Vignesh Subramanian ’24

Figure 1: The South Pool of the 9/11 Memorial in New York, New York

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a progressive loss of memory and cognitive thinking skills that typically worsens with age, and is the leading cause of dementia. Key hallmarks of the disease include buildups of two particular proteins – beta-amyloid peptide and phosphorylated tau – between and inside neurons in the brain. This results in abnormal plaques and tangles forming diffusely across these neurons. Previous studies have found that the accumulation of such toxic deposits is accelerated by cerebral atrophy, the large-scale loss of connections between neurons in the brain, which itself may be caused by a range of factors that include psychological and physiological trauma to the brain. 

Over the last two decades, programs addressing the healthcare needs of first responders to the 9/11/2001 attacks on the World Trade Center (WTC) have identified these individuals as likely having experienced such forms of trauma. WTC responders have been found to experience significantly higher rates of mild cognitive impairment (MCI) and cognitive decline than the broader American public due to their exposure to airborne toxins at Ground Zero and related PTSD. Stony Brook University researchers aimed to determine if material exposures amidst the WTC debris were linked to high levels of neurodegenerative protein aggregates in responders’ brains. 

Led by Drs. Minos Kritikos and Erica Diminich, the researchers analyzed data from nearly 1,200 WTC-exposed adults enrolled in the WTC Aging Study, a longitudinal study examining MCI incidence among this population. The researchers used MRI neuroimaging to quantify and characterize the amyloid, tau, and neurodegeneration (AT[N]) plasma biomarker profiles of each subject, cross-referencing them with data about their cognitive impairment (CI) to determine whether correlations between the two existed. Finally, statistical analyses and self-reported PTSD assessments were performed to distinguish between stress- and memory-centric cognitive outcomes. 

Researchers found that 58% of all responders analyzed had at least one AT[N] biomarker elevated beyond normal levels, with approximately 3.5% having elevations across all measured biomarkers – far outstripping the CI incidence rates of the national populace. Simultaneously, 21% of analyzed responders were found to experience MCI, with nearly 6% having progressed to dementia and responders’ higher rates of PTSD correlating with increased amyloid presence. These findings suggest a direct association between blood-based biomarker levels, cognitive impairment causation, and WTC exposures, underscoring the necessity to enhance Alzheimer’s disease care for 9/11 responders. 

Works Cited:

[1] M. Kritikos, et al., Plasma amyloid beta 40/42, phosphorylated tau 181, and neurofilament light are associated with cognitive impairment and neuropathological changes among World Trade Center responders: A prospective cohort study of exposures and cognitive aging at midlife. Alzheimer’s & Dementia: Diagnosis, Assessment, and Disease Monitoring 15, 1-11 (2023). doi: 10.1002/dad2.12409 

[2] Image retrieved from: https://en.m.wikipedia.org/wiki/File:9-11_Memorial_South_Pool.jpg