ArticleBioscience reports2020
Peripheral inflammation promotes brain tau transmission via disrupting blood-brain barrier.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Cholinergic impairment in the dorsal motor nucleus of the vagus during experimental Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Tau is necessary for Pseudomonas aeruginosa-induced blood-brain barrier dysfunction.Communications biology · 2026Article
- Microbiota and Alzheimer's disease: mechanistic insights from a multi-organ perspective.Translational neurodegeneration · 2026Review
- Linking Lymphedema, Chronic Inflammation, Oxidative Stress, Alzheimer Disease, and Potential Role of Lymphaticovenous Anastomosis.Plastic and reconstructive surgery. Global open · 2025Article
- Microbial Trojan Horses: Virulence Factors as Key Players in Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2025Review
- The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- MRI detects blood-brain barrier alterations in a rat model of Alzheimer's disease and lung infection.Npj imaging · 2025Article
- Circulating Interleukin-17A is associated with executive function in middle aged adults with and without type 2 diabetes.Brain, behavior, & immunity - health · 2024Article
- Peripheral inflammation is associated with brain atrophy and cognitive decline linked to mild cognitive impairment and Alzheimer's disease.Scientific reports · 2024Article
- The endotoxin hypothesis of Alzheimer's disease.Molecular neurodegeneration · 2024Review
- Article
- The role of peripheral inflammatory insults in Alzheimer's disease: a review and research roadmap.Molecular neurodegeneration · 2023Review
- The innate immune response in tauopathies.European journal of immunology · 2023Review
- Recent advances in drug delivery and targeting to the brain.Journal of controlled release : official journal of the Controlled Release Society · 2022Review
- How Microbes Affect Depression: Underlying Mechanisms via the Gut-Brain Axis and the Modulating Role of Probiotics.International journal of molecular sciences · 2022Review
- Interactive Effects of Pulse Pressure and Tau Imaging on Longitudinal Cognition.Journal of Alzheimer's disease : JAD · 2022Article
- The Role of Chronic Infection in Alzheimer's Disease: Instigators, Co-conspirators, or Bystanders?Current clinical microbiology reports · 2021Article
- Irisin treatment lowers levels of phosphorylated tau in the hippocampus of pre-symptomatic female but not male htau mice.Neuropathology and applied neurobiology · 2021Article
- The Impact of Systemic Inflammation on Alzheimer's Disease Pathology.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal aggregation of pathological tau protein is a neuropathological feature of Alzheimer's disease (AD). In the AD patients, the abnormal tau accumulation first appeared in entorhinal cortex (EC) and then propagated to the hippocampus with microglia activation and inflammation, but the mechanism is elusive. Here, we studied the role and mechanisms underlying periphery inflammation on brain tau transmission. By intraperitoneal injection of lipopolysaccharide (LPS) with brain medial entorhinal cortex (MEC)-specific overexpressing P301L human tau (P301L-hTau), we found that both acute and chronic administration of LPS remarkably promoted P301L-hTau transmission from MEC to the hippocampal subsets. Interestingly, the chronic LPS-induced P301L-hTau transmission was still apparent after blocking microglia activation. Further studies demonstrated that LPS disrupted the integrity of blood-brain barrier (BBB) and simultaneous intraperitoneal administration of glucocorticoid (GC) attenuated LPS-promoted P301L-hTau transmission. These data together suggest that a non-microglia-dependent BBB disruption contributes to peripheral LPS-promoted brain P301L-hTau transmission, therefore, maintaining the integrity of BBB can be a novel strategy for preventing pathological tau propagation in AD and other tauopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.