ArticleThe Journal of biological chemistry2010
Beta-amyloid1-42 gene transfer model exhibits intraneuronal amyloid, gliosis, tau phosphorylation, and neuronal loss.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Roles of Ubiquitin Ligases and Deubiquitylases in Alzheimer's Disease.Molecular neurobiology · 2025Review
- The Role of Neuroglial Metabotropic Glutamate Receptors in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Nilotinib Effects on Safety, Tolerability, and Biomarkers in Alzheimer's Disease.Annals of neurology · 2020Article
- Pioglitazone Reduces β Amyloid LevelsFrontiers in aging neuroscience · 2019Article
- Review
- Alzheimer's disease: experimental models and reality.Acta neuropathologica · 2017Review
- Physical Exercise and Brain Mitochondrial Fitness: The Possible Role Against Alzheimer's Disease.Brain pathology (Zurich, Switzerland) · 2016Review
- Weight Loss Predicts Progression of Mild Cognitive Impairment to Alzheimer's Disease.PloS one · 2016Article
- Gene Therapy Models of Alzheimer's Disease and Other Dementias.Methods in molecular biology (Clifton, N.J.) · 2016Article
- The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.Hormones and behavior · 2015Review
- Tau deletion impairs intracellular β-amyloid-42 clearance and leads to more extracellular plaque deposition in gene transfer models.Molecular neurodegeneration · 2014Article
- Choroid plexus implants rescue Alzheimer's disease-like pathologies by modulating amyloid-β degradation.Cellular and molecular life sciences : CMLS · 2014Article
- Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Human APOE genotype affects intraneuronal Aβ1-42 accumulation in a lentiviral gene transfer model.Human molecular genetics · 2014Article
- Fractalkine signaling and Tau hyper-phosphorylation are associated with autophagic alterations in lentiviral Tau and Aβ1-42 gene transfer models.Experimental neurology · 2014Article
- Aging reduces glial uptake and promotes extracellular accumulation of Aβ from a lentiviral vector.Frontiers in aging neuroscience · 2014Article
- Nilotinib reverses loss of dopamine neurons and improves motor behavior via autophagic degradation of α-synuclein in Parkinson's disease models.Human molecular genetics · 2013Article
- Tyrosine kinase inhibition increases functional parkin-Beclin-1 interaction and enhances amyloid clearance and cognitive performance.EMBO molecular medicine · 2013Article
- A transgenic Alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric aβ, and frank neuronal loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Decreased parkin solubility is associated with impairment of autophagy in the nigrostriatum of sporadic Parkinson's disease.Neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer disease is characterized by extracellular beta-amyloid (Abeta) plaques and intracellular inclusions containing neurofibrillary tangles of phospho-Tau and intraneuronal Abeta associated with neuronal cell death. We generated a novel gene transfer animal model using lentiviral Abeta(1-42) that resulted in intracellular but not extracellular Abeta accumulations in the targeted rat primary motor cortex. Expression of intracellular Abeta(1-42) led to pathological changes seen in human Alzheimer disease brains, including cell death, inflammatory signs, activation of two Tau kinases, and Tau hyperphosphorylation. Promoting clearance of lentiviral Abeta(1-42) reversed these effects, demonstrating that intraneuronal Abeta(1-42) is a toxic peptide that lies upstream of Tau modification. These studies reveal the role of intracellular Abeta(1-42) in a novel gene transfer animal model, which is a useful tool to study intraneuronal Abeta(1-42)-induced pathology in the absence of extracellular plaques. Targeted delivery of Abeta will allow speedy delineation of pathological mechanisms associated with specific neurodegenerative lesions.
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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.