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Recent updates

18
FEB

Kick-off Meeting in Mainz, February 2025

From 18 - 19 February 2025 the MARKOPOLO consortium met in Mainz for the first general assembly &...
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01
JAN

Project start on 1st January 2025

Our project kicks off today, and we're ready to tackle the scientific challenges ahead over the next 4...
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About MARKOPOLO

Traffic noise and air pollution, especially particulate matter (PM) and ultrafine particles (UFP), are closely linked environmental risk factors that contribute significantly to the development of diseases such as diabetes, hypertension and atherosclerosis.

MARKOPOLO aims to investigate the impact of traffic noise and air pollution, especially fine and ultrafine particulate matter, on human health through an innovative translational approach. Experimental and computational models are used in clinical, interventional and epidemiological studies.

One of the main objectives is to identify disease-relevant biomarkers and to understand the molecular mechanisms involved in diseases of the brain, lung and cardiovascular system. The “from bench-to-bedside” approach uses extensive knowledge of the brain-heart connection and applies modern methods to better understand the causes of disease.

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Our vision & objectives

MARKOPOLO will advance our understanding of the complex interplay between noise, air pollution, and human well-being.

We aim to close gaps in knowledge and strengthen the evidence base for pollution-disease associations for traffic noise and air pollution (PM including UFP), especially synergetic interactions, and accounting for effects in susceptible groups and in different genders.
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We take a unique translational approach by implementing experimental/computational models, and clinical and epidemiological studies to provide FAIR data on associations between exposures and health outcomes.
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A primary goal is to identify disease-relevant biomarkers and causality mechanisms to understand the biological pathways of cerebral, pulmonary and cardiovascular health outcomes.
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Our “bench to life” approach is entirely driven by profound preclinical mechanistic knowledge and will use novel multiomics methodology (e.g. redox/phospho-proteomics and “spatial” epigenetics), allowing the analysis of key pathomechanisms, to be included in exposure-response models. This will improve risk assessment and allow evaluation of the effectiveness of mitigation strategies.
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We will also consider the societal circumstances and policies at the national level and their impact on different stakeholders.
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