ArticleThe EMBO journal2019
Tau deletion reduces plaque-associated BACE1 accumulation and decelerates plaque formation in a mouse model of Alzheimer's disease.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders.Genomic psychiatry : advancing science from genes to society · 2025Article
- Abnormal behaviors and glial responses in an animal model of tau pathology.Molecular brain · 2025Article
- Axonal tau reduction ameliorates tau and amyloid pathology in a mouse model of Alzheimer's disease.Translational neurodegeneration · 2025Article
- Annexin A6 membrane repair protein protects against amyloid-induced dystrophic neurites and tau phosphorylation in Alzheimer's disease model mice.Acta neuropathologica · 2025Article
- Synthesis and Biological Evaluation of Novel Ramalin Derivatives as Multi-Target Agents for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Article
- Intraneuronal binding of amyloid beta with reelin-Implications for the onset of Alzheimer's disease.PLoS computational biology · 2025Article
- Animal models of Alzheimer's disease: Current strategies and new directions.Zoological research · 2024Review
- Multi-Protective Effects of Petunidin-3-O-(International journal of molecular sciences · 2024Article
- Epilepsy and epileptiform activity in late-onset Alzheimer disease: clinical and pathophysiological advances, gaps and conundrums.Nature reviews. Neurology · 2024Review
- Perinatal Tissue-Derived Stem Cells: An Emerging Therapeutic Strategy for Challenging Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- APP accumulates with presynaptic proteins around amyloid plaques: A role for presynaptic mechanisms in Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Amyloid-beta peptide and tau protein crosstalk in Alzheimer's disease.Neural regeneration research · 2022Review
- Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022Review
- Andrographolide emeliorates maltol aluminium-induced neurotoxicity via regulating p62-mediated Keap1-Nrf2 pathways in PC12 cells.Pharmaceutical biology · 2021Article
- Persistent repression of tau in the brain using engineered zinc finger protein transcription factors.Science advances · 2021Article
- Pregabalin Treatment does not Affect Amyloid Pathology in 5XFAD Mice.Current Alzheimer research · 2021Article
- Therapeutic Effects of Human Amniotic Epithelial Stem Cells in a Transgenic Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice.EMBO reports · 2020Article
- Systems Pharmacology Approach to Investigate the Mechanism of Kai-Xin-San in Alzheimer's Disease.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
In Alzheimer's disease, BACE1 protease initiates the amyloidogenic processing of amyloid precursor protein (APP) that eventually results in synthesis of β-amyloid (Aβ) peptide. Aβ deposition in turn causes accumulation of BACE1 in plaque-associated dystrophic neurites, thereby potentiating progressive Aβ deposition once initiated. Since systemic pharmacological BACE inhibition causes adverse effects in humans, it is important to identify strategies that specifically normalize overt BACE1 activity around plaques. The microtubule-associated protein tau regulates axonal transport of proteins, and tau deletion rescues Aβ-induced transport deficits in vitro. In the current study, long-term in vivo two-photon microscopy and immunohistochemistry were performed in tau-deficient APPPS1 mice. Tau deletion reduced plaque-associated axonal pathology and BACE1 accumulation without affecting physiological BACE1 expression distant from plaques. Thereby, tau deletion effectively decelerated formation of new plaques and reduced plaque compactness. The data revealed that tau reinforces Aβ deposition, presumably by contributing to accumulation of BACE1 in plaque-associated dystrophies. Targeting tau-dependent mechanisms could become a suitable strategy to specifically reduce overt BACE1 activity around plaques, thereby avoiding adverse effects of systemic BACE inhibition.
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