Pesticides, cognitive functions and dementia: A review

Aloizou, Athina‐Maria; Siokas, Vasileios; Vogiatzi, Christina; Peristeri, Eleni; Docea, Anca Oana; Petrakis, Dimitris E.; Provatas, Antonios; Folia, Vasiliki; Chalkia, Charikleia; Vinceti, Marco; Wilks, Martin F.; Izotov, Boris N.; Tsatsakis, Aristidis; Bogdanos, Dimitrios P.; Dardiotis, Efthimios

doi:10.1016/j.toxlet.2020.03.005

Cited by 103 publications

(46 citation statements)

References 184 publications

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“…In order to establish an AD model in a C6 cell, the influence of cell passage and Aβ peptides concentration were investigated, and an in vitro model with astrocyte characteristics was implemented by inducing the differentiation of C6 cells by insulin treatment. This study is expected to be able to study the association of AQP4 expression to natural products such as Panax ginseng [ 42 ] or Scrophularia buergeriana extract [ 43 ] reported as AD prophylactic agents using C6 cells with astrocyte properties [ 44 ]. We believe that our data will facilitate further studies on the astrocytic functions targeting AQP4 in AD.…”

Section: Discussionmentioning

confidence: 99%

Amyloid-ß peptides inhibit the expression of AQP4 and glutamate transporter EAAC1 in insulin-treated C6 glioma cells

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Amyloid-ß peptides inhibit the expression of AQP4 and glutamate transporter EAAC1 in insulin-treated C6 glioma cells

et al. 2020

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“…Another possible environmental agent that could target similar pathways or modify the effects of APAP would be neurotoxic pesticide compounds, which have also been linked to ASD risk [ 9 , 28 ]. Some mechanistic studies have suggested that pesticide compounds that target receptors on the blood-brain barrier prevent drug transport and delivery through the brain, potentially leading to pharmaceutical ineffectiveness and other adverse effects [ 29 ]. One method by which pesticide exposure can alter or worsen the intended effect of medications is by interfering with the P-glycoprotein system, one of the body’s natural detoxification mechanisms found in secretory or barrier tissues such as the placenta and the vascular endothelial cells of the central nervous system [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

In Silico Exploration of the Potential Role of Acetaminophen and Pesticides in the Etiology of Autism Spectrum Disorder

Furnary

García-Milián

Liew

et al. 2021

Toxics

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Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p < 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors.

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“…Exposures throughout the lifespan may impact the later development and progression of cognitive impairment over time. These exposures may range from toxicological to traumatic to infections [ 9 10 11 ]. Infection burden has been studied as a predictor of cognitive decline in several settings and with many different approaches [ 12 13 ].…”

Section: Introductionmentioning

confidence: 99%

Baseline Infection Burden and Cognitive Function in Elders with Essential Tremor

Iglesias-Hernandez

Chapman

Radler

et al. 2021

Tremor and Other Hyperkinetic Movements

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Background: Patients with essential tremor (ET) have an increased risk of cognitive impairment, yet little is known about the predictors of cognitive decline in these patients. Exposures to infectious agents throughout the lifespan may impact the later development of cognitive impairment. For example, high Infection exposure has been associated with lower cognitive performance in Alzheimer's and Parkinson's disease. However, this predictor has not been examined in ET.Objectives: To determine whether a higher baseline infection burden is associated with worse cognitive performance at baseline and greater cognitive decline over time in an ET cohort.Method/Design: 160 elderly non-demented ET participants (80.0 ± 9.5 years) underwent an extensive cognitive evaluation at three time points. At baseline, participants completed an infection burden questionnaire (t-IBQ) that elicited information on previous exposure to infectious agents and number of episodes per disease. Analysis of covariance and generalized estimated equations (GEEs) were used.Results: Overall, infection burden was not associated baseline cognitive performance. Adjusted GEE models for repeated measures yielded a significant time interaction between moderate infection burden at baseline and better performance in the attention domain over time (p = 0.013). Previous history of rubella was associated with faster rate of decline in visuospatial performance (p = 0.046). Conclusion:The data were mixed. Moderate self-reported infection burden was associated with better attention performance over time. Self-reported history of rubella infection was related to lower visuospatial performance over time in this cohort. Follow-up studies with additional design elements would be of value.

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Pesticides, cognitive functions and dementia: A review

Cited by 103 publications

References 184 publications

Amyloid-ß peptides inhibit the expression of AQP4 and glutamate transporter EAAC1 in insulin-treated C6 glioma cells

Amyloid-ß peptides inhibit the expression of AQP4 and glutamate transporter EAAC1 in insulin-treated C6 glioma cells

In Silico Exploration of the Potential Role of Acetaminophen and Pesticides in the Etiology of Autism Spectrum Disorder

Baseline Infection Burden and Cognitive Function in Elders with Essential Tremor

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