ArticleScientific reports2020
Pneumonia-induced endothelial amyloids reduce dendritic spine density in brain neurons.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 91 citations in OpenAlex.
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- The causal association between insomnia and cognitive decline: A 2-sample, 2-step multivariable Mendelian randomization study.Medicine · 2025Article
- Alzheimer's Disease as Type 3 Diabetes: Understanding the Link and Implications.International journal of molecular sciences · 2024Review
- cUMP elicits interendothelial gap formation duringAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- The Impact of Pulmonary Disorders on Neurological Health (Lung-Brain Axis).Immune network · 2024Review
- SARS-CoV-2-Induced Type I Interferon Signaling Dysregulation in Olfactory Networks Implications for Alzheimer's Disease.Current issues in molecular biology · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Gamma secretase activating protein promotes end-organ dysfunction after bacterial pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Infection promotes Ser-214 phosphorylation important for generation of cytotoxic tau variants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Lung infection by Pseudomonas aeruginosa induces neuroinflammation and blood-brain barrier dysfunction in mice.Journal of neuroinflammation · 2023Article
- Lung infection by P. aeruginosa induces neuroinflammation and blood-brain barrier dysfunction in mice.Research square · 2023Article
- Neurovascular Dysfunction in Diverse Communities With Health Disparities-Contributions to Dementia and Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Peripheral Pathways to Neurovascular Unit Dysfunction, Cognitive Impairment, and Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Pneumonia initiates a tauopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa pneumonia elicits endothelial cell release of cytotoxic amyloids that can be recovered from the bronchoalveolar lavage and cerebrospinal fluids of critically ill patients. Introduction of these cytotoxic amyloids into the lateral ventricle impairs learning and memory in mice. However, it is unclear whether the amyloids of lung origin (1) are neurotropic, and (2) cause structural remodeling of hippocampal dendrites. Thus, we used electrophysiological studies in brain slices and structural analysis of post-mortem tissues obtained from animals exposed to endothelium-derived amyloids to assess these issues. The amyloids were administered via three different routes, by intracerebroventricular, intratracheal, and intraperitoneal injections. Synaptic long-term potentiation was abolished following intracerebroventricular amyloid injection. Fluorescence dialysis or Golgi-impregnation labeling showed reduced dendritic spine density and destabilized spines of hippocampal pyramidal neurons 4 weeks after intracerebroventricular amyloid injection. In comparison, endothelial amyloids introduced to the airway caused the most prominent dendritic spine density reduction, yet intraperitoneal injection of these amyloids did not affect spine density. Our findings indicate that infection-elicited lung endothelial amyloids are neurotropic and reduce neuronal dendritic spine density in vivo. Amyloids applied into the trachea may either be disseminated through the circulation and cross the blood-brain barrier to access the brain, initiate feed-forward amyloid transmissibility among cells of the blood-brain barrier or access the brain in other ways. Nevertheless, lung-derived amyloids suppress hippocampal signaling and cause injury to neuronal structure.
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