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Daily Archives for: August 27th, 2008

An hypothesis is presented which attempts to relate the pathogenesis of both manganese neurotoxicity and Parkinson's disease to cytotoxicity from products of catecholamine oxidation. These include the products resulting from the partial reduction of oxygen (superoxide anion, hydroxyl radical, and hydrogen peroxide) and the semiquinones and ortho quinones produced during autoxidation or oxidation of catecholamines initiated by trivalent manganese.

A population-based case-control study was conducted in the Henry Ford Health System (HFHS) in metropolitan Detroit to assess occupational exposures to manganese, copper, lead, iron, mercury and zinc as risk factors for Parkinson's disease (PD). Non-demented men and women 50 years of age who were receiving primary medical care at HFHS were recruited, and concurrently enrolled cases (n = 144) and controls (n = 464) were frequency-matched for sex,

Research into the causes of Parkinson disease (PD) has accelerated recently with the discovery of novel gene mutations. The majority of PD cases, however, remain idiopathic and in those cases environmental causes should be considered. Several recent reports have focused on welding and manganese toxicity as potential risk factors for parkinsonism and some have even proposed that welding is a risk factor for PD.

Alzheimer's disease (AD) is the most common form of dementia. Populations migrating from developing to industrialized countries seem to elicit a higher incidence and prevalence rate of AD, suggesting lifestyle and environmental factors to have a role in the pathophysiology of AD. One of its major neuropathological hallmarks is the deposition of Aβ peptides as amyloid plaques in the brain of AD patients.

The present review is based on presentations from the meeting of the Society of Toxicology in San Diego, CA (March 2006). It addresses recent developments in the understanding of the transport of manganese (Mn) into the central nervous system (CNS), as well as brain imaging and neurocognitive studies in non-human primates aimed at improving our understanding of the mechanisms of Mn neurotoxicity.

Neurodevelopmental disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common, costly, and can cause lifelong disability. Their causes are mostly unknown. A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function.

Background. The fibroblast growth factor (FGF) superfamily of neurotrophic factors plays critical roles in neural cell development, brain assembly, and recovery from neuronal injury.
Objectives. We administered two organophosphate pesticides, chlorpyrifos and diazinon, to neonatal rats on postnatal days 1–4, using doses below the threshold for systemic toxicity or growth impairment,

Manganese neurotoxicity is linked primarily to inhalation exposure, and its clinical features are almost totally based on high doses, such as those experienced by miners. Manifestations of lower level exposures can take two forms. One is the appearance of neurobehavioral deficits. A second, equally subtle, form is as a promoter, borrowing the term used in carcinogenesis,

Manganese (Mn) is an essential trace metal found in all tissues, and it is required for normal amino acid, lipid, protein, and carbohydrate metabolism. While Mn deficiency is extremely rare in humans, toxicity due to overexposure of Mn is more prevalent. The brain appears to be especially vulnerable. Mn neurotoxicity is most commonly associated with occupational exposure to aerosols or dusts that contain extremely high levels (>