Alzheimer's disease (AD) is a progressive and neurodegenerative illness which results in alterations in cognitive development. It is characterized by loss/dysfunction of cholinergic neurons, and formation of
amyloid plaques, and formation of neurofibrillary tangles, among other changes, due to hyperphosphorylation of
tau-protein. Exposure to pesticides in humans occurs frequently due to contact with contaminated food, water, or particles. Organochlorines,
organophosphates,
carbamates,
pyrethroids and
neonicotinoids are associated with the most diagnosed incidents of severe
cognitive impairment. The aim of this study was to determine the effects of these pesticides on the phosphorylation of
tau protein, and its cognitive implications in the development of AD. It was found that exposure to pesticides increased the phosphorylation of
tau protein at sites Ser198, Ser199, Ser202, Thr205, Ser396 and Ser404. Contact with these chemicals altered the enzymatic activities of
cyclin-dependent kinase 5 and
glycogen synthase kinase 3 beta, and
protein phosphatase-2A. Moreover, it altered the expression of the
microtubule associated protein tau gene, and changed levels of intracellular
calcium. These changes affected
tau protein phosphorylation and
neuroinflammation, and also increased oxidative stress. In addition, the exposed subjects had poor level of performance in tests that involved evaluation of novelty, as test on verbal, non-verbal, spatial memory, attention, and problem-solving skills.