sites of pro-neuronal transcription factors during adult neurogenesis, which mostly correlated with transcriptional up-regulation of the associated loci. Inducible deletion of both de novo DNA methyltransferases Dnmt3a and Dnmt3b in adult neural stem cells specifically impaired dendritic outgrowth and synaptogenesis of new neurons, resulting in impaired hippocampal excitability and specific deficits in hippocampus-dependent learning and memory. Our results highlight that, during adult neurogenesis, remodeling of neuronal methylomes is fundamental for proper hippocampal function.
2021-03-02 | GSE167954 | GEO