Abstract
Although cigarette smoking has been postulated to be a potential risk factor for Alzheimer’s disease (AD), the toxic mechanism is still unclear. Additionally, astrocytes have been identified as a potential target, given they play multiple roles in maintaining normal brain function. In this study, we explored the toxic mechanism of whole cigarette smoke condensates (WCSC) using murine astrocytes. Cell proliferation, the percentage of cells in the G2/M phase, and LDH concentrations in the cell supernatants were all reduced in WCSC-treated cells. In addition, oxidative stress was induced, together with shortening of processes, structural damage of organelles, disturbances in mitochondrial function, blockage of autophagic signals, accumulation of amyloid β precursor protein, and loss of chemotactic functions. Based on these results, we hypothesize that dysfunction of astrocytes may contribute to the occurrence of cigarette-smoking-induced AD.
Highlights
IntroductionDementia is the fifth leading cause of death worldwide and affects 50 million people
Dementia is the fifth leading cause of death worldwide and affects 50 million people. many potential causes, including physical, psychological, social, and economic circumstances, are associated with the incidence of dementia, it is clear that age is the most significant risk factor [1]
After 24 h exposure to whole cigarette smoke condensates (WCSC), no features consistent with those of dead cells were evident under phase-contrast microscopy, whereas proliferation appeared to be inhibited
Summary
Dementia is the fifth leading cause of death worldwide and affects 50 million people. Many potential causes, including physical, psychological, social, and economic circumstances, are associated with the incidence of dementia, it is clear that age is the most significant risk factor [1]. The trend toward aging populations and the progressive increase in the number of patients with dementia have become worldwide concerns. Cigarette smoking has been considered an important risk factor for AD, suggesting the possible prevention (or delay) of AD onset (or progress) by quitting smoking [6,7,8]. Oxidative stress increased amyloid β precursor protein (APP) processing and microglial proinflammatory responses, and reduced Aβ clearance by microglia are closely associated with cigarette-smokinginduced AD
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