Fig 1.
The experimental framework for PM2.5 exposure in AD mice.
Table 1.
The water-soluble ion composition of the PM2.5 around exposure period.
Fig 2.
The histopathological views of H&E staining (100X & 400X) in AD mouse brain after PM2.5 exposure.
Fig 3.
The histopathological views of Nissl staining (100X & 400X) in AD mouse brain after PM2.5 exposure.
Fig 4.
The histopathological views of IHC staining (100X & 400X) of TNFα and Iba-1 in AD mouse brain after PM2.5 exposure.
The red arrow indicates the representative IHC positively stained neurons.
Table 2.
The numbers of neuronal cells in the cortex sections after 3-month exposure of PM2.5.
Fig 5.
The levels of AD-related protein expression (a) p-tau, (b) total tau, (c) Iba-1, (d) Aβ42, and (e) LC3B in AD mouse brains after PM2.5 exposure (n = 6) compared to control mice (n = 7). The values are presented as mean ± SD. * indicates the significant differences between two groups with a p value lower than 0.05.
Fig 6.
The MDA levels of individual AD mouse brain regions after PM2.5 exposure (n = 6) compared to control mice (n = 7).
The values are presented as mean ± SD. * indicates the significant differences between two groups with a p value lower than 0.05.
Fig 7.
The possible mechanisms of subchronic exposure to environmental levels of PM2.5-mediated neuronal dysfunction in AD mouse brains.
The black words and arrows indicated the observations (such as neuronal death and p-tau accumulation) and their biological roles found in this study. The gray parts were described the PM-mediated evidences and mechanisms reported from previous researches, but not in the current studies.
Table 3.
PM-induced neuronal dysfunction on brains of AD disease models.