Sick Building: Fungi Release Toxin Directly Into Air, Study Finds - NBC News

 "Jean-Denis Bailly of the University of Toulouse in France and colleagues tested three common types of fungi that can grow inside buildings and found that their mycotoxins could and did disperse into the air until normal conditions.

“These toxins can subsequently be aerosolized, at least partly, from moldy material,” they wrote in their report in the journal Applied and Environmental Microbiology, published by the American Society for Microbiology.

“This transfer to air requires air velocities that can be encountered in ‘real life conditions’ in buildings.

The three species they tested were Penicillium brevicompactum, Aspergillus versicolor and Stachybotrys chartarum, all of which grew on wallpaper in their lab.

They all also produce mycotoxins."



Here's the paper:-

Aerosolization of mycotoxins after growth of toxinogenic fungi on wallpaper


The joint effect of air pollution exposure and copy number variation on risk for autism - Kim - 2017 - Autism Research - Wiley Online Library

 Autism spectrum disorder is a complex trait with a high degree of heritability as well as documented susceptibility from environmental factors. In this study the contributions of copy number variation, exposure to air pollutants, and the interaction between the two on autism risk, were evaluated in the population-based case-control Childhood Autism Risks from Genetics and Environment (CHARGE) Study. For the current investigation, we included only those CHARGE children (a) who met criteria for autism or typical development and (b) for whom our team had conducted both genetic evaluation of copy number burden and determination of environmental air pollution exposures based on mapping addresses from the pregnancy and early childhood. This sample consisted of 158 cases of children with autism and 147 controls with typical development. Multiple logistic regression models were fit with and without environmental variable-copy number burden interactions. We found no correlation between average air pollution exposure from conception to age 2 years and the child's CNV burden. We found a significant interaction in which a 1SD increase in duplication burden combined with a 1SD increase in ozone exposure was associated with an elevated autism risk (OR 3.4, P < 0.005) much greater than the increased risks associated with either genomic duplication (OR 1.85, 95% CI 1.25–2.73) or ozone (OR 1.20, 95% CI 0.93–1.54) alone. Similar results were obtained when CNV and ozone were dichotomized to compare those in the top quartile relative to those having a smaller CNV burden and lower exposure to ozone, and when exposures were assessed separately for pregnancy, the first year of life, and the second year of life. No interactions were observed for other air pollutants, even those that demonstrated main effects; ozone tends to be negatively correlated with the other pollutants examined. While earlier work has demonstrated interactions between the presence of a pathogenic CNV and an environmental exposure [Webb et al., 2016], these findings appear to be the first indication that global copy number variation may increase susceptibility to certain environmental factors, and underscore the need to consider both genomics and environmental exposures as well as the mechanisms by which each may amplify the risks for autism associated with the other.



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Frontiers | 16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain | Frontiers in Aging Neuroscience

The neurological deterioration associated with Alzheimer’s disease (AD), involving accumulation of amyloid-beta peptides and neurofibrillary tangles, is associated with evident neuroinflammation. This is now seen to be a significant contributor to pathology. Recently the tenet of the privileged status of the brain, regarding microbial compromise, has been questioned, particularly in terms of neurodegenerative diseases. It is now being considered that microbiological incursion into the central nervous system could be either an initiator or significant contributor to these. This is a novel study using 16S ribosomal gene-specific Next generation sequencing (NGS) of extracted brain tissue. A comparison was made of the bacterial species content of both frozen and formaldehyde fixed sections of a small cohort of Alzheimer-affected cases with those of cognitively unimpaired (normal). Our findings suggest an increase in bacterial populations in Alzheimer brain tissue compared with normal."




Environmental Health Perspectives – The Florence Statement on Triclosan and Triclocarban

The Florence Statement on Triclosan and Triclocarban documents a consensus of more than 200 scientists and medical professionals on the hazards of and lack of demonstrated benefit from common uses of triclosan and triclocarban. These chemicals may be used in thousands of personal care and consumer products as well as in building materials. Based on extensive peer-reviewed research, this statement concludes that triclosan and triclocarban are environmentally persistent endocrine disruptors that bioaccumulate in and are toxic to aquatic and other organisms. Evidence of other hazards to humans and ecosystems from triclosan and triclocarban is presented along with recommendations intended to prevent future harm from triclosan, triclocarban, and antimicrobial substances with similar properties and effects. Because antimicrobials can have unintended adverse health and environmental impacts, they should only be used when they provide an evidence-based health benefit. Greater transparency is needed in product formulations, and before an antimicrobial is incorporated into a product, the long-term health and ecological impacts should be evaluated. "



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CRISPR Reverses Huntington’s Disease in Mice | GEN

  Huntington disease is an inherited, progressive brain disorder that causes uncontrolled movements, emotional problems, and loss of thinking ability (cognition). [NIH]
The potential of genome-editing techniques, such as CRISPR/Cas9, to alleviate disease burden has ignited the imagination for thousands of researchers looking for new therapeutic strategies. Scientists were very quickly able to show that this gene-altering technique could eliminate disease-causing mutations within a variety of tissues in vitro. More recently, CRISPR is being positioned to help treat patients directly, with clinical trials in humans already under way in China and soon to begin in the U.S. Yet, no current clinical trials feature drugs made using the technique for the treatment of neurodegenerative diseases.

