ReviewMolecular neurobiology2025
Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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
3 citing papers in PubMed.
- Synaptic vs. Non-Synaptic Glycine Receptors: Physiological Role and Implications in Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Mitochondrial dysfunction in Alzheimer's disease: connecting pathophysiology with neuroimaging.Frontiers in aging neuroscience · 2026Review
- Metabolic dysfunction and mitochondrial failure in Alzheimer's disease: integrating pathophysiology, clinical evidence and emerging interventions.Frontiers in neurology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial calcium has emerged as a critical player in Alzheimer's disease (AD), closely linked to neuronal dysfunction and cognitive decline seen in patients. Intracellular calcium signaling is essential for processes like synaptic plasticity, neuronal survival, and differentiation. When this balance is disturbed, it can trigger early pathological changes in AD, including the accumulation of amyloid-β (Aβ) peptides and the development of neurofibrillary tangles (NFTs), the hallmark features of the disease. Calcium imbalance in mitochondria disrupts their function, leading to reduced adenosine triphosphate (ATP) production, increased reactive oxygen species (ROS), and ultimately neuronal death. Aβ and tau act synergistically to further disturb calcium regulation, intensifying neurodegeneration. Excess mitochondrial calcium is also linked to altered activity of key calcium transporters, such as the mitochondrial calcium uniporter (MCU) and sodium/calcium/lithium exchanger (NCLX). Moreover, several genetic risk factors for AD, including ApoE4, PS1, PS2, and CALHM1, are known to influence intracellular calcium homeostasis. Building on this, the present study investigates how calcium dysregulation impairs mitochondrial function in AD. Understanding the mechanisms of calcium-induced mitochondrial dysfunction and identifying potential targets to control mitochondrial calcium levels could provide valuable insights for developing therapies against AD and other neurodegenerative diseases.
Indexed as
Identifiers
41317260What Socratic 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 Socratic graph.