Abstract
Background
Amyloid-β proteins, a hallmark of Alzheimer's disease, are believed to play an adaptive role in the cerebral immune response.
Objective
Amyloid is believed to play a role in cerebral immune response and could play a similar role in response to air pollution exposures. In the present study, we examined whether WTC exposure duration was associated with cerebral amyloidosis in WTC responders.
Methods
WTC responders (aged 44–65 years) who varied in exposure duration but did not use personalized protective equipment were assessed using positron-emission tomography with [18F]-Florbetaben. The outcome was the cortical [18F]-Florbetaben burden, measured using regional standardized uptake value ratios (SUVRs) in 34 Desikan-Killiany regions of interest. Spearman's ρ and generalized linear models were used to estimate correlations between WTC exposure duration and cortical [18F]-Florbetaben SUVR. Cognitive and behavioral symptoms were measured. Magnetic resonance imaging was used to measure cortical thickness and diffusivity.
Results
The mean age of imaged responders was 56 years old. WTC exposure duration was associated with olfactory [18F]-Florbetaben SUVR (Spearman's ρ = 0.43, p = 0.011), which was in turn associated with elevated [18F]-Florbetaben SUVR in ventral regions (ρ = 0.41, p = 0.016). Cortical [18F]-Florbetaben in ventral regions was associated with reduced response speed (ρ = −0.72, p < 0.001), was co-located with cortical diffusivity across regions in the parietal and frontal lobes and reduced cortical thickness in the isthmus cingulate (ρ = −0.53, p = 0.001).
Conclusions
Low-grade amyloidosis in the olfactory and frontal lobes was associated with WTC exposure duration. Future work should examine whether low-grade amyloidosis is correlated with the location or distribution of neurofibrillary tangles in WTC responders.
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Supplementary Material
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