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Proteasome 20S and Rab5 alteration after 24 h and 14 days chlorpyrifos exposure lead to β-amyloid and Tau protein levels increase and SN56 neuronal cell death.

The biocide Chlorpyrifos (CPF) was shown to produce cognition impairment, following single and long-term exposure. The complete mechanisms that lead to the CPF induced cognitive disorders remain to be discovered. Aβ and tau proteins pro-duction was induced in basal forebrain SN56 cholinergic cells, by CPF, through proteasome 20S inhibition and Rab5 over-expression, leading to cell death both after acute and repeated administration, which was related with cognitive disorders induction. The results obtained in our study procure novel information related to the mechanisms involved in CPF neuro-degeneration, which could be responsible for cognitive dysfunction and may lead to a promising alternative treatment of these effects.