ArticleJournal of Alzheimer's disease : JAD2015
Impact of CRFR1 Ablation on Amyloid-β Production and Accumulation in a Mouse Model of Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Stress, stress systems, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Review
- The Aggravating Role of Failing Neuropeptide Networks in the Development of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease.Neurobiology of disease · 2023Article
- Research Progress on the Etiology and Pathogenesis of Alzheimer's Disease from the Perspective of Chronic Stress.Aging and disease · 2023Review
- Anxiety and Alzheimer's disease pathogenesis: focus on 5-HT and CRF systems in 3xTg-AD and TgF344-AD animal models.Frontiers in aging neuroscience · 2023Review
- Emerging Alzheimer's disease therapeutics: promising insights from lipid metabolism and microglia-focused interventions.Frontiers in aging neuroscience · 2023Review
- Hippocampal Reduction of α-Synuclein via RNA Interference Improves Neuropathology in Alzheimer's Disease Mice.Journal of Alzheimer's disease : JAD · 2023Article
- Intrinsically disordered proteins and proteins with intrinsically disordered regions in neurodegenerative diseases.Biophysical reviews · 2022Review
- Targeting the cannabinoid system to counteract the deleterious effects of stress in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Neuroprotection of Tropical Fruit Juice Mixture via the Reduction of iNOS Expression and CRH Level inEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Corticotropin releasing factor-binding protein (CRF-BP) as a potential new therapeutic target in Alzheimer's disease and stress disorders.Translational psychiatry · 2019Review
- Localization of amyloid beta peptides to locus coeruleus and medial prefrontal cortex in corticotropin releasing factor overexpressing male and female mice.Brain structure & function · 2019Article
- Risk Factors for Alzheimer's Disease: Focus on Stress.Frontiers in pharmacology · 2019Review
- Cerebellar Learning Properties Are Modulated by the CRF Receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Stress induced neural reorganization: A conceptual framework linking depression and Alzheimer's disease.Progress in neuro-psychopharmacology & biological psychiatry · 2018Review
- The relationship between stress and Alzheimer's disease.Neurobiology of stress · 2018Review
- Sex differences in chronic stress responses and Alzheimer's disease.Neurobiology of stress · 2018Review
- Brain Under Stress and Alzheimer's Disease.Cellular and molecular neurobiology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Stress exposure and the corticotropin-releasing factor (CRF) system have been implicated as mechanistically involved in both Alzheimer's disease (AD) and associated rodent models. In particular, the major stress receptor, CRF receptor type 1 (CRFR1), modulates cellular activity in many AD-relevant brain areas, and has been demonstrated to impact both tau phosphorylation and amyloid-β (Aβ) pathways. The overarching goal of our laboratory is to develop and characterize agents that impact the CRF signaling system as disease-modifying treatments for AD. In the present study, we developed a novel transgenic mouse to determine whether partial or complete ablation of CRFR1 was feasible in an AD transgenic model and whether this type of treatment could impact Aβ pathology. Double transgenic AD mice (PSAPP) were crossed to mice null for CRFR1; resultant CRFR1 heterozygous (PSAPP-R1(+/-)) and homozygous (PSAPP-R1(-/-)) female offspring were used at 12 months of age to examine the impact of CRFR1 disruption on the severity of AD Aβ levels and pathology. We found that both PSAPP-R1(+/-) and PSAPP-R1(-/-) had significantly reduced Aβ burden in the hippocampus, insular, rhinal, and retrosplenial cortices. Accordingly, we observed dramatic reductions in Aβ peptides and AβPP-CTFs, providing support for a direct relationship between CRFR1 and Aβ production pathways. In summary, our results suggest that interference of CRFR1 in an AD model is tolerable and is efficacious in impacting Aβ neuropathology.
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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.