Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mitochondrial dysfunction and Ca2+ dysregulation in human iPSC-derived neurons carrying presenilin-1 mutation arise under stress via an MCU-1-independent mechanism.

Scientific reports - 22 Jan 2026

Wilson Carlos, Galeano Pablo, Remedi María Mónica, Novack Gisela Vanina, Campanelli Lorenzo, Gastaldi Laura, Miglietta Esteban, Rossi Andres Hugo, Olivar Natividad, Brusco Luis Ignacio, Castaño Eduardo Miguel, Cáceres Alfredo, Morelli Laura

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Calcium

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calcium Channels

Share to Induced Pluripotent Stem Cells

Share to Mitochondria

Share to Neurons

Share to Presenilin-1

Share to Reactive Oxygen Species

Source

Open in PubMed Open full text

Identifiers

PMID: 41571873
DOI: 10.1038/s41598-026-35597-0
PMCID: PMC12902014

Genes

MCU

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mitochondrial dysfunction and Ca2+ dysregulation in human iPSC-derived neurons carrying presenilin-1 mutation arise under stress via an MCU-1-independent mechanism.PMID 41571873Read ↗

Dysregulation of energy metabolism and calcium homeostasis in iPSC-derived neurons carrying Presenilin-1 M146L gene mutationSemantic proximity Read ↗

Mitochondrial dysfunction in neurodegenerative diseases: A focus on iPSC-derived neuronal modelsSemantic proximity Read ↗

Alzheimer's disease-causing presenilin-1 mutations have deleterious effects on mitochondrial function.Semantic proximity Read ↗

Impaired mitochondrial function due to familial Alzheimer's disease-causing presenilins mutants via Ca2+ disruptionsSemantic proximity Read ↗

Physiological phenotype and vulnerability in Parkinson's disease.Semantic proximity Read ↗

Carvedilol suppresses ryanodine receptor-dependent Ca <sup>2+</sup> bursts in human neurons bearing <i>PSEN1</i> variants found in early onset Alzheimer’s diseaseSemantic proximity Read ↗

Calcium, bioenergetics, and neuronal vulnerability in Parkinson's disease.Semantic proximity Read ↗

Susceptibility to cellular stress in PS1 mutant N2a cells is associated with mitochondrial defects and altered calcium homeostasis.Semantic proximity Read ↗

The gain-of-function enhancement of IP3-receptor channel gating by familial Alzheimer's disease-linked presenilin mutants increases the open probability of mitochondrial permeability transition pore.Semantic proximity Read ↗

Role of Presenilin in Mitochondrial Oxidative Stress and Neurodegeneration in <em>Caenorhabditis elegans</em>Semantic proximity Read ↗

Presenilin 1 (PS1) located at mitochondrial inner membrane regulates mitochondrial cristae junction proteins arrangement and cristae formation in HEK293 cellsSemantic proximity Read ↗

Mitochondria, calcium and cell death: a deadly triad in neurodegeneration.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.