ArticleCell reports2019
Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer's Disease.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.
- Associations between cerebrospinal fluid markers and cognition in ageing and dementia: A systematic review.The European journal of neuroscience · 2022Pooled it
- Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer's disease.Nature aging · 2021Trial
- Review
- Xanthones and Their Nitrogen and Sulfur Analogs in Alzheimer's Disease: Recent Progress Toward Multifunctional Therapeutics.ChemMedChem · 2026Review
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial-oligodendrocyte responses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Corticothalamic circuit and executive dysfunction in Alzheimer's disease and related tauopathies.The Journal of physiology · 2026Article
- Maintaining and regaining episodic memory in Alzheimer disease: a circuit-based perspective.Nature reviews. Neurology · 2026Review
- Tau and β-Amyloid Relevant Pathology as a Central Therapeutic Target in Alzheimer's Disease.Biomolecules · 2026Review
- Presenilin-dependent regulation of neuronal tau pathology via the autophagy and proteasome pathways.Acta neuropathologica communications · 2026Article
- Modulation of Tau Protein Neurotoxic Hallmarks by Novel σChemMedChem · 2026Article
- Synthesis of 3-desoxycollinoketone B and its ability to reduce Alzheimer-associated misfolded proteins.Nature communications · 2026Article
- Blood level of β-amyloid, Tau, and p-Tau in mild cognitive impairment and Alzheimer disease: A follow up study.The Indian journal of medical research · 2026Article
- Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.Cell death & disease · 2026Review
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
- APP E590D mutation increases generation of Aβ and Aη peptides and exacerbates tauopathy.NPJ dementia · 2026Article
- Exploring the Biological Connection Between Tau and PrPMolecular neurobiology · 2025Review
- Emerging Concepts in Diagnosis, Pathologic Features, and Treatment of Limbic-Predominant Amnestic Neurodegenerative Syndrome (LANS): A Narrative Review.Advances in therapy · 2025Review
- Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Neuroprotective Effects of Hesperidin and CK2 Inhibitor DRB on AβMolecular neurobiology · 2025Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
30 authors at 3 institutions in 3 countries.
Funding
Abstract
A key knowledge gap blocking development of effective therapeutics for Alzheimer's disease (AD) is the lack of understanding of how amyloid beta (Aβ) peptide and pathological forms of the tau protein cooperate in causing disease phenotypes. Within a mouse tau-deficient background, we probed the molecular, cellular, and behavioral disruption triggered by the influence of wild-type human tau on human Aβ-induced pathology. We find that Aβ and tau work cooperatively to cause a hyperactivity behavioral phenotype and to cause downregulation of transcription of genes involved in synaptic function. In both our mouse model and human postmortem tissue, we observe accumulation of pathological tau in synapses, supporting the potential importance of synaptic tau. Importantly, tau reduction in the mice initiated after behavioral deficits emerge corrects behavioral deficits, reduces synaptic tau levels, and substantially reverses transcriptional perturbations, suggesting that lowering synaptic tau levels may be beneficial in AD.
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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.