ArticleFrontiers in physiology2017
The Cerebral Brain-Derived Neurotrophic Factor Pathway, Either Neuronal or Endothelial, Is Impaired in Rats with Adjuvant-Induced Arthritis. Connection with Endothelial Dysfunction.
Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Joint-brain communication in rheumatoid arthritis: glial mechanisms, pain phenotypes, and translational evidence.Frontiers in immunology · 2026Review
- G-protein coupled receptor kinase 2 mediates rheumatoid arthritis-induced depression-like behaviors via the hippocampal CRHR1 signaling pathway.Acta pharmacologica Sinica · 2025Article
- Brain-immune interactions: implication for cognitive impairments in Alzheimer's disease and autoimmune disorders.Journal of leukocyte biology · 2024Review
- Role of Nitric Oxide in the Altered Calcium Homeostasis of Platelets from Rats with Biliary Cirrhosis.International journal of molecular sciences · 2023Article
- Molecular mechanisms underlying physical exercise-induced brain BDNF overproduction.Frontiers in molecular neuroscience · 2023Review
- Article
- Cognitive Decline in Rheumatoid Arthritis: Insight into the Molecular Pathogenetic Mechanisms.International journal of molecular sciences · 2021Review
- Endothelial Dysfunction and Extra-Articular Neurological Manifestations in Rheumatoid Arthritis.Biomolecules · 2021Review
- Brain-derived neurotrophic factor secreted by the cerebral endothelium: A new actor of brain function?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia.Frontiers in aging neuroscience · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive abilities are largely dependent on activation of cerebral tropomyosin-related kinase B receptors (TrkB) by brain-derived neurotrophic factor (BDNF) that is secreted under a bioactive form by both neurons and endothelial cells. In addition, there is mounting evidence for a link between endothelial function and cognition even though the underlying mechanisms are not well known. Therefore, we investigated the cerebral BDNF pathway, either neuronal or endothelial, in rheumatoid arthritis (RA) that combines both endothelial dysfunction (ED) and impaired cognition. Adjuvant-induced arthritis (AIA) in rats was used as a model of RA. Clinical inflammatory symptoms were evaluated from an arthritis score and brains were collected at day 31 ± 2 post-immunization. Neuronal expression of BDNF and TrkB phosphorylated at tyrosine 816 (p-TrkB) was examined in brain slices. Endothelial BDNF and p-TrkB expression was examined on both brain slices (hippocampal arterioles) and isolated cerebral microvessels-enriched fractions (vessels downstream to arterioles). The connection between endothelial nitric oxide (NO) and BDNF production was explored on the cerebrovascular fractions using endothelial NO synthase (eNOS) levels as a marker of NO production,
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