In one paragraphArticle in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
12 authors.
Fuling Wu *Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0006-8887-0589 Yingxue Wu *Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0002-2110-4020 Bingbing QinKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0007-6190-2330 Jinfeng ZhangKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0003-6506-4611 Xinyu ZhuKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0008-7236-9532 Shuji LiKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0000-0230-513X Yuehao ChenKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0009-9684-0234 Jingyi LinKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0005-3829-7924 Xiaofei ZhengKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0004-9130-1278 Feng YiKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-0049-742X Nannan GuoKey Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. guonannan@smu.edu.cn.ORCID http://orcid.org/0009-0006-9212-9670 Funding
National Natural Science Foundation of China (National Science Foundation of China) 32170990National Natural Science Foundation of China (National Science Foundation of China) 32371031
6 · The paper itselfAbstract
Age-related cognitive decline is associated with altered inhibitory signaling in hippocampal circuits, but the mechanisms underlying this dysfunction remain incompletely understood. Neural stem cells (NSCs) persist in the adult hippocampus and influence brain function beyond generating new neurons, although the molecular signals involved remain unclear. Here we show that phospholipase A2 group VII (PLA2G7), a secreted lipid-metabolizing enzyme expressed in NSCs, negatively regulates inhibitory circuit function in the dentate gyrus. Conditional deletion of Pla2g7 in NSCs enhanced inhibitory inputs onto dentate granule cells and improved hippocampal cognition. Lipidomic profiling revealed PLA2G7-dependent remodeling of phospholipid composition, linking NSC-derived lipid metabolism to inhibitory synaptic regulation. Supplementation with phosphatidylcholine rescued PLA2G7-associated inhibitory synapse deficits. In aged mice, PLA2G7 suppression restored inhibitory circuit function, partially normalized circuit imbalance and improved cognition. These findings identify a non-neurogenic mechanism through which NSCs modulate hippocampal circuits and suggest PLA2G7 as a target for promoting cognitive function during aging.
Indexed as
AgingCognitionDentate GyrusNeural Stem CellsPhospholipases A2AnimalsCognitive EnhancementHippocampusMaleMiceMice, Inbred C57BLPhosphatidylcholinesPhosphatidylcholinesPhospholipases A2
What OpenQuestion holds
Textmetadata
Read underepoch 390