ROLE OF PESTICIDES IN INTESTINAL DYSBIOSIS AND DEVELOPMENT OF NEURODEGENERATIVE DISEASES

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Giovanni Tomasello, Angelo Miceli, Olga Maria Manna, Stefano Burgio, Adelaide Carista, Elisa Tripoli, Marco Giammanco, Federica Scalia, Francesco Carini

The analysis of recent literature on the correlation between intestinal dysbiosis and chronic degenerative diseases shows an increased risk of developing spondyloartropatia seronegative, chronic inflammatory bowel diseases, autoimmune diseases and neurodegenerative diseases (Alzheimer’s, Parkinson’s and Amyotrophic Lateral Sclerosis) in subjects suffering from dysbiosis. The aim of the study is, to investigate through a metanalysis, the existence of the causal relationship between the use of pesticides in the work environment and the development of neurodegenerative diseases and then to formulate a physiopathological model valid to explain the development of dysbiosis-induced neurodegeneration in subjects exposed to pesticides. A careful analysis of the studies produced that investigate the relationship between the use of pesticides and the development of intestinal dysbiosis and the relationship between the latter and the development of neurodegenerative diseases has been carried out. To reduce the scope of the study we decided to consider, among the various neurodegenerative diseases, exclusively Alzheimer’s Dementia, Parkinson’s disease and Amyotrophic Lateral Sclerosis (SLA). Examination of the results shows, an increased risk of neurodegenerative diseases and in particular Parkinson’s, Alzheimer’s and SLA, in subjects exposed to pesticides. Alzheimer’s disease, Parkinson’s disease and SLA all have common pathological characteristics. The hallmark of these neurological disorders is, in fact, protein misfolding (i.e. incorrect folding) and the consequent aggregation and deposition of proteins in the CNS with progressive neuronal loss. The condition of dysbiosis, favors the stabilization of an imbalance between bacterial strains producing intestinal amyloid and non-producing strains; this triggers the enhancement of the endogenous response to neuronal amyloids via the intestine-brain axis.

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