Cortical Synaptic Reorganization Under Chronic Arsenic Exposure

Niño, Sandra A.; Vázquez-Hernández, Nallely; Arévalo-Villalobos, Jaime I.; Chi‐Ahumada, Erika; Martín-Amaya-Barajas, Fabiola L.; Dı́az-Cintra, Sofı́a; Martel-Gallegos, Guadalupe; González-Burgos, Ignacio; Jiménez‐Capdeville, María E.

doi:10.1007/s12640-021-00409-y

Cited by 6 publications

(3 citation statements)

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“…Some researchers have hypothesized that early exposure to heavy metals is associated with the later development of AD. Based on their observations of experimental animals, they concluded that early-life exposure to As [ 54 ], Pb [ 55 ], and Cd [ 56 ] may contribute to the development of neurodegeneration later in life, which is consistent with the developmental hypothesis of AD [ 57 , 58 , 59 ].…”

Section: Heavy Metals In Alzheimer’s Diseasementioning

confidence: 73%

Metals in Alzheimer’s Disease

et al. 2023

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The role of metals in the pathogenesis of Alzheimer’s disease (AD) is still debated. Although previous research has linked changes in essential metal homeostasis and exposure to environmental heavy metals to the pathogenesis of AD, more research is needed to determine the relationship between metals and AD. In this review, we included human studies that (1) compared the metal concentrations between AD patients and healthy controls, (2) correlated concentrations of AD cerebrospinal fluid (CSF) biomarkers with metal concentrations, and (3) used Mendelian randomization (MR) to assess the potential metal contributions to AD risk. Although many studies have examined various metals in dementia patients, understanding the dynamics of metals in these patients remains difficult due to considerable inconsistencies among the results of individual studies. The most consistent findings were for Zn and Cu, with most studies observing a decrease in Zn levels and an increase in Cu levels in AD patients. However, several studies found no such relation. Because few studies have compared metal levels with biomarker levels in the CSF of AD patients, more research of this type is required. Given that MR is revolutionizing epidemiologic research, additional MR studies that include participants from diverse ethnic backgrounds to assess the causal relationship between metals and AD risk are critical.

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Section: Heavy Metals In Alzheimer’s Diseasementioning

confidence: 73%

Metals in Alzheimer’s Disease

et al. 2023

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“…3,4 Epidemiological studies have shown an association between chronic arsenic exposure and poor cognitive performance in both children and adults. 5 In addition, many rodent studies revealed that arsenic could induce neural dysfunction by altering epigenetics, hippocampal function, glucocorticoid and hypothalamus−pituitary−adrenal axis pathway, as well as glutamatergic, cholinergic, and monoaminergic signaling. 6 The hippocampus is a crucial brain structure in the process of learning and memory, and its lesions can destroy spatial learning and working memory.…”

Section: ■ Introductionmentioning

confidence: 99%

“…It was estimated that 94–220 million people are potentially exposed to high concentrations of arsenic via consumption of groundwater globally, which poses a significant threat to human health. As a highly toxic substance, arsenic exposure has been demonstrated to cause a variety of adverse health outcomes, including neurotoxicity. , Epidemiological studies have shown an association between chronic arsenic exposure and poor cognitive performance in both children and adults . In addition, many rodent studies revealed that arsenic could induce neural dysfunction by altering epigenetics, hippocampal function, glucocorticoid and hypothalamus–pituitary–adrenal axis pathway, as well as glutamatergic, cholinergic, and monoaminergic signaling .…”

Section: Introductionmentioning

confidence: 99%

Transgenerational Effects of Arsenic Exposure on Learning and Memory in Rats: Crosstalk between Arsenic Methylation, Hippocampal Metabolism, and Histone Modifications

Hua,

Han,

et al. 2024

Environ. Sci. Technol.

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Arsenic (As) is widely present in the natural environment, and exposure to it can lead to learning and memory impairment. However, the underlying epigenetic mechanisms are still largely unclear. This study aimed to reveal the role of histone modifications in environmental levels of arsenic (sodium arsenite) exposure-induced learning and memory dysfunction in male rats, and the inter/transgenerational effects of paternal arsenic exposure were also investigated. It was found that arsenic exposure impaired the learning and memory ability of F0 rats and down-regulated the expression of cognition-related genes Bdnf, c-Fos, mGlur1, Nmdar1, and Gria2 in the hippocampus. We also observed that inorganic arsenite was methylated to DMA and histone modification-related metabolites were altered, contributing to the dysregulation of H3K4me1/2/3, H3K9me1/2/3, and H3K4ac in rat hippocampus after exposure. Therefore, it is suggested that arsenic methylation and hippocampal metabolism changes attenuated H3K4me1/2/3 and H3K4ac while enhancing H3K9me1/2/3, which repressed the key gene expressions, leading to cognitive impairment in rats exposed to arsenic. In addition, paternal arsenic exposure induced transgenerational effects of learning and memory disorder in F2 male rats through the regulation of H3K4me2 and H3K9me1/2/3, which inhibited c-Fos, mGlur1, and Nmdar1 expression. These results provide novel insights into the molecular mechanism of arsenic-induced neurotoxicity and highlight the risk of neurological deficits in offspring with paternal exposure to arsenic.

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