ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017
TLR2 knockout protects against diabetes-mediated changes in cerebral perfusion and cognitive deficits.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- TLR2 promotes the progression of diabetes mellitus with atherosclerosis via activating NLRP3 inflammasome and MyD88/NF-κB signaling pathway.Scientific reports · 2025Article
- Novel insights into immune-related genes associated with type 2 diabetes mellitus-related cognitive impairment.World journal of diabetes · 2024Article
- Exploring the common mechanism of vascular dementia and inflammatory bowel disease: a bioinformatics-based study.Frontiers in immunology · 2024Article
- Magnetic resonance imaging reveals microemboli-mediated pathological changes in brain microstructure in diabetic rats: relevance to vascular cognitive impairment/dementia.Clinical science (London, England : 1979) · 2022Article
- Identification of Molecular Signatures and Candidate Drugs in Vascular Dementia by Bioinformatics Analyses.Frontiers in molecular neuroscience · 2022Article
- Identification of TLR2 as a Key Target in Neuroinflammation in Vascular Dementia.Frontiers in genetics · 2022Article
- Diabetic rats are more susceptible to cognitive decline in a model of microemboli-mediated vascular contributions to cognitive impairment and dementia.Brain research · 2020Article
- Glu-mGluR2/3-ERK Signaling Regulates Apoptosis of Hippocampal Neurons in Diabetic-Depression Model Rats.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy.Frontiers in endocrinology · 2019Article
- Post-stroke neovascularization and functional outcomes differ in diabetes depending on severity of injury and sex: Potential link to hemorrhagic transformation.Experimental neurology · 2019Article
- In vivo imaging and analysis of cerebrovascular hemodynamic responses and tissue oxygenation in the mouse brain.Nature protocols · 2018Article
- Impact of Metabolic Diseases on Cerebral Circulation: Structural and Functional Consequences.Comprehensive Physiology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The risk of cognitive decline in diabetes (Type 1 and Type 2) is significantly greater compared with normoglycemic patients, and the risk of developing dementia in diabetic patients is doubled. The etiology for this is likely multifactorial, but one mechanism that has gained increasing attention is decreased cerebral perfusion as a result of cerebrovascular dysfunction. The innate immune system has been shown to play a role in diabetic vascular complications, notably through the Toll-like receptor (TLR)-stimulated release of proinflammatory cytokines and chemokines that lead to vascular damage. TLR2 has been implicated in playing a crucial role in the development of diabetic microvascular complications, such as nephropathy, and thus, we hypothesized that TLR2-mediated cerebrovascular dysfunction leads to decreased cerebral blood flow (CBF) and cognitive impairment in diabetes. Knockout of TLR2 conferred protection from impaired CBF in early-stage diabetes and from hyperperfusion in long-term diabetes, prevented the development of endothelium-dependent vascular dysfunction in diabetes, created a hyperactive and anxiolytic phenotype, and protected against diabetes-induced impairment of long-term hippocampal and prefrontal cortex-mediated fear learning. In conclusion, these findings support the involvement of TLR2 in the pathogenesis of diabetic vascular disease and cognitive impairment.
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