ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Convergence of presenilin- and tau-mediated pathways on axonal trafficking and neuronal function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Altered expression of Presenilin2 impacts endolysosomal homeostasis and synapse function in Alzheimer's disease-relevant brain circuits.Nature communications · 2024Article
- miR-200a-3p Regulates PRKACB and Participates in Aluminium-Induced Tau Phosphorylation in PC12 Cells.Neurotoxicity research · 2022Article
- Differential Transcriptome Profiling Unveils Novel Deregulated Gene Signatures Involved in Pathogenesis of Alzheimer's Disease.Biomedicines · 2022Article
- Loss of presenilin function enhances tau phosphorylation and aggregation in mice.Acta neuropathologica communications · 2021Article
- Review
- Presenilin/γ-secretase-dependent EphA3 processing mediates axon elongation through non-muscle myosin IIA.eLife · 2019Article
- Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons.Journal of Alzheimer's disease : JAD · 2017Review
- Neurodegenerative Disease Related Proteins Have Negative Effects on SNARE-Mediated Membrane Fusion in Pathological Confirmation.Frontiers in molecular neuroscience · 2017Article
- Synergistic effects of particulate matter (PMToxicology research · 2017Article
- Pharmocologic treatment with histone deacetylase 6 inhibitor (ACY-738) recovers Alzheimer's disease phenotype in amyloid precursor protein/presenilin 1 (APP/PS1) mice.Alzheimer's & dementia (New York, N. Y.) · 2015Article
- Article
- Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB.EMBO molecular medicine · 2014Article
- Overexpression of p62/SQSTM1 promotes the degradations of abnormally accumulated PrP mutants in cytoplasm and relieves the associated cytotoxicities via autophagy-lysosome-dependent way.Medical microbiology and immunology · 2014Article
- Cytosolic carboxypeptidase 5 removes α- and γ-linked glutamates from tubulin.The Journal of biological chemistry · 2013Article
- Axonal degeneration in Alzheimer's disease: when signaling abnormalities meet the axonal transport system.Experimental neurology · 2013Review
- Axonal transport deficits and neurodegenerative diseases.Nature reviews. Neuroscience · 2013Review
- Presenilins in synaptic function and disease.Trends in molecular medicine · 2011Review
- Convergent pathogenic pathways in Alzheimer's and Huntington's diseases: shared targets for drug development.Nature reviews. Drug discovery · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is a significant and growing health problem in the aging population. Although definitive mechanisms of pathogenesis remain elusive, genetic and histological clues have implicated the proteins presenilin (PS) and tau as key players in AD development. PS mutations lead to familial AD, and although tau is not mutated in AD, tau pathology is a hallmark of the disease. Axonal transport deficits are a common feature of several neurodegenerative disorders and may represent a point of intersection of PS and tau function. To investigate the contribution of wild-type, as opposed to mutant, tau to axonal transport defects in the context of presenilin loss, we used a mouse model postnatally deficient for PS (PS cDKO) and expressing wild-type human tau (WtTau). The resulting PS cDKO;WtTau mice exhibited early tau pathology and axonal transport deficits that preceded development of these phenotypes in WtTau or PS cDKO mice. These deficits were associated with reduced neurotrophin signaling, defective learning and memory and impaired synaptic plasticity. The combination of these effects accelerated neurodegeneration in PS cDKO;WtTau mice. Our results strongly support a convergent role for PS and tau in axonal transport and neuronal survival and function and implicate their misregulation as a contributor to AD pathogenesis.
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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.