Understanding the Links Between Air Pollution and Increased Alzheimer Disease Risk

Alzheimer disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide. It typically begins with episodic memory decline and progresses to impairments in language, executive function, and behavior. Pathologically, AD is marked by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss, particularly in the hippocampus.¹ Neuropsychiatric symptoms, including depression and agitation, are common and contribute substantially to caregiver burden and reduced quality of life.²

As AD prevalence continues to rise, attention has increasingly turned toward identifying modifiable environmental risk factors. In a new national cohort study, lead author Yanling Deng, MBBS, PhD, postdoctoral researcher at Emory University, and colleagues examined the association between air pollution exposure and AD risk. Published in PLOS Medicine, findings suggest that PM2.5 exposure is linked to increased AD risk, largely through direct pathways rather than through comorbid conditions.³

To gain more perspective on these new nationwide findings linking PM2.5 exposure to increased AD risk, NeurologyLive^® recently spoke with AD expert R. Scott Turner, PhD, MD, the director of the memory disorders program at MedStar Georgetown University Hospital. In this Q&A, he underscored the importance of identifying modifiable environmental factors as AD prevalence is projected to rise. He also noted that PM2.5 may function as an independent risk factor through mechanisms such as inflammation, oxidative stress, and amyloid accumulation.

NeurologyLive: Beginning with a more general question, why is research of this nature important to conduct?

R Scott Turner, PhD, MD: There are many causes of dementia with aging, but AD is the most common cause of dementia in the United States. Current therapies are limited and can slow but not stop or reverse progressive cognitive and functional decline. AD currently affects approximately 7 million individuals (and their families) in the US alone, and this number will double by 2050. One way to tease out the cause of disease is to discover its risk factors. Other ways are to examine tissues for pathologic changes (such as amyloid plaques and tangles found in brain tissue of AD), and to discover genetic forms of the disease (rare families carrying a genetic mutation that causes early-onset AD).

What does this new research tell us about the relationship between air pollution and AD?

Prior studies have suggested air pollution as a risk factor for AD, but this new study is the largest and most comprehensive to date. This new nationwide study confirms that air pollution – specifically fine particulate matter, or PM2.5 – is indeed a risk factor for AD, and this effect is not mediated by stroke, hypertension, or depression (although stroke was implicated in approximately 4%). This means air pollution is likely a direct risk factor.

What population is most vulnerable to air pollution?

Those with other lung diseases – asthma, chronic obstructive pulmonary disease, etc. - are vulnerable to air pollution. The population at risk for AD because of air pollution are older individuals, especially those with other known AD risk factors. The nonmodifiable risk factors for AD are aging and genetics/family history. Potentially modifiable risk factors include hearing loss, high cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, social isolation, and visual loss, and air pollution. Risk factors may be additive or synergistic in promoting AD.

This new study examined air pollution levels by zip code. Those who live in regions of the US with high air pollution (such as the smog of the Los Angeles basin) may be more vulnerable. Particulates also come from forest fires – which spread smoke to large regions of the country. A website tracks the air quality index (and PM2.5) across the US (www.airNow.gov). Protective measures for air pollution include facemasks, home filters, and staying indoors when air quality is poor. And, of course, no smoking of any kind.

From a mechanistic perspective, how is air pollution thought to contribute to the pathophysiology of AD?

How air pollution contributes to AD is not known, but theories include inflammation, oxidative stress, and amyloid accumulation in the brain. If fine particulates are able to cross the blood brain barrier into brain, they may seed amyloid plaques - similar to seeding clouds to make rain – but this is speculative. Further research is needed to determine mechanism.

In your mind, what needs to be studied further?

We have made tremendous progress with our understanding of AD in recent years. This includes prognosis (including healthy individuals at risk of impending dementia), diagnosis, and treatment. We now have blood tests to determine whether dementia may be because of AD. Newly-approved treatments – antibodies that remove amyloid from the brain and slow dementia progression - are available for those with early AD.

Much research is still needed – for example, validating new blood tests, finding more effective and safer treatments, and preventing disease. We need more studies with diverse populations since AD affects all races and ethnicities. Other dementing illnesses of aging also warrant further study, such as dementia with Lewy bodies and frontotemporal dementia.

Transcript edited for clarity. Click here to view more of our coverage in AD.

REFERENCES
1. Knopman DS, Amieva H, Petersen RC, et al. Alzheimer disease. Nat Rev Dis Primers. 2021;7(1):33. doi:10.1038/s41572-021-00269-y
2. Lanctôt KL, Amatniek J, Ancoli-Israel S, et al. Neuropsychiatric signs and symptoms of Alzheimer disease. Alzheimers Dement. 2017;13(11):1316-1336. doi:10.1016/j.jalz.2017.05.008
3. Deng Y, Liu Y, Hao H, et al. The role of comorbidities in the associations between air pollution and Alzheimer's disease: A national cohort study in the American Medicare population. PLoS Med. 2026;23(2):e1004912. Published 2026 Feb 17. doi:10.1371/journal.pmed.1004912