ArticleCell calcium2016
Impaired mitochondrial function due to familial Alzheimer's disease-causing presenilins mutants via Ca(2+) disruptions.
Article in Cell calcium, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Pluripotent stem-cell-based screening uncovers sildenafil as a mitochondrial disease therapy.Cell · 2026Article
- MAMs and Mitochondrial Quality Control: Overview and Their Role in Alzheimer's Disease.Neurochemical research · 2024Review
- Neurodegenerative disorders, metabolic icebergs, and mitohormesis.Translational neurodegeneration · 2024Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Presenilins and mitochondria-an intriguing link: mini-review.Frontiers in neuroscience · 2023Review
- Intracellular Injection of Brain Extracts from Alzheimer's Disease Patients Triggers Unregulated CaCells · 2022Article
- Significance of mitochondrial activity in neurogenesis and neurodegenerative diseases.Neural regeneration research · 2022Review
- Impact of β-Amyloids Induced Disruption of CaCells · 2022Article
- Limonin Isolated From Pomelo Seed Antagonizes Aβ25-35-Mediated Neuron Injury via PI3K/AKT Signaling Pathway by Regulating Cell Apoptosis.Frontiers in nutrition · 2022Article
- Expression of tiRNA and tRF inAnnals of translational medicine · 2021Article
- The Relevance of Amyloid β-Calmodulin Complexation in Neurons and Brain Degeneration in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Review
- Review
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- Protein-protein interactions underlying the behavioral and psychological symptoms of dementia (BPSD) and Alzheimer's disease.PloS one · 2020Article
- Mitochondrial dysfunction and role in spreading depolarization and seizure.Journal of computational neuroscience · 2019Article
- Presenilin 1 Regulates [CaOxidative medicine and cellular longevity · 2019Article
- CellSpecks: A Software for Automated Detection and Analysis of Calcium Channels in Live Cells.Biophysical journal · 2018Article
- Data-driven modeling of mitochondrial dysfunction in Alzheimer's disease.Cell calcium · 2018Article
- Analyzing optical imaging of CaCell calcium · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutants in presenilins (PS1 or PS2) is the major cause of familial Alzheimer's disease (FAD). FAD causing PS mutants affect intracellular Ca(2+) homeostasis by enhancing the gating of inositol trisphosphate (IP3) receptor (IP3R) Ca(2+) release channel on the endoplasmic reticulum, leading to exaggerated Ca(2+) release into the cytoplasm. Using experimental IP3R-mediated Ca(2+) release data, in conjunction with a computational model of cell bioenergetics, we explore how the differences in mitochondrial Ca(2+) uptake in control cells and cells expressing FAD-causing PS mutants affect key variables such as ATP, reactive oxygen species (ROS), NADH, and mitochondrial Ca(2+). We find that as a result of exaggerated cytosolic Ca(2+) in FAD-causing mutant PS-expressing cells, the rate of oxygen consumption increases dramatically and overcomes the Ca(2+) dependent enzymes that stimulate NADH production. This leads to decreased rates in proton pumping due to diminished membrane potential along with less ATP and enhanced ROS production. These results show that through Ca(2+) signaling disruption, mutant PS leads to mitochondrial dysfunction and potentially to cell death.
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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.