Tremor, olfactory and motor changes in Italian adolescents exposed to historical ferro-manganese emission

Lucchini, Roberto; Guazzetti, Stefano; Zoni, Silvia; Donna, Filippo; Peter, Stephanie; Zacco, Annalisa; Salmistraro, Marco; Bontempi, Elza; Zimmerman, Neil J.; Smith, Donald R.

doi:10.1016/j.neuro.2012.01.005

Cited by 227 publications

(287 citation statements)

References 30 publications

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“…High concentrations in soil and biomarkers associated with deficits in olfactory and motor function are the rule in children age 11-14 years [22].…”

Section: Cognition Effects and Brain Structural Changesmentioning

confidence: 99%

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

et al. 2016

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Air pollution (indoor and outdoor air) is a major issue in public health as epidemiological studies haven pointed to the numerous detrimental health consequences (notably, respiratory and cardiovascular pathology). In the last fifteen years, air pollution has also been considered as a potent environmental risk factor for neurological diseases and neuropathology. In this review, the authors examine the impact of air pollution on children's brain development and its clinical, cognitive, brain structural and metabolic consequences. Long-term potential consequences for adults' brain and effects on multiple sclerosis are also discussed. One challenge is assessing lifetime exposures to outdoor and indoor environments, including occupational exposures: how much, for how long and what type. The diffuse neuroinflammation, the damage to the neurovascular unit, and the production of auto-antibodies to neural and tight junction proteins are worrisome findings in children chronically exposed to concentrations above current standards for ozone and fine particulate matter (PM 2.5 ) and may constitute significant risk factors for the development of Article Outline

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“…High concentrations in soil and biomarkers associated with deficits in olfactory and motor function are the rule in children age 11-14 years [22].…”

Section: Cognition Effects and Brain Structural Changesmentioning

confidence: 99%

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

et al. 2016

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“…Manganese toxicity is commonly observed under certain occupational settings where workers are chronically exposed to high levels of manganese (1). Recent evidence suggests that individuals exposed to elevated manganese from environmental sources may also develop aspects of the disease (6). Furthermore, as the primary mode of manganese excretion is by secretion into bile, individuals who fail to excrete manganese due to hepatic dysfunction, secondary to diseases such as cirrhosis, may develop manganese-induced parkinsonism in the absence of exposure to elevated manganese (7).…”

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confidence: 99%

Structural Elements in the Transmembrane and Cytoplasmic Domains of the Metal Transporter SLC30A10 Are Required for Its Manganese Efflux Activity

Zogzas

Aschner

Mukhopadhyay

2016

Journal of Biological Chemistry

105

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Homozygous mutations in SLC30A10 lead to the development of familial manganese-induced parkinsonism. We previously demonstrated that SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its trafficking and efflux activity. Interestingly, other transporters in the SLC30 family mediate zinc efflux. Determining the mechanisms that allow SLC30A10 to transport manganese, which are unclear, is essential to understand its role in parkinsonism. Here, we generated a predicted structure of SLC30A10, based on the structure of the bacterial zinc transporter YiiP, and performed functional studies. In YiiP, side chains of residues Asp-45 and Asp-49 in the second and His-153 and Asp-157 in the fifth transmembrane segments coordinate zinc and are required for transport. In SLC30A10, the corresponding residues are Asn-43 and Asp-47 in the second and His-244 and Asp-248 in the fifth transmembrane segments. Surprisingly, although alanine substitution of Asp-248 abolished manganese efflux, that of Asn-43 and Asp-47 did not. Instead, side chains of charged or polar residues adjacent to Asp-248 in the first (Glu-25) or fourth (Asn-127) transmembrane segments were required. Further analyses revealed that residues His-333 and His-350 in the cytoplasmic C-terminal domain were required for full activity. However, the C-terminal domain failed to transfer manganese transport capability to a related zinc transporter. Overall, our results indicate that residues in the transmembrane and C-terminal domains together confer optimal manganese transport capability to SLC30A10 and suggest that the mechanism of ion coordination in the transmembrane domain of SLC30A10 may be substantially different from that in YiiP/other SLC30 proteins.

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“…The two conditions also share non-motor signs and symptoms, including depression, dementia, loss of smell, reduced contrast vision, and sleep disturbances [47][48][49][50][51] . Mn has been invoked as a risk factor for PD based on evidence from welders 52,53 and other occupational exposures 54 .…”

Section: Introductionmentioning

confidence: 99%

Manganese and aging

Parmalee

Aschner

2016

NeuroToxicology

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Tremor, olfactory and motor changes in Italian adolescents exposed to historical ferro-manganese emission

Cited by 227 publications

References 30 publications

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: The clinical impact on children and beyond

Structural Elements in the Transmembrane and Cytoplasmic Domains of the Metal Transporter SLC30A10 Are Required for Its Manganese Efflux Activity

Manganese and aging

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