Ultrafine particles, UFPs, the smallest contributors to air pollution, hinder the function of mitochondria in human olfactory mucosa cells, a new study shows. Led by the University of Eastern Finland, the study showed that traffic-related UFPs impair mitochondrial functions in primary human olfactory mucosa cells by hampering oxidative phosphorylation and redox balance. Furthermore, the responses of olfactory mucosa cells of individuals with Alzheimer's disease differed from those of cognitively healthy controls.
The findings were published in Redox Biology . Air pollution forms a major global burden to health, and it has been identified as a risk factor for dementia, including Alzheimer's disease, AD. Despite the growing body of evidence, the role of UFPs in the cellular and molecular changes in the human brain leading to Alzheimer's disease remains obscure.
The olfactory mucosa is a sensory tissue responsible for odour detection, and it is directly exposed to the environment and in contact with the brain. Interestingly, one of the earliest clinical symptoms of Alzheimer's disease is an impaired sense of smell. The Kanninen Lab at the University of Eastern Finland uses a physiologically relevant human-based in-vitro model of the olfactory mucosa, which is generated from cells obtained from voluntary donors and collected in collaboration with Kuopio University Hospital.
Earlier studies by the Kanninen Lab have shown that this model recapitulates AD-related alterations, which .