ArticleMolecular neurobiology2016
Angiotensin-(1-7) is Reduced and Inversely Correlates with Tau Hyperphosphorylation in Animal Models of Alzheimer's Disease.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Current updates on latest basic research of scientific relevance in hypertensive dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.Inflammopharmacology · 2025Article
- Rescuing ACE2-Deficiency-Mediated Nucleus Pulposus Senescence and Intervertebral Disc Degeneration by a Nanotopology-Enhanced RNAi System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Angiotensin-(1-7) protective effects in neurocognitive disorders: molecular mechanisms to therapeutic implications.Frontiers in physiology · 2025Review
- The Contribution of the Renin-Angiotensin System to Alzheimer's Disease.Current topics in behavioral neurosciences · 2025Review
- Review
- The Influence of SARS-CoV-2 Infection on the Development of Selected Neurological Diseases.International journal of molecular sciences · 2024Review
- Targeting the Renin-Angiotensin System (RAS) for Neuropsychiatric Disorders.Current neuropharmacology · 2024Article
- Angiotensin Receptor Blockers and Cognition: a Scoping Review.Current hypertension reports · 2024Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Multiomics profiling of the impact of an angiotensin (1-7)-expressing probiotic combined with exercise training in aged male rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Links between COVID-19 and Alzheimer's Disease-What Do We Already Know?International journal of environmental research and public health · 2023Review
- The COVID-19 pandemic and Alzheimer's disease: mutual risks and mechanisms.Translational neurodegeneration · 2022Review
- Renin-Angiotensin System in Huntington's Disease: Evidence from Animal Models and Human Patients.International journal of molecular sciences · 2022Article
- Alzheimer's-like signaling in brains of COVID-19 patients.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Angiotensin-(1-7) reduces α-synuclein aggregation by enhancing autophagic activity in Parkinson's disease.Neural regeneration research · 2022Article
- Multiple Aspects of Inappropriate Action of Renin-Angiotensin, Vasopressin, and Oxytocin Systems in Neuropsychiatric and Neurodegenerative Diseases.Journal of clinical medicine · 2022Review
- Can SARS-CoV-2 Infection Exacerbate Alzheimer's Disease? An Overview of Shared Risk Factors and Pathogenetic Mechanisms.Journal of personalized medicine · 2022Review
- Safety and biomarker effects of candesartan in non-hypertensive adults with prodromal Alzheimer's disease.Brain communications · 2022Article
- Probiotic Releasing Angiotensin (1-7) in a Drosophila Model of Alzheimer's Disease Produces Sex-Specific Effects on Cognitive Function.Journal of Alzheimer's disease : JAD · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a recently identified bioactive peptide of brain renin-angiotensin system (RAS), angiotensin-(1-7) [Ang-(1-7)] along with its metabolic enzyme angiotensin-converting enzyme (ACE) 2 and its receptor Mas forms ACE2/Ang-(1-7)/Mas axis. Accumulating evidence suggests an essential role of ACE2/Ang-(1-7)/Mas axis in maintaining normal cognitive functions in both animals and human subjects, and dysregulation of this axis contributed to the pathogenesis of several neurodegenerative diseases such as hypertension-induced neurodegeneration and vascular dementia. To date, whether this axis was associated with the etiology and progression of Alzheimer's disease (AD), the most prevalent neurodegenerative disease in the elderly, remains unclear. In the current study, by using senescence-accelerated mouse prone 8 (SAMP8) mice, an animal model of sporadic AD, we showed for the first time that the level of Ang-(1-7) in the brain was significantly reduced during disease progression. More importantly, an inverse correlation was found between Ang-(1-7) level and tau hyperphosphorylation, a pathological hallmark of AD, in cerebral cortex and hippocampus of SAMP8 mice. Meanwhile, this has been further confirmed in P301S mice, an animal model of pure tauopathy. All these findings suggested that Ang-(1-7), the main effector of brain ACE2/Ang-(1-7)/Mas axis, might be implicated in the etiology and progression of AD, possibly via modulation of tau hyperphosphorylation.
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