ArticleMolecular neurodegeneration2014
Tau pathogenesis is promoted by Aβ1-42 but not Aβ1-40.
Article in Molecular neurodegeneration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Tau acetylation at K331 has limited impact on tau pathology in vivo.FEBS letters · 2026Article
- Preeclampsia as a reversible risk factor for Alzheimer's disease: A prospective MRI study on morphological changes of the cerebral cortex and impairment of cognitive functions.The journal of prevention of Alzheimer's disease · 2026Article
- The association between mean arterial pressure and memory decline in preeclampsia patients: a mediation analysis of serum amyloid-β 1-42 and phosphorylated tau 181.BMC pregnancy and childbirth · 2025Article
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- LncRNA NORAD sponging to miR-26b-5p represses the progression of Alzheimer's disease in vitro by upregulating MME expression.Cytotechnology · 2025Article
- The effects of amyloidosis and aging on glutamatergic and GABAergic synapses, and interneurons in the barrel cortex and non-neocortical brain regions.Frontiers in neuroanatomy · 2025Article
- N-Acetylcysteine Amide against Aβ-Induced Alzheimer's-like Pathology in Rats.International journal of molecular sciences · 2023Article
- Necrostatin-1 Relieves Learning and Memory Deficits in a Zebrafish Model of Alzheimer's Disease Induced by Aluminum.Neurotoxicity research · 2022Article
- Probing Protein Aggregation Using the Coarse-Grained UNRES Force Field.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The Effects of AβInternational journal of molecular sciences · 2021Article
- Characterization of a Mouse Model of Alzheimer's Disease Expressing Aβ4-42 and Human Mutant Tau.International journal of molecular sciences · 2021Article
- Relationship between neuropsychiatric symptoms and Alzheimer's disease pathology: An in vivo positron emission tomography study.International journal of geriatric psychiatry · 2021Article
- The Positive Side of the Alzheimer's Disease Amyloid Cross-Interactions: The Case of the Aβ 1-42 Peptide with Tau, TTR, CysC, and ApoA1.Molecules (Basel, Switzerland) · 2020Review
- The Interplay Between Beta-Amyloid 1-42 (AβFrontiers in molecular neuroscience · 2020Article
- Article
- Dependence of the Formation of Tau and Aβ Peptide Mixed Aggregates on the Secondary Structure of the N-Terminal Region of Aβ.The journal of physical chemistry. B · 2018Article
- Mitochondrial Molecular Abnormalities Revealed by Proteomic Analysis of Hippocampal Organelles of Mice Triple Transgenic for Alzheimer Disease.Frontiers in molecular neuroscience · 2018Article
- TREM2 in Neurodegenerative Diseases.Molecular neurodegeneration · 2017Review
- Neuroprotective Effect of Fisetin Against Amyloid-Beta-Induced Cognitive/Synaptic Dysfunction, Neuroinflammation, and Neurodegeneration in Adult Mice.Molecular neurobiology · 2017Article
- Neuritic and Diffuse Plaque Associations with Memory in Non-Cognitively Impaired Elderly.Journal of Alzheimer's disease : JAD · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe relationship between the pathogenic amyloid β-peptide species Aβ1-42 and tau pathology has been well studied and suggests that Aβ1-42 can accelerate tau pathology in vitro and in vivo. The manners if any in which Aβ1-40 interacts with tau remains poorly understood. In order to answer this question, we used cell-based system, transgenic fly and transgenic mice as models to study the interaction between Aβ1-42 and Aβ1-40.
resultsIn our established cellular model, live cell imaging (using confocal microscopy) combined with biochemical data showed that exposure to Aβ1-42 induced cleavage, phosphorylation and aggregation of wild-type/full length tau while exposure to Aβ1-40 didn't. Functional studies with Aβ1-40 were carried out in tau-GFP transgenic flies and showed that Aβ1-42, as previously reported, disrupted cytoskeletal structure while Aβ1-40 had no effect at same dose. To further explore how Aβ1-40 affects tau pathology in vivo, P301S mice (tau transgenic mice) were injected intracerebrally with either Aβ1-42 or Aβ1-40. We found that treatment with Aβ1-42 induced tau phosphorylation, cleavage and aggregation of tau in P301S mice. By contrast, Aβ1-40 injection didn't alter total tau, phospho-tau (recognized by PHF-1) or cleavage of tau, but interestingly, phosphorylation at Ser262 was shown to be significantly decreased after direct inject of Aβ1-40 into the entorhinal cortex of P301S mice.
conclusionsThese results demonstrate that Aβ1-40 plays different role in tau pathogenesis compared to Aβ1-42. Aβ1-40 may have a protective role in tau pathogenesis by reducing phosphorylation at Ser262, which has been shown to be neurotoxic.
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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.