A new study by Cacciottolo and colleagues indicates that J20-APPswe mice exposed to nano-sized traffic-related particulate matter (nPM) for 150 hours have increased markers of lipid oxidation (4-HNE) and increased the pro-amyloidogenic processing of APP in lipid raft fractions in cerebral cortex but not in the cerebellum a find which parallels that seen for selectivity of Aβ deposits in Alzheimer's disease (AD). In addition, in vitro, studies showed that nPM induced similar oxidative responses in N2a-APPswe cells, which showed dose-dependent production of NO, oxidative damage (4-HNE, 3NT), and lipid raft alterations of APP with increased Aβ peptides. Furthermore, treatment with the antioxidant N-acetyl-cysteine (NAC) attenuated nPM-induced oxidative damage and alterations of APP processing.
These findings provide additional evidence of the mechanisms via which exogenous toxicants found in the environment and workplace interact with neuropathological mechanisms implicated in the onset and progression of AD.
Link to orignal article in PubMed
These findings provide additional evidence of the mechanisms via which exogenous toxicants found in the environment and workplace interact with neuropathological mechanisms implicated in the onset and progression of AD.
Link to orignal article in PubMed
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