ArticleAging2019
Studies on APP metabolism related to age-associated mitochondrial dysfunction in APP/PS1 transgenic mice.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Requirement for oxidation of neuronal ketone bodies in aging and neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Caffeine Sodium Benzoate Promotes Endothelial Dysfunction of Human Umbilical Vein Endothelial Cells by Promoting M1 Macrophage Polarization.Molecular biotechnology · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Diastolic dysfunction in Alzheimer's disease model mice is associated with Aβ-amyloid aggregate formation and mitochondrial dysfunction.Scientific reports · 2024Article
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- Trazodone rescues dysregulated synaptic and mitochondrial nascent proteomes in prion neurodegeneration.Brain : a journal of neurology · 2024Article
- Peripheral blood amyloid-β involved in the pathogenesis of Alzheimer's disease via impacting on peripheral innate immune cells.Journal of neuroinflammation · 2024Review
- Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus.Antioxidants (Basel, Switzerland) · 2023Article
- A CHCHD6-APP axis connects amyloid and mitochondrial pathology in Alzheimer's disease.Acta neuropathologica · 2022Article
- Proteomics-based evaluation of the mechanism underlying vascular injury via DNA interstrand crosslinks, glutathione perturbation, mitogen-activated protein kinase, and Wnt and ErbB signaling pathways induced by crotonaldehyde.Clinical proteomics · 2022Article
- Implications of miR-148a-3p/p35/PTEN signaling in tau hyperphosphorylation and autoregulatory feedforward of Akt/CREB in Alzheimer's disease.Molecular therapy. Nucleic acids · 2022Article
- The emerging possibility of the use of geniposide in the treatment of cerebral diseases: a review.Chinese medicine · 2021Review
- Wide-Ranging Effects on the Brain Proteome in a Transgenic Mouse Model of Alzheimer's Disease Following Treatment with a Brain-Targeting Somatostatin Peptide.ACS chemical neuroscience · 2021Article
- Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer's disease mouse model.Communications biology · 2021Article
- Zero Echo TimeMetabolites · 2021Article
- Article
- Neuroprotective Effect of Danggui Shaoyao San via the Mitophagy-Apoptosis Pathway in a Rat Model of Alzheimer's Disease.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats.Aging · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aging brain with mitochondrial dysfunction and a reduced adenosine 5'-triphosphate (ATP) has been implicated in the onset and progression of β-Amyloid (Aβ)-induced neuronal toxicity in AD. To unravel the function of ATP and the underlying mechanisms on AD development, APP/PS1 double transgenic mice and wild-type (WT) C57 mice at 6 and 10 months of age were studied. We demonstrated a decreased ATP release in the hippocampus and platelet of APP/PS1 mice, comparing to C57 mice at a relatively early age. Levels of Aβ were raised in both hippocampus and platelet of APP/PS1 mice, accompanied by a decrease of α-secretase activity and an increase of β-secretase activity. Moreover, our results presented an age-dependent rise in mitochondrial vulnerability to oxidation in APP/PS1 mice. In addition, we found decreased pSer473-Akt levels, increased GSK3β activity by inhibiting phosphorylation at Ser9 in aged APP/PS1 mice and these dysfunctions probably due to down-regulation of Bcl-2 and up-regulation of cleaved caspase-3. Therefore, we demonstrate that PI3K/Akt/GSK3β signaling pathway could be involved in Aβ-associated mitochondrial dysfunction of APP/PS1 mice and APP abnormal metabolism in platelet might provide potential biomarkers for early diagnosis of AD.
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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.