Now, a group of investigators led by scientists at Emory University is hoping to open up new avenues of neurodegenerative research and rapidly move toward human trials after the release of their new findings. The research team showed that the CRISPR/Cas9 system could snip part of a gene that produces toxic protein aggregates in the brains of 9-month-old mice used as a model for Huntington’s disease. Moreover, the scientists noted that when they looked at the brain region where the vector was applied, some weeks later, the aggregated proteins had almost disappeared. Amazingly, the motor abilities of the mice had improved, although not to the level of control mice.            

Findings from the new study were published today in the Journal of Clinical Investigation through an article entitled, “CRISPR/Cas9-mediated gene editing ameliorates neurotoxicity in mouse model of Huntington’s disease.”"



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House cleaning chemicals may cause birth defects - Medical News Today

 "Hrubec and colleagues investigated the effect of a large class of common household chemicals called "quaternary ammonium compounds," or "quats."

Due to their antimicrobial and antistatic properties, these products are routinely used as disinfectants in the form of household cleaning products, laundry detergent, and fabric softener. They are also used as preservatives in personal hygiene products, such as shampoo, conditioner, and eye drops. The study found that neural tube defects (NTDs) increased proportionally with the ambient exposure to the chemicals."




Glutamine suppresses herpes in mice and guinea pigs | National Institutes of Health (NIH)

 "Glutamine supplements can suppress reactivation of herpes simplex virus (HSV) in mice and guinea pigs, according to findings recently published in the Journal of Clinical Investigation. The research was conducted by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and at the U.S. Food and Drug Administration."



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Prenatal fever and autism risk. - PubMed - NCBI

 Some studies suggest that prenatal infection increases risk of autism spectrum disorders (ASDs). This study was undertaken in a prospective cohort in Norway to examine whether we could find evidence to support an association of the prenatal occurrence of fever, a common manifestation of infection, with ASD risk. Prospective questionnaires provided maternal exposure data; case status was established from clinical assessments and registry linkages. In a large, prospectively ascertained cohort of pregnant mothers and their offspring, we examined infants born ⩾32 weeks for associations between fever exposure in each trimester and ASD risk using logistic regression. Maternal exposure to second-trimester fever was associated with increased ASD risk, adjusting for presence of fever in other trimesters and confounders (adjusted odds ratio (aOR), 1.40; 95% confidence interval, 1.09-1.79), with a similar, but nonsignificant, point estimate in the first trimester. Risk increased markedly with exposure to three or more fever episodes after 12 weeks' gestation (aOR, 3.12; 1.28-7.63). ASD risk appears to increase with maternal fever, particularly in the second trimester. Risk magnified dose dependently with exposure to multiple fevers after 12 weeks' gestation. Our findings support a role for gestational maternal infection and innate immune responses to infection in the pathogenesis of at least some cases of ASD"



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Aluminium in brain tissue in familial Alzheimer’s disease

 The genetic predispositions which describe a diagnosis of familial Alzheimer’s disease can be considered as cornerstones of the amyloid cascade hypothesis. Essentially they place the expression and metabolism of the amyloid precursor protein as the main tenet of disease aetiology. However, we do not know the cause of Alzheimer’s disease and environmental factors may yet be shown to contribute towards its onset and progression. One such environmental factor is human exposure to aluminium and aluminium has been shown to be present in brain tissue in sporadic Alzheimer’s disease. We have made the first ever measurements of aluminium in brain tissue from 12 donors diagnosed with familial Alzheimer’s disease. The concentrations of aluminium were extremely high, for example, there were values in excess of 10 μg/g tissue dry wt. in 5 of the 12 individuals. Overall, the concentrations were higher than all previous measurements of brain aluminium except cases of known aluminium-induced encephalopathy. We have supported our quantitative analyses using a novel method of aluminium-selective fluorescence microscopy to visualise aluminium in all lobes of every brain investigated. The unique quantitative data and the stunning images of aluminium in familial Alzheimer’s disease brain tissue raise the spectre of aluminium’s role in this devastating disease."



