A new study from the University of Eastern Finland shows that exposure to ultrafine particles (UFP) from traffic can interfere with how our genes function, without altering the genetic code itself. These changes happen through epigenetic mechanisms – switches that turn genes on or off.
The researchers focused on how UFPs affect cells in the olfactory mucosa, the tissue at the top of our nasal cavity that is in direct contact with both the outside air and the brain. This area is especially vulnerable as it’s one of the main pathways through which air pollution can reach the brain. Disruptions in the sense of smell, which this tissue helps control, are also known to be one of the earliest warning signs of Alzheimer’s disease.
This study is the first to take a broad, integrative approach by combining several advanced genetic analysis methods to investigate how UFPs affect cellular functions. The team looked closely at a key biological pathway called PI3K/AKT, which helps regulate cell growth and survival. This pathway is already known to be affected in many diseases, including Alzheimer’s, and previous research has shown it can be disturbed by pollutants.
Their findings suggest that UFPs may disrupt the normal function of this pathway by altering how genes are regulated. While they found changes in the expression of genes related to cell death and growth, the cells didn’t die – implying that they might be trying to adapt or protect themselves. However, cells taken from individuals with Alzheimer’s reacted differently, showing more signs of vulnerability to UFP exposure than healthy cells.
This research adds to concerns about the long-term impacts of air pollution on brain health and highlights the potential for even small particles like UFPs to trigger complex biological responses.
First author, Doctoral Researcher Laura Mussalo of the Kanninen Lab. said: ‘The association between air pollution and Alzheimer’s disease is well established, however, the understanding of the molecular mechanisms of how air pollutants are involved in AD pathobiology remain obscure. This study deep dives into one signaling pathway connected to AD to understand these complex interactions of how environmental stressors shape our bodily responses.’
The study is part of the TUBE project, funded by the European Union to study the adverse effects of extremely fine particles in the human lung and brain.
The full research can be read here.
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