Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain | Proceedings of the Royal Society of London B: Biological Sciences

Neurofibrillary tangles (NFT) and β-amyloid plaques are the neurological hallmarks of both Alzheimer's disease and an unusual paralytic illness suffered by Chamorro villagers on the Pacific island of Guam. Many Chamorros with the disease suffer dementia, and in some villages one-quarter of the adults perished from the disease. Like Alzheimer's, the causal factors of Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC) are poorly understood. In replicated experiments, we found that chronic dietary exposure to a cyanobacterial toxin present in the traditional Chamorro diet, β-N-methylamino-L-alanine (BMAA), triggers the formation of both NFT and β-amyloid deposits similar in structure and density to those found in brain tissues of Chamorros who died with ALS/PDC. Vervets (Chlorocebus sabaeus) fed for 140 days with BMAA-dosed fruit developed NFT and sparse β-amyloid deposits in the brain. Co-administration of the dietary amino acid L-serine with L-BMAA significantly reduced the density of NFT. These findings indicate that while chronic exposure to the environmental toxin BMAA can trigger neurodegeneration in vulnerable individuals, increasing the amount of L-serine in the diet can reduce the risk.

2-Amino-1-Methyl-6-Phenylimidazo[4,5-b]Pyridine (PhIP) (from cooked meat) is Selectively Toxic to Primary Dopaminergic Neurons In Vitro.

Parkinson's disease (PD) is the second most common neurodegenerative
disease. Much data has linked the etiology of PD to a variety of
environmental factors. The majority of cases are thought to arise from a
combination of genetic susceptibility and environmental factors.
Chronic exposures to dietary factors, including meat, have been
identified as potential risk factors. Although heterocyclic amines that
are produced during high-temperature meat cooking are known to be
carcinogenic, their effect on the nervous system has yet to be studied
in depth. In this study, we investigated neurotoxic effects of
2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a highly
abundant heterocyclic amine in cooked meat, in vitro. We tested toxicity
of PhIP and the two major Phase I metabolites, N-OH-PhIP and
4'-OH-PhIP, using primary mesencephalic cultures from rat embryos. This
culture system contains both dopaminergic and non-dopaminergic neurons,
which allows specificity of neurotoxicity to be readily examined. We
find that exposure to PhIP or N-OH-PhIP is selectively toxic to
dopaminergic neurons in primary cultures, resulting in a decreased
percentage of dopaminergic neurons. Neurite length is decreased in
surviving dopaminergic neurons. Exposure to 4'-OH-PhIP did not produce
significant neurotoxicity. PhIP treatment also increased formation of
oxidative damage markers, 4-hydroxy-2-nonenal (HNE) and 3-nitrotyrosine
in dopaminergic neurons. Pre-treatment with N-acetylcysteine was
protective. Finally, treatment with blueberry extract, a dietary factor
with known antioxidant and other protective mechanisms, prevented
PhIP-induced toxicity. Collectively, our study suggests, for the first
time, that PhIP is selectively toxic to dopaminergic neurons likely
through inducing oxidative stress.

Opinion: Toxicants and the Brain | The Scientist Magazine®

The recent US and European BRAIN initiative do not  identify brain development as a key area of research, nor the possible effects of environmental toxicants on brain health.

This is a shame. A wealth of research shows that metals, pesticides, solvents, and other chemicals can seriously impede brain development in children. So far, we have identified about a dozen chemicals that can harm brain development in children and result in lasting deficits and disease, and there are more than 200 additional substances, the majority commonly present in the environment, that are known to be neurotoxic in adults, but for which we have little or no evidence for the effects on brain development. Furthermore, animal models suggest that brain toxicity during early development may lead to degenerative brain disease, such as Parkinson’s and autism, later in life. We need to understand better the causation and emergence of brain diseases as a result of toxic chemicals.

Agent Orange Linked To Fatal Prostate Cancer

"A new study of US Veterans has found that exposure to Agent Orange is linked to a two-fold higher risk of developing the most lethal forms of prostate cancer. The researchers suggest a history of exposure to the agent, which contains the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a dangerous toxin and carcinogen, should be one of the first things to look for when screening Veterans as it could lead to earlier diagnosis and treatment and prolong survival."

( Agent orange was liberally sprayed onto Vietnam, eastern Laos and parts of Cambodia during the Vietnam War) Wikipedia Agent Orange

News in Brief: Chemical tied to intergenerational obesity | Environment | Science News

Exposure in the womb to a chemical used in PVC and ship paint promotes obesity in mice. And the effect is long-lasting: The mice’s grandchildren were also fat despite no exposure to the chemical.

The work shows that the effects of an obesogen — a chemical that encourages fat accumulation — can be passed on to future generations not exposed to the chemical, researchers report online January 15 inEnvironmental Health Perspectives.

Futurity.org – Germ killer in hand soap may weaken muscles (Triclosan)

Triclosan, an antibacterial chemical, hinders muscle contractions at a cellular level, slows swimming in fish, and reduces muscular strength in mice, according to researchers at the University of California, Davis, and the University of Colorado. The team reported full findings in the Proceedings of the National Academy of Sciences.

Ecstasy harms memory with one year of recreational use

New research published online July 25 by the scientific journal Addiction, gives some of the first information available on the actual risk of using ecstasy. It shows that even in recreational amounts over a relatively short time period, ecstasy users risk specific memory impairments. Further, as the nature of the impairments may not be immediately obvious to the user, it is possible people wouldn't get the signs that they are being damaged by drug use until it is too late.

Poisoning from industrial compounds can cause similar effects to ALS

Researchers from the Bellvitge Biomedical Research Institute (IDIBELL) at the University of Barcelona (UB) have coordinated a research into how the IDPN nitrile causes neurological syndromes similar to those of the amyotrophic lateral sclerosis (ALS), a severe neuromuscular degenerative disease. The study, led by Jordi Llorens, has been recently published in Neuropathology and Applied Neurobiology journal.

Today's environment influences behavior generations later: Chemical exposure raises descendants' sensitivity to stress

Researchers at The University of Texas at Austin and Washington State University have seen an increased reaction to stress in animals whose ancestors were exposed to an environmental compound (vinclozolin, a popular fruit and vegetable fungicide) generations earlier.

PNAS: Brain anomalies in children exposed prenatally to a common organophosphate pesticide

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. High-exposure 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.