ArticleMolecular neurobiology2026
Mechanistic Investigation of TSPO-Mediated Dysregulation of Mitochondrial Copper Homeostasis in Microglia and its Role in Perioperative Neurocognitive Disorders.
Article in Molecular neurobiology, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perioperative neurocognitive disorders (PND) are common complications in elderly surgical patients; their mechanisms remain unclear and no effective therapeutic targets exist. This study aims to determine whether copper dyshomeostasis contributes to PND via 18 kDa translocator protein (TSPO)-mediated pathways and to evaluate the therapeutic potential of a TSPO inhibitor. An aged-mouse model of PND was established by right carotid exposure, and BV-2 microglia were stimulated with lipopolysaccharide (LPS) to mimic neuroinflammation. Copper ions, TSPO expression, and mitochondrial function were assessed in the hippocampus, serum, and cultured cells. Postoperative mice exhibited elevated copper levels in both the hippocampus and serum, accompanied by a significant increase in hippocampal TSPO expression. In vitro, LPS-induced TSPO over-expression in BV-2 cells led to copper accumulation and mitochondrial dysfunction, both of which were reversed by the TSPO inhibitor PK11195. TSPO-mediated disruption of copper homeostasis is a critical mechanism in PND, and targeting TSPO offers a novel strategy for PND prevention and treatment.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.