ReviewJournal of neurochemistry2024
The reciprocal relationship between amyloid precursor protein and mitochondrial function.
Review in Journal of neurochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed.
- Mitochondria-associated endoplasmic reticulum membranes and calcium ion exchange: A novel direction for aging and neurodegenerative diseases.Neural regeneration research · 2026Article
- Inter-Organelle Membrane Contact Sites as Physiological Regulatory Hubs in the Brain: From Neurons to Glial Cells.Biomolecules · 2026Review
- Estrogen Withdrawal-Induced Cognitive Impairment in Menopausal Women: Mechanisms and Prospects for Integrated Interventions.International journal of molecular sciences · 2026Review
- Amyloid precursor protein interacts with the mitochondrial phosphatase PGAM5 and regulates mitochondrial respiration.bioRxiv : the preprint server for biology · 2026Article
- Amyloid-β and Mitochondrial Membranes: A Missing Link in Alzheimer's Pathogenesis.Molecular neurobiology · 2026Review
- MicroRNA-502-3p Modulates the GABA A Subunits, Synaptic Proteins, and Mitochondrial Morphology in Hippocampal Neurons.Molecular neurobiology · 2025Article
- Review
- Organelle perturbation in Alzheimer's disease: do intracellular amyloid-ß and the fragmented Golgi mediate early intracellular neurotoxicity?Frontiers in cell and developmental biology · 2025Review
- Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Amyloid precursor protein (APP), secretase enzymes, and amyloid beta (Aβ) have been extensively studied in the context of Alzheimer's disease (AD). Despite this, the function of these proteins and their metabolism is not understood. APP, secretase enzymes, and APP processing products (Aβ and C-terminal fragments) localize to endosomes, mitochondria, endoplasmic reticulum (ER), and mitochondrial/ER contact sites. Studies implicate significant relationships between APP, secretase enzyme function, APP metabolism, and mitochondrial function. Mitochondrial dysfunction is a key pathological hallmark of AD and is intricately linked to proteostasis. Here, we review studies examining potential functions of APP, secretase enzymes, and APP metabolites in the context of mitochondrial function and bioenergetics. We discuss implications and limitations of studies and highlight knowledge gaps that remain in the field.
Indexed as
Identifiers
What 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.