ArticleThe American journal of pathology2013
The bradykinin B1 receptor regulates Aβ deposition and neuroinflammation in Tg-SwDI mice.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
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- A human telomerase reverse transcriptase-derived peptide GV1001 rescues neurodegeneration in a mouse model of Alzheimer disease.Experimental & molecular medicine · 2026Article
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- Angiotensin Receptor Blockers and Cognition: a Scoping Review.Current hypertension reports · 2024Article
- The Effects of Serping1 siRNA in α-Synuclein Regulation in MPTP-Induced Parkinson's Disease.Biomedicines · 2023Article
- Evaluation of Novel B1R/B2R Agonists Containing TRIOZAN™ Nanoparticles for Targeted Brain Delivery of Antibodies in a Mouse Model of Alzheimer Disease.Molecules (Basel, Switzerland) · 2023Article
- Characterization and preclinical evaluation of the cGMP grade DNA based vaccine, AV-1959D to enter the first-in-human clinical trials.Neurobiology of disease · 2020Review
- A MultiTEP platform-based epitope vaccine targeting the phosphatase activating domain (PAD) of tau: therapeutic efficacy in PS19 mice.Scientific reports · 2019Article
- fMRI Reveals Mitigation of Cerebrovascular Dysfunction by Bradykinin Receptors 1 and 2 Inhibitor Noscapine in a Mouse Model of Cerebral Amyloidosis.Frontiers in aging neuroscience · 2019Article
- The Dual Role of Kinin/Kinin Receptors System in Alzheimer's Disease.Frontiers in molecular neuroscience · 2019Article
- Insights From Dynamic Neuro-Immune Imaging on Murine Immune Responses to CNS Damage.Frontiers in neuroscience · 2019Review
- A novel detection method of cleaved plasma high-molecular-weight kininogen reveals its correlation with Alzheimer's pathology and cognitive impairment.Alzheimer's & dementia (Amsterdam, Netherlands) · 2018Article
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- Comparison of Efficacy of Preventive and Therapeutic Vaccines Targeting the N Terminus of β-Amyloid in an Animal Model of Alzheimer's Disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Neuroprotective Effects of Aged Garlic Extract on Cognitive Dysfunction and Neuroinflammation Induced by β-Amyloid in Rats.Nutrients · 2017Article
- Involvement of the Bradykinin BFrontiers in endocrinology · 2017Article
- Visualization of microbleeds with optical histology in mouse model of cerebral amyloid angiopathy.Microvascular research · 2016Article
- Physiological amyloid-beta clearance in the periphery and its therapeutic potential for Alzheimer's disease.Acta neuropathologica · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The deposition of amyloid-β peptides (Aβ) in the cerebral vasculature, a condition known as cerebral amyloid angiopathy, is increasingly recognized as an important component leading to intracerebral hemorrhage, neuroinflammation, and cognitive impairment in Alzheimer disease (AD) and related disorders. Recent studies demonstrated a role for the bradykinin B1 receptor (B1R) in cognitive deficits induced by Aβ in mice; however, its involvement in AD and cerebral amyloid angiopathy is poorly understood. Herein, we investigated the effect of B1R inhibition on AD-like neuroinflammation and amyloidosis using the transgenic mouse model (Tg-SwDI). B1R expression was found to be up-regulated in brains of Tg-SwDI mice, specifically in the vasculature, neurons, and astrocytes. Notably, administration of the B1R antagonist, R715, to 8-month-old Tg-SwDI mice for 8 weeks resulted in higher Aβ40 levels and increased thioflavin S-positive fibrillar Aβ deposition. Moreover, blockage of B1R inhibited neuroinflammation, as evidenced by the decreased accumulation of activated microglia and reactive astrocytes, diminished NF-κB activation, and reduced cytokine and chemokine levels. Together, our results indicate that B1R activation plays an important role in limiting the accumulation of Aβ in AD-like brain, likely through the regulation of activated glial cell accumulation and release of pro-inflammatory mediators. Therefore, the modulation of the receptor may represent a novel therapeutic approach for AD.
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