Culprit hidden in plain sight in Alzheimer’s disease development: Combustion-derived nanoparticles in key brain target cells and organelles in young urbanites | Journal of Alzheimer's Disease

Culprit hidden in plain sight in Alzheimer’s disease development: Combustion-derived nanoparticles in key brain target cells and organelles in young urbanites | Journal of Alzheimer's Disease: "Missoula, MT, June 8, 2017 — A new study by researchers at the University of Montana, Universidad del Valle de México, Instituto Nacional de Pediatría, Boise State, and Universidad Nacional Autónoma de México, heightens concerns over the detrimental short- and long-term impact of airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) present in young urbanites’ brains. Using transmission electron microscopy, the researchers documented by abundant combustion nanoparticles in neurons, glial cells, choroid plexus, and neurovascular units of Mexico City children, teens and young adults chronically exposed to concentrations above the US-EPA standards for fine particulate matter. Residents in Mexico City are exposed from conception to harmful neurotoxic air pollutants. These findings are published in the Journal of Alzheimer’s Disease."



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Drinking diet beverages during pregnancy linked to child obesity, NIH study suggests | National Institutes of Health (NIH)

  "Children born to women who had gestational diabetes and drank at least one artificially sweetened beverage per day during pregnancy were more likely to be overweight or obese at age 7, compared to children born to women who had gestational diabetes and drank water instead of artificially sweetened beverages, according to a study led by researchers at the National Institutes of Health. Childhood obesity is known to increase the risk for certain health problems later in life, such as diabetes, heart disease, stroke and some cancers. The study appears online in the International Journal of Epidemiology. "


Here's the paper :-

Maternal consumption of artificially sweetened beverages during pregnancy, and offspring growth through 7 years of age: a prospective cohort study: Int J Epidemiol 

Synergistic effects of influenza and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can be eliminated by the use of influenza therapeutics: experimental evidence for the multi-hit hypothesis | npj Parkinson's Disease

H1N1 virus
H1N1 virus (Photo credit: Wikipedia)
"Central Nervous System inflammation has been implicated in neurodegenerative disorders including Parkinson’s disease (Ransohoff, Science 353: 777–783, 2016; Kannarkat et al. J. Parkinsons Dis. 3: 493–514, 2013). Here, we examined if the H1N1 influenza virus (Studahl et al. Drugs 73: 131–158, 2013) could synergize with the parkinsonian toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (Jackson-Lewis et al. in Mark LeDoux (ed) Movement Disorders: Genetics and Models: 287–306, Elsevier, 2015) to induce a greater microglial activation and loss of substantia nigra pars compacta dopaminergic neurons than either insult alone. H1N1-infected animals administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine exhibit a 20% greater loss of substantia nigra pars compacta dopaminergic neurons than occurs from the additive effects of H1N1 or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine alone (p < 0.001). No synergistic effects were found in microglial activation. The synergistic dopaminergic neuron loss is eliminated by influenza vaccination or treatment with oseltamivir carboxylate. This work shows that multiple insults can induce synergistic effects; and even these small changes can be significant as it might allow one to cross a phenotypic disease threshold that would not occur from individual non-interacting exposures. Our observations also have important implications for public health, providing impetus for influenza vaccination or prompt treatment with anti-viral medications upon influenza diagnosis."



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Common acne medication, minocycline, offers new treatment for multiple sclerosis

 "A Canadian clinical trial led by researchers at the University of Calgary's Hotchkiss Brain Institute (HBI), at the Cumming School of Medicine (CSM), shows that minocycline, a common acne medication, can slow the progress of relapsing-remitting multiple sclerosis (MS) in people who have recently experienced their first symptoms.

In addition to being an unexpected discovery - an acne drug benefitting a neurological disorder - the discovery is significant as it offers a safe and affordable treatment option for those with early onset MS. This discovery could impact thousands of newly diagnosed MS patients around the world."

Here's the paper

Trial of Minocycline in a Clinically Isolated Syndrome of Multiple Sclerosis New England Journal of medicine 


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Fetal and postnatal metal dysregulation in autism : Nature Communications

 Genetic and environmental factors contribute to the etiologies of autism spectrum disorder (ASD), but evidence of specific environmental exposures and susceptibility windows is limited. Here we study monozygotic and dizygotic twins discordant for ASD to test whether fetal and postnatal metal dysregulation increases ASD risk. Using validated tooth-matrix biomarkers, we estimate pre- and post-natal exposure profiles of essential and toxic elements. Significant divergences are apparent in metal uptake between ASD cases and their control siblings, but only during discrete developmental periods. Cases have reduced uptake of essential elements manganese and zinc, and higher uptake of the neurotoxin lead. Manganese and lead are also correlated with ASD severity and autistic traits. Our study suggests that metal toxicant uptake and essential element deficiency during specific developmental windows increases ASD risk and severity, supporting the hypothesis of systemic elemental dysregulation in ASD. Independent replication in population-based studies is needed to extend these findings."



