ArticleFrontiers in aging neuroscience2023
Article in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Presenilin-dependent regulation of neuronal tau pathology via the autophagy and proteasome pathways.Acta neuropathologica communications · 2026Article
- Phase separation in mitochondrial fate and mitochondrial diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Review
- Integrating multi-omics data to identify the role of Aggrephagy-related genes in tumor microenvironment and key tumorigenesis factors of GB from the perspective of single-cell sequencing.Discover oncology · 2025Article
- Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Novel insights into presenilin 1 mutation associated with a distinctive dementia phenotype and cotton wool plaques.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Article
- Respiratory Dysfunction in Alzheimer's Disease-Consequence or Underlying Cause? Applying Animal Models to the Study of Respiratory Malfunctions.International journal of molecular sciences · 2024Review
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Alzheimer's disease remains the most common neurodegenerative disorder, depicted mainly by memory loss and the presence in the brain of senile plaques and neurofibrillary tangles. This disease is related to several cellular alterations like the loss of synapses, neuronal death, disruption of lipid homeostasis, mitochondrial fragmentation, or raised oxidative stress. Notably, changes in the autophagic pathway have turned out to be a key factor in the early development of the disease. The aim of this research is to determine the impact of the Methods: Fibroblasts from Alzheimer's patients with Results: We observed that the Conclusion: The findings suggest that all these modifications could eventually contribute to the neuronal degeneration that underlies the pathogenesis of Alzheimer's disease. Further research in this area may help to develop targeted therapies for the treatment of Alzheimer's disease.
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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.