ReviewCurrent opinion in neurobiology2023
Amyloid precursor protein and mitochondria.
Review in Current opinion in neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Variecolactone, a Natural PDE4 Inhibitor from Marine-DerivedBiomolecules · 2026Article
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Targeted intestinal barrier repairActa pharmaceutica Sinica. B · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Amyloid precursor protein interacts with the mitochondrial phosphatase PGAM5 and regulates mitochondrial respiration.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- Copper Homeostasis and Cuproptosis in Neurological Disorders.Drug design, development and therapy · 2026Review
- Unraveling the Function of PPARα in Neurodegenerative Disorders: A Potential Pathway to Novel Therapies.Biomedicines · 2025Review
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Cell-specific protein expression in Alzheimer's disease prefrontal cortex.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Oxidative stress and inflammation in the pathogenesis of neurological disorders: Mechanisms and implications.Acta pharmaceutica Sinica. B · 2025Review
- The manipulator behind "Scissors": γ -secretase and its modulators in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- SIRT2 as a potential new therapeutic target for Alzheimer's disease.Neural regeneration research · 2024Review
- Expression of Human L-Dopa Decarboxylase (DDC) under Conditions of Oxidative Stress.Current issues in molecular biology · 2023Article
- Mitochondrial Complex I and β-Amyloid Peptide Interplay in Alzheimer's Disease: A Critical Review of New and Old Little Regarded Findings.International journal of molecular sciences · 2023Review
- Amyloid Precursor Protein and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- APOE Peripheral and Brain Impact: APOE4 Carriers Accelerate Their Alzheimer Continuum and Have a High Risk of Suicide in PMBiomolecules · 2023Review
- Article
- Article
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 at 1 institution in 1 country.
Funding
Abstract
Amyloid Precursor Protein (APP) processing to amyloid beta (Aβ) is a major hallmark of Alzheimer's disease (AD). The amyloid cascade hypothesis postulates that Aβ accumulation and aggregation causes AD, however many therapeutics targeting Aβ have failed recently. Decades of research describe metabolic deficits in AD. Mitochondrial dysfunction is observed in AD subjects within the brain and systemically. APP and γ-secretase are localized to mitochondria. APP can be processed within mitochondria and its localization to mitochondria affects function. Here we discuss the evidence showing APP and γ-secretase localize to mitochondria. We also discuss the implications for the function of APP and its cleavage products in regulating mitochondrial function.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.