Neurodegenerative diseases involve an exacerbated neuroinflammatory response led by microglia that triggers cytokine storm and leukocyte infiltration into the brain. PPARα agonists partially dampen this neuroinflammation in some models of brain insult, but neuronal loss was not the triggering cause in any of them. This study examines the anti-inflammatory and immunomodulatory properties of the PPARα agonist oleoylethanolamide (OEA) in the Purkinje Cell Degeneration (PCD) mouse, which exhibits striking neuroinflammation caused by aggressive loss of cerebellar Purkinje neurons. Using real-time quantitative polymerase chain reaction and immunostaining, we quantified changes in pro- and anti-inflammatory markers, microglial density and marker-based phenotype, and overall leukocyte recruitment at different time points after OEA administration. OEA was found to modulate cerebellar neuroinflammation by increasing the gene expression of proinflammatory mediators at the onset of neurodegeneration and decreasing it over time. OEA also enhanced the expression of anti-inflammatory and neuroprotective factors and the Pparα gene. Regarding microgliosis, OEA reduced microglial density—especially in regions where it is preferentially located in PCD mice—and shifted the microglial phenotype towards an anti-inflammatory state. Finally, OEA prevented massive leukocyte infiltration into the cerebellum. Overall, our findings suggest that OEA may change the environment to protect neurons from degeneration caused by exacerbated inflammation.

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality globally. Early detection and personalised prevention strategies are crucial for reducing the burden of CVD. The use of biomarkers plays a pivotal role in identifying individuals at risk and facilitating timely interventions. This rapid scoping review aims to identify and evaluate current research on biomarkers used for primary and secondary personalised prevention of CVD, highlighting evidence gaps and the integration of digital technologies. A comprehensive search was conducted in Medline and Embase databases from January 2020 to February 2023. Joanna Briggs Institute (JBI) Manual for Evidence Synthesis and PRISMA-ScR guidelines were followed. A total of 775 studies were included, with ischemic heart disease (IHD) and stroke being the most investigated CVDs. Molecular, cellular, imaging, physiological, and anthropometric biomarkers were included. Molecular biomarkers, particularly genetic and biochemical, were the most researched. For secondary prevention, there was considerable research using imaging biomarkers. Genetic biomarker research was the most frequent category of biomarker identified, particularly using variant analysis and polygenic scores, followed by biochemical, imaging, and physiological biomarkers. There was also evidence of the integration of artificial intelligence to enhance the predictive capabilities of these biomarkers. Despite progress, research gaps were identified for less common CVDs, such as aortic aneurysm and nonrheumatic valvular heart disease, and limited research investigating other molecular biomarker types, such as epigenetics and transcriptomics.

Background and Aims: Chronic inflammation contributes to various chronic diseases, emphasizing the need for reliable biomarkers for early detection and understanding its causes. Measuring chronic inflammation poses challenges since most biomarkers are influenced by both acute and chronic states and recent exposures. Joint analysis of inflammatory biomarkers may help identify specific biological signatures linked to chronic inflammation. The scoping review whose protocol is described here, aims to map the existing literature identifying these signatures in adults using data reduction methods in epidemiological studies. Methods: The review will follow the Joanna Briggs Institute methodology and the extension for Scoping Reviews of the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis checklist (PRISMA‐ScR). An electronic search will be performed in Medline (via PubMed) and Embase (via Elsevier) for studies published until October 2023, using relevant terms related to inflammation biomarkers, and data reduction methods. Eligible studies include systematic reviews and primary experimental, quasi‐experimental, and observational research analyzing inflammation biomarkers in blood, urine, or saliva from adults. Studies focused on acute infectious diseases, transient inflammatory conditions, and those not published in English or Spanish will be excluded. Four independent reviewers will conduct a two‐phase screening of studies (title/abstract and full‐text), with a third reviewer resolving disagreements. Data extraction will be handled by one reviewer and verified by another using a predefined form. Results: Findings will be summarized in a PRISMA flowchart. Interactive visual maps will illustrate the identified inflammatory signatures, categorized by study design, data reduction method, population type, and clinical condition. All resources will be publicly available. Conclusion: This review will provide a comprehensive overview of inflammation biomarker signatures derived from data reduction methods while identifying existing knowledge gaps in the field. Scoping Review Registration: This protocol was registered on January 25, 2024, on Open Science Framework ( https://doi.org/10.17605/OSF.IO/85XUF ).