Background: Neuropathological studies supported by experimental animal studies show that the constituents of the innate immunity are intimately involved in the early steps of the pathological cascade of Alzheimer's disease (AD).
Objectives: To show the evidence that constituents of the innate immunity contribute to the etiology of late-onset AD.
Methods: Evaluation of the relationship between the constituents of the innate immunity and genetic risk factors for late-onset AD.
Results: Complement activation and activated microglia are early neuropathogical events in AD brains. Genome-wide association studies have demonstrated gene loci that are linked to the complement system. The production capacity for inflammatory cytokines is under genetic control and the offspring with a parental history of late-onset AD have a higher production capacity for inflammatory cytokines.
Conclusion: Epidemiological and genetic data suggest that the innate immunity is involved in the etiology of late-onset AD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1159/000334287 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Prior vaccination prevents overactivation of innate immune responses during COVID-19 breakthrough infection.
Sci Transl Med
January 2025
Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
At this stage in the COVID-19 pandemic, most infections are "breakthrough" infections that occur in individuals with prior severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure. To refine long-term vaccine strategies against emerging variants, we examined both innate and adaptive immunity in breakthrough infections. We performed single-cell transcriptomic, proteomic, and functional profiling of primary and breakthrough infections to compare immune responses from unvaccinated and vaccinated individuals during the SARS-CoV-2 Delta wave.
View Article and Find Full Text PDFAdaptive Immunity Determines the Cancer Treatment Outcome of Oncolytic Virus and Anti-PD-1.
Bull Math Biol
January 2025
Department of Mathematics, University of Manitoba, 340 UMSU University Centre, Winnipeg, MB, R3T 2N2, Canada.
The immune checkpoint inhibitor, anti-programmed death protein-1 (anti-PD-1), enhances adaptive immunity to kill tumor cells, and the oncolytic virus (OV) triggers innate immunity to clear the infected tumor cells. We create a mathematical model to investigate how the interaction between adaptive and innate immunities under OV and anti-PD-1 affects tumor reduction. For different immunity strength, we create the corresponding virtual baseline patients and cohort patients to decipher the major factors determining the treatment outcome.
View Article and Find Full Text PDFA comprehensive review of current insights into the virulence factors of SARS-CoV-2.
J Virol
January 2025
State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
The evolution of SARS-CoV-2 pathogenicity has been a major focus of attention. However, the determinants of pathogenicity are still unclear. Various hypotheses have attempted to elucidate the mechanisms underlying the evolution of viral pathogenicity, but a definitive conclusion has yet to be reached.
View Article and Find Full Text PDFInnate Immunity Never "NODs" Off: NLRs Regulate the Host Anti-Viral Immune Response.
Immunol Rev
March 2025
Graduate Program in Translational Biology, Medicine, and Health, Virginia Tech, Roanoke, Virginia, USA.
A robust innate immune response is essential in combating viral pathogens. However, it is equally critical to quell overzealous immune signaling to limit collateral damage and enable inflammation resolution. Pattern recognition receptors are critical regulators of these processes.
View Article and Find Full Text PDFHost cell responses to biofilm-derived extracellular vesicles.
Front Cell Infect Microbiol
January 2025
Department of Comparative Biochemistry and Bioanalytics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.
is a prevalent fungal pathogen responsible for infections in humans. As described recently, nanometer-sized extracellular vesicles (EVs) produced by play a crucial role in the pathogenesis of infection by facilitating host inflammatory responses and intercellular communication. This study investigates the functional properties of EVs released by biofilms formed by two strains-3147 (ATCC 10231) and SC5314-in eliciting host responses.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!