ArticleCNS neuroscience & therapeutics2026
MCC-135 Exerts Antiepileptic and Neuroprotective Effects by Downregulating NCX1 Expression to Decrease Intracellular Calcium Overload in the Hippocampus.
Article in CNS neuroscience & therapeutics, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundApproximately 30% of epilepsy patients still develop drug resistance after standard antiepileptic treatment. Therefore, there is an urgent need to identify new drug targets to improve seizure control. Previous studies have shown that NCX1 can regulate the intracellular Ca
methodsThis study employed single-cell analysis and molecular docking to identify the potential molecular targets of MCC-135 in treating epilepsy. Additionally, we used a KA-induced epileptic mouse model to validate these molecular levels and the therapeutic effects and mechanisms of MCC-135.
resultsRelative to controls, NCX1 expression was significantly upregulated in the hippocampus of KA-induced epileptic mice. Immunofluorescence staining revealed that NCX1 was co-localized with both astrocytes and neurons. MCC-135 treatment significantly prolonged the seizure latency in KA-induced epileptic mice and alleviated hippocampal neuronal damage. Furthermore, MCC-135 effectively reduced NCX1 expression, alleviated intracellular calcium overload, and downregulated glutamate levels in the epileptic mice.
conclusionMCC-135 exerts neuroprotective and antiepileptic effects by downregulating NCX1 expression, thereby alleviating calcium overload and reducing glutamate levels in the hippocampus. We are the first to propose the role and mechanism of MCC-135 in epilepsy treatment, providing novel insights into its potential as a therapeutic agent for epilepsy.
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.