ArticleMolecular psychiatry2026
NTPDase2 suppresses hippocampal astrocyte-supplied cholesterol through hydrolyzing eATP in depression.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
The 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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Depression is associated with cholesterol metabolism dysregulation, but the exact correlation and underlying mechanism remain unclear. Here, our finding reveals a notable reduction in cholesterol, specifically in apolipoprotein E lipoprotein (ApoE-Lps)-carried cholesterol, in cerebrospinal fluid (CSF) of depressed rats exposing to chronic unpredictable mild stress (CUMS) or stress-level corticosterone. Consistently, Mendelian randomization (MR) analysis also showed that low level of total cholesterol in CSF may be as a risk factor associated with the characteristic symptom of depression such as anhedonia. More importantly, intracerebroventricular cholesterol administration alleviates changes in hippocampal neuronal morphology and depressive-like behaviors in CUMS rats. In astrocyte-neuron co-culture in vitro, astrocytic cholesterol release is decreased under corticosterone exposure. Mechanistically, increased nucleoside triphosphate diphosphohydrolase-2 (NTPDase2) suppresses ATP-binding cassette G1 (ABCG1)-mediated cholesterol efflux by hydrolyzing extracellular ATP (eATP) in corticosterone-exposed astrocytes. Knockdown of Ntpdase2 in rat hippocampal astrocytes via adeno-associated virus (AAV) exhibits beneficial effects in increasing hippocampal neuronal cholesterol level, protecting neuronal morphology and improving depressive-like behaviors compared with vehicle-injected corticosterone model. Collectively, this study suggests impaired astrocytic cholesterol efflux as a cause of abnormality in hippocampal neuronal structure and identifies NTPDase2 as a potential therapeutic target for depression.
Indexed as
Identifiers
42297933What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.