ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
p75NTR regulates Abeta deposition by increasing Abeta production but inhibiting Abeta aggregation with its extracellular domain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
- p75 neurotrophin receptor signaling through the RhoA/ROCK pathway contributes to Tau-mediated neurodegeneration.Molecular psychiatry · 2026Article
- Palmitoylation of death receptor p75Alzheimer's research & therapy · 2026Article
- Amelioration of Symptomatic Alzheimer's Disease after Selective Impairment of p75The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Rigor & Reproducibility: pH Adjustments of Papain with L-Cysteine Dissociation Solutions and Cell Media Using Phenol Red Spectrophotometry.Biosensors · 2025Article
- Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches.Journal of neuroscience research · 2025Review
- The Molecular Pathway of p75 Neurotrophin Receptor (p75NTR) in Parkinson's Disease: The Way of New Inroads.Molecular neurobiology · 2024Review
- Soluble p75 neurotrophic receptor as a reliable biomarker in neurodegenerative diseases: what is the evidence?Neural regeneration research · 2024Review
- Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.Aging and disease · 2024Review
- Nerve growth factor receptor (Ngfr) induces neurogenic plasticity by suppressing reactive astroglial Lcn2/Slc22a17 signaling in Alzheimer's disease.NPJ Regenerative medicine · 2023Article
- Basal forebrain cholinergic signalling: development, connectivity and roles in cognition.Nature reviews. Neuroscience · 2023Review
- Deletion of p75Frontiers in molecular neuroscience · 2023Article
- Association of rs2072446 in the NGFR gene with the risk of Alzheimer's disease and amyloid-β deposition in the brain.CNS neuroscience & therapeutics · 2022Article
- Integrated Analysis of DNA methylation and transcriptome profile to identify key features of age-related macular degeneration.Bioengineered · 2021Article
- Integrated phylogeny of the human brain and pathobiology of Alzheimer's disease: A unifying hypothesis.Neuroscience letters · 2021Review
- Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Pharmacokinetic Modelling of Human Recombinant Protein, p75ECD-Fc: A Novel Therapeutic Approach for Treatment of Alzheimer's Disease, in Serum and Tissue of Sprague Dawley Rats.European journal of drug metabolism and pharmacokinetics · 2021Article
- Inactive variants of death receptor p75The EMBO journal · 2021Article
- Estradiol Replacement at the Critical Period Protects Hippocampal Neural Stem Cells to Improve Cognition in APP/PS1 Mice.Frontiers in aging neuroscience · 2020Article
- Knockout of p75 neurotrophin receptor attenuates the hyperphosphorylation of Tau in pR5 mouse model.Aging · 2019Article
- Neurotrophin Receptor p75 mRNA Level in Peripheral Blood Cells of Patients with Alzheimer's Disease.Neurotoxicity research · 2019Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of toxic amyloid-β (Aβ) in the cerebral cortex and hippocampus is a major pathological feature of Alzheimer's disease (AD). The neurotrophin receptor p75NTR has been proposed to mediate Aβ-induced neurotoxicity; however, its role in the development of AD remains to be clarified. The p75NTR/ExonIII-/- mice and APPSwe/PS1dE9 mice were crossed to generate transgenic AD mice with deletion of p75NTR gene. In APPSwe/PS1dE9 transgenic mice, p75NTR expression was localized in the basal forebrain neurons and degenerative neurites in neocortex, increased with aging, and further activated by Aβ accumulation. Deletion of the p75NTR gene in APPSwe/PS1dE9 mice reduced soluble Aβ levels in the brain and serum, but increased the accumulation of insoluble Aβ and Aβ plaque formation. There was no change in the levels of amyloid precursor protein (APP) and its proteolytic derivatives, or α-, β-, and γ-secretase activities, or in levels of BACE1, neprilysin (NEP), and insulin-degrading enzyme (IDE) proteins. Aβ production by cortical neurons of APPSwe/PS1dE9 mice was reduced by deletion of p75NTR gene in vitro. Recombinant extracellular domain of p75NTR attenuated the oligomerization and fibrillation of synthetic Aβ(42) peptide in vitro, and reduced local Aβ plaques after hippocampus injection in vivo. In addition, deletion of p75NTR attenuated microgliosis but increased the microhemorrhage profiles in the brain. The deletion of p75NTR did not significantly change the cognitive function of the mice up to the age of 9 months. Our data suggest that p75NTR plays a critical role in regulating Aβ levels by both increasing Aβ production and attenuating its aggregation, and they caution that a therapeutic intervention simply reducing p75NTR may exacerbate AD pathology.
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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.