ArticleNeural regeneration research2022
Presenilin mutations and their impact on neuronal differentiation in Alzheimer's disease.
Article in Neural regeneration research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Exploring the Potential Neurotoxic Links Between 6PPD/6PPD-Q and Parkinson's Disease Through Network Toxicology and Multi-Dimensional Bioinformatics Analysis.Neurotoxicity research · 2026Article
- Neurodevelopmental origins of age-related neurodegenerative diseases.EBioMedicine · 2026Review
- Innovative Approaches to Alzheimer's Treatment: Utilizing Tacrine Hybrids to Inhibit Amyloid Beta Aggregation as a Strategic Focus.Mini reviews in medicinal chemistry · 2026Review
- PF-04691502, a PI3K/mTOR Dual Inhibitor, Ameliorates AD-like Pathology in a Mouse Model of AD.Cells · 2025Article
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- PF-06447475 Molecule Attenuates the Neuropathology of Familial Alzheimer's and Coexistent Parkinson's Disease Markers in PSEN1 I416T Dopaminergic-like Neurons.Molecules (Basel, Switzerland) · 2025Article
- Alzheimer's Disease as Type 3 Diabetes: Understanding the Link and Implications.International journal of molecular sciences · 2024Review
- MAMs and Mitochondrial Quality Control: Overview and Their Role in Alzheimer's Disease.Neurochemical research · 2024Review
- Lost in translation: Inconvenient truths on the utility of mouse models in Alzheimer's disease research.eLife · 2024Review
- Genetic and epigenetic targets of natural dietary compounds as anti-Alzheimer's agents.Neural regeneration research · 2024Review
- Insights on the Use of Transgenic Mice Models in Alzheimer's Disease Research.International journal of molecular sciences · 2024Review
- Long-read sequencing revealing intragenic deletions in exome-negative spastic paraplegias.Journal of human genetics · 2023Article
- The Unfolded Protein Response: A Double-Edged Sword for Brain Health.Antioxidants (Basel, Switzerland) · 2023Review
- GS-SMD server for steered molecular dynamics of peptide substrates in the active site of the γ-secretase complex.Nucleic acids research · 2023Article
- Presenilins and mitochondria-an intriguing link: mini-review.Frontiers in neuroscience · 2023Review
- Cogs in the autophagic machine-equipped to combat dementia-prone neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Neurogenesis in aging and age-related neurodegenerative diseases.Ageing research reviews · 2022Review
- Excessive/Aberrant and Maladaptive Synaptic Plasticity: A Hypothesis for the Pathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- Epigenetic and Immune-Cell Infiltration Changes in the Tumor Microenvironment in Hepatocellular Carcinoma.Frontiers in immunology · 2021Article
- Zinc Finger Proteins in Neuro-Related Diseases Progression.Frontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presenilin genes (PSEN1 and PSEN2) are mainly responsible for causing early-onset familial Alzheimer's disease, harboring ~300 causative mutations, and representing ~90% of all mutations associated with a very aggressive disease form. Presenilin 1 is the catalytic core of the γ-secretase complex that conducts the intramembranous proteolytic excision of multiple transmembrane proteins like the amyloid precursor protein, Notch-1, N- and E-cadherin, LRP, Syndecan, Delta, Jagged, CD44, ErbB4, and Nectin1a. Presenilin 1 plays an essential role in neural progenitor maintenance, neurogenesis, neurite outgrowth, synaptic function, neuronal function, myelination, and plasticity. Therefore, an imbalance caused by mutations in presenilin 1/γ-secretase might cause aberrant signaling, synaptic dysfunction, memory impairment, and increased Aβ
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