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Role of WHO.

Neuropsychopharmacology: The Fifth Generation of Progress

Prenatal exposure to chlorpyrifos (CPF), an organophosphate insecticide, is associated with neurobehavioral deficits in humans and animal models. We investigated associations between CPF exposure and brain morphology using magnetic resonance imaging in 40 children, 5.9–11.2 y, selected from a nonclinical, representative community-based cohort. Twenty high-exposure children (upper tertile of CPF concentrations in umbilical cord blood) were compared with 20 low-exposure children on cortical surface features; all participants had minimal prenatal exposure to environmental tobacco smoke and polycyclic aromatic hydrocarbons. High CPF exposure was associated with enlargement of superior temporal, posterior middle temporal, and inferior postcentral gyri bilaterally, and enlarged superior frontal gyrus, gyrus rectus, cuneus, and precuneus along the mesial wall of the right hemisphere. Group differences were derived from exposure effects on underlying white matter. A significant exposure × IQ interaction was derived from CPF disruption of normal IQ associations with surface measures in low-exposure children. In preliminary analyses, high-exposure children did not show expected sex differences in the right inferior parietal lobule and superior marginal gyrus, and displayed reversal of sex differences in the right mesial superior frontal gyrus, consistent with disruption by CPF of normal behavioral sexual dimorphisms reported in animal models. Highexposure children also showed frontal and parietal cortical thinning, and an inverse dose–response relationship between CPF and cortical thickness. This study reports significant associations of prenatal exposure to a widely used environmental neurotoxicant, at standard use levels, with structural changes in the developing human brain.

https://www.pnas.org/content/pnas/109/20/7871.full.pdf

Brain anomalies in children exposed prenatally to a common organophosphate pesticide.

The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154, 2007) and Bowman et al. (Metals and neurodegeneration, 2009).

/pdf/manganese-and-its-role-in-parkinson-s-disease-from-transport-3dpxtp91p2.pdf

Manganese and its Role in Parkinson's disease: from Transport to Neuropathology.

Occupational or environmental exposure to manganese (Mn) can lead to the development of "Manganism," a neurological condition showing certain motor symptoms similar to Parkinson's disease (PD). Like PD, Mn toxicity is seen in the central nervous system mainly affecting nigrostriatal neuronal circuitry and subsequent behavioral and motor impairments. Since the first report of Mn-induced toxicity in 1837, various experimental and epidemiological studies have been conducted to understand this disorder. While early investigations focused on the impact of high concentrations of Mn on the mitochondria and subsequent oxidative stress, current studies have attempted to elucidate the cellular and molecular pathways involved in Mn toxicity. In fact, recent reports suggest the involvement of Mn in the misfolding of proteins such as α-synuclein and amyloid, thus providing credence to the theory that environmental exposure to toxicants can either initiate or propagate neurodegenerative processes by interfering with disease-specific proteins. Besides manganism and PD, Mn has also been implicated in other neurological diseases such as Huntington's and prion diseases. While many reviews have focused on Mn homeostasis, the aim of this review is to concisely synthesize what we know about its effect primarily on the nervous system with respect to its role in protein misfolding, mitochondrial dysfunction, and consequently, neuroinflammation and neurodegeneration. Based on the current evidence, we propose a 'Mn Mechanistic Neurotoxic Triad' comprising (1) mitochondrial dysfunction and oxidative stress, (2) protein trafficking and misfolding, and (3) neuroinflammation.

Manganese-Induced Neurotoxicity: New Insights Into the Triad of Protein Misfolding, Mitochondrial Impairment, and Neuroinflammation.

Exposure of adult humans to manganese (Mn) has long been known to cause neurotoxicity. Recent evidence also suggests that exposure of children to Mn is associated with developmental neurotoxicity. Astrocytes are critical for the proper functioning of the nervous system, and they play active roles in neurogenesis, synaptogenesis and synaptic neurotransmission. In this report, to help elucidate the molecular events underlying Mn neurotoxicity, we systematically identified the molecular targets of Mn in primary human astrocytes at a genome-wide level, by using microarray gene expression profiling and computational data analysis algorithms. We found that Mn altered the expression of diverse genes ranging from those encoding cytokines and transporters to signal transducers and transcriptional regulators. Particularly, 28 genes encoding proinflammatory chemokines, cytokines and related functions were up-regulated, whereas 15 genes encoding functions involved in DNA replication and repair and cell cycle checkpoint control were down-regulated. Consistent with the increased expression of proinflammatory factors, analysis of common regulators revealed that 16 targets known to be positively affected by the interferon-γ signaling pathway were up-regulated by Mn 2+ . In addition, 68 genes were found to be similarly up- or down-regulated by both Mn 2+ and hypoxia. These results from genomic analysis are further supported by data from real-time RT-PCR, Western blotting, flow cytometric and toxicological analyses. Together, these analyses show that Mn 2+ selectively affects cell cycle progression, the expression of hypoxia-responsive genes, and the expression of proinflammatory factors in primary human astrocytes. These results provide important insights into the molecular mechanisms underlying Mn neurotoxicity.

https://academiccommons.columbia.edu/doi/10.7916/D8KK9HKD/download

Gene expression profiling of human primary astrocytes exposed to manganese chloride indicates selective effects on several functions of the cells.

The development of CNS drugs has been the most challenging task in drug design. Only an abysmal one per- cent of nervous system drugs tested in human clinical trials ever reach market. This is largely attributable to the difficul- ties in both identifying appropriate targets and in understanding the toxicology, pharmacology, and pharmaceutical prop- erties of therapeutic compounds. Pesticides have not attracted much attention in the field of CNS drug design. However, the toxicological and molecular actions of certain pesticides, such as chlorpyrifos and pyrethroids, have been well studied. Furthermore, recent epidemiological data have provided important insights into the actions of pesticides in the human brain. Therefore, in this review we seek to examine and summarize the toxicological and molecular actions of common pesticides, organophosphates and pyrethroids. We will also summarize and compare the effects of common pesticides on the neurological functions in animals and in humans. Common pesticides have been shown to act on molecular targets such as the serotonin receptors, brain-derived neurotrophic factor (BDNF), and the transcription factor CREB. Likewise, pesticides can affect multiple neurological functions, such as motor coordination, habituation, attention, cognition, and psychomotor development. A comprehensive review of the toxicological and molecular roles of pesticides in the CNS might provide insights into the actions of CNS agents.

Unique Insights into the Actions of CNS Agents: Lessons from Studies of Chlorpyrifos and Other Common Pesticides

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Gene expression profiling of human primary astrocytes exposed to manganese chloride indicates selective effects on several functions of the cells.

Unique Insights into the Actions of CNS Agents: Lessons from Studies of Chlorpyrifos and Other Common Pesticides