Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Tang, Bor Luen

doi:10.3390/toxics8020021

Cited by 43 publications

(16 citation statements)

References 170 publications

(221 reference statements)

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“…Exposure to the residual amount of pesticides, such as maneb and paraquat, was found to increase the risk of developing Parkinson's disease [ [8] , [9] , [10] ]. Similar reports exist for Alzheimer's disease as well [ [11] , [12] , [13] ]. Indeed pesticide-induced animal models of Parkinson's disease and Alzheimer's disease recapitulate many of the pathologies seen in human patients and have become popular models to study [ 12 , 14 ].…”

Section: Introductionsupporting

confidence: 82%

“…Similar reports exist for Alzheimer's disease as well [ [11] , [12] , [13] ]. Indeed pesticide-induced animal models of Parkinson's disease and Alzheimer's disease recapitulate many of the pathologies seen in human patients and have become popular models to study [ 12 , 14 ]. However, the specific effect of pesticides at the cellular and molecular levels is yet to be fully established.…”

Section: Introductionsupporting

confidence: 82%

“…Of these three pesticides, fipronil and maneb are known to induce Parkinson's disease in animal models [ 26 , 27 ]. Similarly, exposure to pesticides also results in a neurodegenerative condition in humans [ [8] , [9] , [10] , [11] , [12] , [13] ]. Our results suggest that chronic exposure to pesticides may have a long-term impact on neuronal translation, eventually leading to cell death.…”

Section: Discussionmentioning

confidence: 99%

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Pesticides DEET, fipronil and maneb induce stress granule assembly and translation arrest in neuronal cells

Bhadauriya¹,

Parihar²,

Ganesh³

2021

Biochemistry and Biophysics Reports

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Pesticides entering our body, either directly or indirectly, are known to increase the risk of developing neurodegenerative disorders. The pesticide-induced animal models of Parkinson's disease and Alzheimer's disease recapitulates many of the pathologies seen in human patients and have become popular models for studying disease biology. However, the specific effect of pesticides at the cellular and molecular levels is yet to be fully established. Here we investigated the cellular effect of three commonly used pesticides: DEET, fipronil and maneb. Specifically, we looked at the effect of these pesticides in the formation of stress granules and the concomitant translational arrest in a neuronal cell line. Stress granules represent an ensemble of non-translating mRNAs and appear in cells under physiological stress. Growing evidence indicates that chronic stress may covert the transient stress granules into amyloids and may thus induce neurodegeneration. We demonstrate here that all three pesticides tested induce stress granules and translation arrest through the inactivation of the eukaryotic initiation factor, eIF2α. We also show that oxidative stress could be one of the major intermediary factors in the pesticide-induced stress granule formation and that it is a reversible process. Our results suggest that prolonged pesticide exposure may result in long-lived stress granules, thus compromising the neuronal stress response pathway and leading to neurodegeneration.

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Section: Introductionsupporting

confidence: 82%

Section: Introductionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

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Pesticides DEET, fipronil and maneb induce stress granule assembly and translation arrest in neuronal cells

Bhadauriya¹,

Parihar²,

Ganesh³

2021

Biochemistry and Biophysics Reports

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“…[216] Exposure to pesticides, fungicides, and herbicide is a risk factor for AD. [217] Meta-analysis of data from cohort and case-control studies have shown a positive association between pesticide exposure and AD. [218] SYEDA AND CANNON | 5 of 15…”

Section: Metalsmentioning

confidence: 99%

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

Syeda

Cannon

2021

J Biochem & Molecular Tox

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Alzheimer's disease (AD) is a major public health crisis due to devastating cognitive symptoms, a lack of curative treatments, and increasing prevalence. Most cases are sporadic (>95% of cases) after the age of 65 years, implicating an important role of environmental factors in disease pathogenesis. Environmental neurotoxicants have been implicated in neurodegenerative disorders including Parkinson's Disease and AD. Animal models of AD and in vitro studies have shed light on potential neuropathological mechanisms, yet the biochemical and molecular underpinnings of AD‐relevant environmental neurotoxicity remain poorly understood. Beta‐site amyloid precursor protein cleaving enzyme 1 (BACE1) is a potentially critical pathogenic target of environmentally induced neurotoxicity. BACE1 clearly has a critical role in AD pathophysiology: It is required for amyloid beta production and expression and activity of BACE1 are increased in the AD brain. Though the literature on BACE1 in response to environmental insults is limited, current studies, along with extensive AD neurobiology literature suggest that BACE1 deserves attention as an important neurotoxic target. Here, we critically review research on environmental neurotoxicants such as metals, pesticides, herbicides, fungicides, polyfluoroalkyl substances, heterocyclic aromatic amines, advanced glycation end products, and acrolein that modulate BACE1 and potential mechanisms of action. Though more research is needed to clearly understand whether BACE1 is a critical mediator of AD‐relevant neurotoxicity, available reports provide convincing evidence that BACE1 is altered by environmental risk factors associated with AD pathology, implying that BACE1 inhibition and its use as a biomarker should be considered in AD management and research.

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“…Several epidemiological analyses have affirmed a link between pesticides and incidence of sporadic Alzheimer's disease (AD). Meanwhile, in vitro and animal models of AD have shed light on potential neuropathological mechanisms [1].…”

Section: Introductionmentioning

confidence: 99%

The interaction effect of abamectin and tramadol on brain neurotransmitters in rats

Hussein¹,

Ahmed²

2020

World J. Adv. Res. Rev.

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A single -oral dose of abamectin (10 mg/Kg body weight; LD50) and tramadol dose of 40 mg kg -1 was given orally by gavage to the rats and the brain samples were examined biologically and histopathologically at various times (0.5, 1, 1.5, 2, 2.5, 3, 3.5 and 24 h) after dosing. Results revealed that oxidative stress was noticed, since it provokes a significant in brain due to insecticides administration. A significant reduction in, acetylcholinesterase (AchE), Nor-epinephrine (NE), serotonin (5-HT), epinephrine (E) and dopamine (DA) in treated group as compared to control group (P< 0.05). We found that there were neurotoxic effects of pesticides such as abamectin on brain activities, neurotransmitters and alterations in brain tissue. Tramadol, abamectin alone or in combination produced a significant increase in AchE of the brain of treated rats. In normal brain, the activity of acetylcholine esterase, is necessary for the healthy function of the brain, and changes in AchE activity are accompanied by clear signs of neurotoxicity. The central cholinergic neurotransmission in the brain is a crucial factor in cognitive functions including memory and learning.

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Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

Cited by 43 publications

References 170 publications

Pesticides DEET, fipronil and maneb induce stress granule assembly and translation arrest in neuronal cells

Pesticides DEET, fipronil and maneb induce stress granule assembly and translation arrest in neuronal cells

Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target

The interaction effect of abamectin and tramadol on brain neurotransmitters in rats

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