ArticleScientific reports2026
Mitochondrial dysfunction and Ca
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Mechanotransduction Failure and Molecular Rescue in Gastric Cancer: Kinetotherapy Across the IL-6/STAT3-Myostatin/ACVR2B-Akt/mTOR Axis.Medical sciences (Basel, Switzerland) · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
Impaired cellular activities in Alzheimer’s disease (AD) are linked to metabolic defects and Ca²⁺ dysregulation, but the underlying mechanisms in human neurons are unclear. We performed an integrative analysis using human iPSC-derived neurons (iNs) carrying the Presenilin-1 M146L mutation (PS1M146L). Mutant iNs displayed abnormal Ca²+ dynamics, enhanced mitochondrial respiration, and elevated reactive oxygen species (ROS). KCl-evoked depolarization was reduced, indicating a compromised plasma membrane electrochemical gradient. Under thapsigargin-induced stress, mitochondrial Ca²⁺ ([Ca²⁺]m) was significantly lower in PS1M146L iNs, while bradykinin stimulation (implying an intact IP3 pathway) showed no genotypic difference. Since both genotypes remained sensitive to an MCU-1 inhibitor, the observed [Ca²⁺]m deficits likely stem from impaired ER-mitochondria contacts rather than MCU-1 dysfunction. The present results generalise previous observations and provide evidence of the role of the MCU-1 on Ca²⁺ homeostasis in human neurons bearing this specific familial AD mutation.
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