Tiffany Ang, Class of 2026

Amyloid-B (AB) proteins, a hallmark of Alzheimer’s disease, have been linked to air pollution exposure, potentially contributing to neurodegenerative diseases. Dr. Kritikos and colleagues at Stony Brook University investigated whether exposure to particulate matter (PM), particularly from the World Trade Center (WTC) site following the 9/11 attacks, was associated with increased cerebral amyloidosis, a condition characterized by the accumulation of AB plaques in the brain, which contribute to cognitive decline in responders. Fine particulate matter (PM_2.5), particles smaller than 2.5 micrometers, is known to contribute to cognitive decline and an elevated risk of dementia.

WTC responders, aged 44-65, who had varying durations of exposure and did not have personalized protective equipment, were assessed using positron-emission tomography (PET) with ¹⁸F-florbetaben to detect amyloid plaques, which are commonly associated with Alzheimer’s disease and related dementias (ADRD). PET visualizes metabolic activity in cells, and ¹⁸F-florbetaben binds to amyloid plaques, making them visible on PET scans. These amyloid plaques, which accumulate as part of a neuroimmune response, are accelerated by air pollution, leading to faster aggregation and deposition, even in younger individuals. Dr. Kritikos and colleagues hypothesized that amyloidosis would be most prominent in the olfactory cortex, as PM enters through the nasal cavities. Responders were recruited from a WTC health monitoring program and assessed for cognitive impairment. Cognitive performance was measured using the CogState computerized battery and the Montreal Cognitive Assessment. This study is particularly relevant as many WTC responders are aging, and Dr. Kritikos’ team sought to understand how long-term exposure to air pollution contributes to cognitive deficits. 

The results showed increased ¹⁸F-florbetaben uptake in the frontal regions, indicative of fibrillary amyloidosis, a hallmark of Alzheimer’s disease. Amyloid clusters were detected in the medial orbitofrontal, superior frontal, and precentral regions, further supporting the presence of fibrillary amyloidosis. Elevated amyloid burden is associated with lower neurocognitive scores, including declines in cognitive speed, memory, learning, information processing, and impaired motor function. Dr. Kritikos’s team concluded that cerebral amyloidosis likely can arise from inhaled neurotoxic dust, particularly PM_2.5, which can cross the blood-brain barrier and deposit in the olfactory cortex. The olfactory cortex is responsible for sensory perception, and damage to this area can impair one’s sense of smell, a potential indicator of neurodegeneration. These findings highlight the role of air pollution in dementia and emphasize the need for protective measures, such as respiratory masks and health monitoring programs to reduce long-term cognitive risks in affected populations.

Figure 1: The One World Trade Center and the 9/11 Memorial is a testament to resilience and the ongoing effects of World Trade Center related neurodegeneration.

Works Cited:

[1] Kritikos M, Zhou J-W, Huang C, et al. Exposure duration and cerebral amyloidosis in the olfactory cortex of World Trade Center responders: A positron emission tomography and magnetic resonance imaging study. Journal of Alzheimer’s Disease. 2025;103(2):383-395. doi:10.1177/13872877241302350
[2] Image retrieved from: https://commons.wikimedia.org/wiki/File:September_11_Memorial,_1_World_Trade_Center,_New_York_City.jpg