Could Air Pollution Be Linked to Alzheimer’s Disease?

         Hypothesizing about the environmental triggers of Alzheimer’s disease (AD) can quickly lead down a proverbial rabbit hole. Such a discussion occurred last week in my Neurochemistry course at Concordia College as we discussed the role that obesity, insulin resistance, and genetics play in the development of AD.
        And while I won’t reach any foregone conclusion today about how Alzheimer’s arises, I will share concerning new research about a possible link between air pollution and AD. This research is important because in today’s world, whether you live in Fargo, ND or Los Angeles, we all experience some level of air pollution. The findings are important to acknowledge for the sake of our health and should leave us to reconsider the safety of our current means of energy production.
        In July of 2016, a study from the Lancaster Environment Center at the University of Lancaster in England provided evidence of exogenous magnetite nanoparticles in the human brain. The study used common imaging and chemical analysis techniques to examine the composition of the nanoparticles from the brains of about 40 human subjects who had previously lived in either Mexico City or Manchester, England.
        Endogenous biological processes can actually form angular nanoparticles composed of iron oxide that are similar to the exogenous nanoparticles found by Lancaster. What was unique, however, concerning the aforementioned study was the identification of nanoparticles with more rounded shapes.
        While the rounded particles were a new finding in the human brain, the particles themselves were recognizable. That’s because the rounded particles in the brain share a striking resemblance with nanoparticles in our air that arise from high-temperature (combustion-derived) particulate matter (PM). But how could the nanospheres in the air around us also appear in our brains?
        It turns out that nanoparticles less than 200 nanometers in diameter have a direct route into the brain through the axons of the olfactory bulb. And although some of the highest levels of nanoparticles were found in the oldest subjects from Manchester, equivalent and even higher levels have been found in many young Mexico City residents. In previous studies, these increased metal concentrations have corresponded to hallmarks of AD. All of this, then, provides compelling evidence that nanoparticles from external sources can end up in the brain, but what role does this play in AD?
        The most common neuropathology of AD is the accumulation of beta-amyloid plaques in the brain. Research has shown that magnetite nanoparticles are sometimes associated with beta-amyloid plaques and that the particles work to enhance the toxicity of beta-amyloid. That’s because when beta-amyloid is associated with the nanoparticles, it can generate dangerous reactive oxygen species that cause oxidative brain damage. Consequently, oxidative brain damage is an early feature of AD.
        With the incidence of AD increasing, it’s important that efforts are ramped up to identify early risk factors. Most importantly, we must be impartial in our inquiries towards possible risk factors, even if those factors could be arising from our most necessary forms of transportation. It might seem like a tall (and frankly unlikely) task for an unbiased review of our air pollution’s effects on AD, but it is definitely necessary. In the end, it could finally provide a nonpartisan reason to invest in cleaner and less nanoparticle forming energy sources. Most importantly, it could save lives.