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Crack in CRISPR Facade after Unanticipated In Vivo Mutations Arise | GEN

 "The CRISPR/Cas9 genome-editing technique set the molecular biology field ablaze when its game-changing potential was realized only a few short years ago. In the time since this wildfire of excitement and hope, it has spread to almost every life science endeavor imaginable and shows little sign of slowing down. However, new data from a team of scientists lead by investigators at Columbia University Medical Center (CUMC) has uncovered that the gene-editing technology can introduce hundreds of unintended mutations into the genome—a concerning find, considering the technology is beginning to move full steam ahead into clinical trials. The findings from the new study were published recently in Nature Methods in an article entitled "Unexpected Mutations after CRISPR-Cas9 Editing In Vivo.""



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Suramin and Autism - UC San Diego Health

 "Suramin is a 100-year-old drug developed to treat African sleeping sickness and river blindness. Though it has been investigated for other diseases, including cancer, it is not approved for any therapeutic use in the United States.
However, a small, randomized clinical trial conducted by Robert Naviaux, MD, PhD, professor of medicine, pediatrics and pathology, and colleagues at University of California San Diego School of Medicine have found that a single intravenous dose of suramin produced dramatic, but transient, improvement of core symptoms of autism spectrum disorder (ASD). Currently, there are no drugs approved for treating the core symptoms of ASD.
More broadly, the trial findings support the “cell danger response theory,” which posits that autism and other chronic conditions are fundamentally driven by metabolic dysfunction—and thus treatable. Naviaux and his co-authors propose larger, longer clinical trials to assess suramin (or similar drugs) as an ASD treatment."



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Statins a new hope for treatment of Multiple Sclerosis an autoimmune disease - ShoutasScience

University college of London (UCL) researchers in the initial phase of clinical trial have found out that taking high doses of Statins (Simvastatin), a cholesterol-lowering drug by the people with the secondary progressive form of multiple sclerosis (MS) had a significant reduction in the rate of brain atrophy (brain shrinkage) over two years and also had better disability scores at the end of study. The phase 2 Clinical trial was conducted in collaboration with National Institute for Health Research (NIHR), the MS Society (UK), the National MS Society (US), the NHS and UK universities."




Can Omega-3 Help Prevent Alzheimer’s Disease? Brain SPECT Imaging Shows Possible Link | Journal of Alzheimer's Disease

 Amsterdam, NL – The incidence of Alzheimer’s disease (AD) is expected to triple in the coming decades and no cure has been found. Recently, interest in dietary approaches for prevention of cognitive decline has increased. In particular, the omega-3 fatty acids have shown anti-amyloid, anti-tau and anti-inflammatory actions in the brains of animals. In a new article published in the Journal of Alzheimer’s Disease, researchers have found that for patients with high omega-3 levels, blood flow in specific areas of the brain is increased."



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CX3CR1+ monocytes modulate learning and learning-dependent dendritic spine remodeling via TNF-[alpha] : Nature Medicine : Nature Research

Impaired learning and cognitive function often occurs during systemic infection or inflammation. Although activation of the innate immune system has been linked to the behavioral and cognitive effects that are associated with infection, the underlying mechanisms remain poorly understood. Here we mimicked viral immune activation with poly(I:C), a synthetic analog of double-stranded RNA, and longitudinally imaged postsynaptic dendritic spines of layer V pyramidal neurons in the mouse primary motor cortex using two-photon microscopy. We found that peripheral immune activation caused dendritic spine loss, impairments in learning-dependent dendritic spine formation and deficits in multiple learning tasks in mice. These observed synaptic alterations in the cortex were mediated by peripheral-monocyte-derived cells and did not require microglial function in the central nervous system. Furthermore, activation of CX3CR1highLy6Clow monocytes impaired motor learning and learning-related dendritic spine plasticity through tumor necrosis factor (TNF)-α-dependent mechanisms. Taken together, our results highlight CX3CR1high monocytes and TNF-α as potential therapeutic targets for preventing infection-induced cognitive dysfunction.

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Lithium May Prevent Neuron Damage In traumatic brain injury Patients - Neuroscience News

According to researchers, lithium, a drug commonly used to treat bipolar disorder, and rapamycin can help to protect neurons from further damage in those with TBI.

Source: Rutgers.

A drug used to treat bipolar disorder and other forms of depression may help to preserve brain function and prevent nerve cells from dying in people with a traumatic brain injury, according to a new Rutgers University study.

In research published in Scientific Reports, Rutgers scientists discovered that lithium – used as a mood stabilizer and to treat depression and bipolar disorder – and rapamycin, a treatment for some forms of cancer, protected nerve cells in the brain and stopped the chemical glutamate from sending signals to other cells and creating further brain cell damage."



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