Occupational silicosis caused by long-term inhalation of silica is a serious public-health problem in the world and is known to be a risk factor for the development of dementia. However, the progression of silicosis, including its impact on the brain and its relationship with β-Amyloid (Aβ), the early biomarker of Alzheimer's disease, remains unclear. In this study, we categorized silicosis into four stages in a mouse model and employed [18F] AV45 PET imaging to quantify Aβ deposition across 19 cerebral sub-regions. We compared the differences in Aβ accumulation across various stages of silicosis and observed a significant increase in Aβ deposition in key brain areas such as the cortex and olfactory bulb, correlating with the severity of lung fibrosis. Notably, Aβ accumulation was also detected in the ocular region, indicating its potential as a non-invasive biomarker for cognitive impairment. These findings highlight a direct link between pulmonary health and neurodegeneration, suggesting that occupational exposure may lead to structural brain changes and cognitive decline. The study underscores the importance of managing silicosis to mitigate its neurological impacts, providing insights into the systemic effects of occupational hazards on brain health and emphasizing the need to monitor these risks to prevent cognitive decline.Copyright © 2025 Elsevier Inc. All rights reserved.