A common atmospheric pollutant, magnetite, may be involved in inducing the accumulation of toxic proteins and neuronal loss associated with Alzheimer’s disease. Research conducted on mice exposed to magnetite particles showed increased buildup of amyloid plaques and behavioral changes within just 4 months of exposure. Scientists are hopeful that this study will aid in the development of preventive healthcare and governmental measures against the disease.
Magnetite (Fe3O4) is an atmospheric pollutant originating from the combustion products of fossil fuels such as coal, oil, and natural gas. It is commonly found in emissions from coal-fired power plants, vehicle exhausts, as well as in smoke from brake pads and engine wear.
Studies have revealed that once inhaled, atmospheric particles can accumulate in the lower respiratory tract and subsequently migrate into the systemic circulation by crossing the alveolar-capillary barrier. These particles can also reach the brain through the olfactory bulb and breach the blood-brain barrier.
It has been suggested that upon entering the brain, these particles may play a role in the etiology of various neurodegenerative diseases, including Alzheimer’s. Abnormally high levels of magnetite particles have been found in post-mortem brain samples of individuals living in heavily polluted areas, aged between 40 to 65 at the time of their death. While iron and iron oxides are naturally present in the brain and essential for numerous metabolic processes, excessive presence can be toxic, leading to oxidative damage.
Researchers from the University of Technology Sydney, the University of New South Wales, and the Singapore University of Technology collaborated to delve into the molecular mechanisms behind this correlation in a detailed study published in Environment International.
A new study aimed at investigating the biological activities of atmospheric pollutants potentially involved in Alzheimer’s, conducted in vivo and in vitro analysis on human neurons and healthy as well as Alzheimer’s-prone (genetically modified) mouse models exposed to pollutants for 4 months.
The findings indicated that magnetite triggered pathological processes commonly associated with Alzheimer’s in all models. This included exacerbated loss of neurons in the hippocampus (vital for memory) and the somatosensory cortex (involved in sensation processing). Additionally, behavior changes consistent with disease symptoms were observed, such as increased anxiety-related stress and short-term memory impairments.
Magnetite also elicited abnormally elevated immune responses and oxidative stress in all animals, leading to neuronal damage. Inflammation and oxidative stress are recognized as significant factors contributing to dementia.
Furthermore, it was noted that magnetite-induced neurodegeneration is independent of the pathological state, as Alzheimer’s signs were observed in the brains of healthy mice aside from amyloid plaque accumulation. These results could potentially guide the development of guidelines for disease prevention, suggesting the inclusion of magnetite particles in air quality assessments and appropriate actions.
