ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Presenilin-1 mutations reduce cytoskeletal association, deregulate neurite growth, and potentiate neuronal dystrophy and tau phosphorylation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 111 citations in OpenAlex.
- Increasing expression of presenilin 1, β-catenin, and p-PTEN and its regulatory roles on cell invasion in gastric cancer.World journal of gastrointestinal oncology · 2026Article
- Aberrant accumulation of age- and disease-associated factors following neural probe implantation in a mouse model of Alzheimer's disease.Journal of neural engineering · 2023Article
- Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration.Journal of neuroinflammation · 2023Review
- Glycogen synthase kinase 3β (GSK3β) and presenilin (PS) are key regulators of kinesin-1-mediated cargo motility within axons.Frontiers in cell and developmental biology · 2023Review
- Use of Zebrafish Genetic Models to Study Etiology of the Amyloid-Beta and Neurofibrillary Tangle Pathways in Alzheimer's Disease.Current neuropharmacology · 2022Review
- Patient-Derived Fibroblasts With Presenilin-1 Mutations, That Model Aspects of Alzheimer's Disease Pathology, Constitute a Potential Object for Early Diagnosis.Frontiers in aging neuroscience · 2022Article
- Preferential Involvement of BRCA1/BARD1, Not Tip60/Fe65, in DNA Double-Strand Break Repair in Presenilin-1 P117L Alzheimer Models.Neural plasticity · 2022Article
- Presenilin mutations and their impact on neuronal differentiation in Alzheimer's disease.Neural regeneration research · 2022Article
- Loss of presenilin function enhances tau phosphorylation and aggregation in mice.Acta neuropathologica communications · 2021Article
- Presenilin/γ-secretase-dependent EphA3 processing mediates axon elongation through non-muscle myosin IIA.eLife · 2019Article
- proBDNF is modified by advanced glycation end products in Alzheimer's disease and causes neuronal apoptosis by inducing p75 neurotrophin receptor processing.Molecular brain · 2018Article
- Presenilin PS1∆E9 disrupts mobility of secretory organelles in rat astrocytes.Acta physiologica (Oxford, England) · 2018Article
- Prion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.PloS one · 2017Article
- Extract of Fructus Cannabis Ameliorates Learning and Memory Impairment Induced by D-Galactose in an Aging Rats Model.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- The Role of Presenilin in Protein Trafficking and Degradation-Implications for Metal Homeostasis.Journal of molecular neuroscience : MN · 2016Review
- Diosmin reduces cerebral Aβ levels, tau hyperphosphorylation, neuroinflammation, and cognitive impairment in the 3xTg-AD mice.Journal of neuroimmunology · 2016Article
- Postnatal dysregulation of Notch signal disrupts dendrite development of adult-born neurons in the hippocampus and contributes to memory impairment.Scientific reports · 2016Article
- Anabolic actions of Notch on mature bone.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- MiR-126 Regulates Growth Factor Activities and Vulnerability to Toxic Insult in Neurons.Molecular neurobiology · 2016Article
- The BET-Bromodomain Inhibitor JQ1 Reduces Inflammation and Tau Phosphorylation at Ser396 in the Brain of the 3xTg Model of Alzheimer's Disease.Current Alzheimer research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in presenilin genes are linked to early onset familial Alzheimer's disease (FAD). Previous work in non-neuronal cells indicates that presenilin-1 (PS1) associates with cytoskeletal elements and that it facilitates Notch1 signaling. Because Notch1 participates in the control of neurite growth, cultured hippocampal neurons were used to investigate the cytoskeletal association of PS1 and its potential role during neuronal development. We found that PS1 associates with microtubules (MT) and microfilaments (MF) and that its cytoskeletal association increases dramatically during neuronal development. PS1 was detected associated with MT in the central region of neuronal growth cones and with MF in MF-rich areas extending into filopodia and lamellipodia. In differentiated neurons, PS1 mutations reduced the interaction of PS1 with cytoskeletal elements, diminished the nuclear translocation of the Notch1 intracellular domain (NICD), and promoted a marked increase in total neurite length. In developing neurons, PS1 overexpression increased the nuclear translocation of NICD and inhibited neurite growth, whereas PS1 mutations M146V, I143T, and deletion of exon 9 (D9) did not facilitate NICD nuclear translocation and had no effect on neurite growth. In cultures that were treated with amyloid beta (Abeta), PS1 mutations significantly increased neuritic dystrophy and AD-like changes in tau such as hyperphosphorylation, release from MT, and increased tau protein levels. We conclude that PS1 participates in the regulation of neurite growth and stabilization in both developing and differentiated neurons. In the Alzheimer's brain PS1 mutations may promote neuritic dystrophy and tangle formation by interfering with Notch1 signaling and enhancing pathological changes in tau.
Indexed as
Identifiers
11157069PMC6762317W1785214340What 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.