ArticleAging cell2016
Beta-amyloid 1-42 monomers, but not oligomers, produce PHF-like conformation of Tau protein.
Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022Pooled it
- Article
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- The AβFrontiers in cellular neuroscience · 2024Article
- Estrogens still represent an attractive therapeutic approach for Alzheimer's disease.Neural regeneration research · 2022Article
- Acetylation of Aβ42 at Lysine 16 Disrupts Amyloid Formation.ACS chemical neuroscience · 2020Article
- Vascular Dysfunction in Alzheimer's Disease: A Prelude to the Pathological Process or a Consequence of It?Journal of clinical medicine · 2019Review
- Epigenetics of chronic inflammatory diseases.Journal of inflammation research · 2019Review
- Promising Results from Alzheimer's Disease Passive Immunotherapy Support the Development of a Preventive Vaccine.Research (Washington, D.C.) · 2019Review
- Cellular Prion Protein Mediates the Disruption of Hippocampal Synaptic Plasticity by Soluble TauThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The effect of amyloid-β peptide on synaptic plasticity and memory is influenced by different isoforms, concentrations, and aggregation status.Neurobiology of aging · 2018Article
- The Transcriptional Regulatory Properties of Amyloid Beta 1-42 may Include Regulation of Genes Related to Neurodegeneration.Neuromolecular medicine · 2018Article
- Tau reduction in the presence of amyloid-β prevents tau pathology and neuronal death in vivo.Brain : a journal of neurology · 2018Article
- A silver lining for 24-hydroxycholesterol in Alzheimer's disease: The involvement of the neuroprotective enzyme sirtuin 1.Redox biology · 2018Article
- The Unexpected Role of Aβ1-42 Monomers in the Pathogenesis of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- The Emerging Role of Altered Cerebellar Synaptic Processing in Alzheimer's Disease.Frontiers in aging neuroscience · 2018Review
- Dual Mechanism of Toxicity for Extracellular Injection of Tau Oligomers versus Monomers in Human Tau Mice.Journal of Alzheimer's disease : JAD · 2017Article
- The Decrease of Uch-L1 Activity Is a Common Mechanism Responsible for Aβ 42 Accumulation in Alzheimer's and Vascular Disease.Frontiers in aging neuroscience · 2017Article
- Review
Corrections and comments
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Authors and funding
11 authors at 9 institutions in 2 countries.
Funding
Abstract
The mechanistic relationship between amyloid β1-42 (Aβ1-42) and the alteration of Tau protein are debated. We investigated the effect of Aβ1-42 monomers and oligomers on Tau, using mice expressing wild-type human Tau that do not spontaneously develop Tau pathology. After intraventricular injection of Aβ1-42, mice were sacrificed after 3 h or 4 days. The short-lasting treatment with Aβ monomers, but not oligomers, showed a conformational PHF-like change of Tau, together with hyperphosphorylation. The same treatment induced increase in concentration of GSK3 and MAP kinases. The inhibition of the kinases rescued the Tau changes. Aβ monomers increased the levels of total Tau, through the inhibition of proteasomal degradation. Aβ oligomers reproduced all the aforementioned alterations only after 4 days of treatment. It is known that Aβ1-42 monomers foster synaptic activity. Our results suggest that Aβ monomers physiologically favor Tau activity and dendritic sprouting, whereas their excess causes Tau pathology. Moreover, our study indicates that anti-Aβ therapies should be targeted to Aβ1-42 monomers too.
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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.