Exposure To Antiepileptic Drug In Womb Linked To Autism Risk

MNT "Children whose mothers take the antiepileptic drug sodium valproate while pregnant are at significantly increased risk of autism and other neurodevelopmental disorders, suggests a small study published online in the Journal of Neurology Neurosurgery and Psychiatry."

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Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut.

Recently, we discovered that depression is accompanied by increased IgM and IgA responses directed against gram negative gut commensals. The aim of this study was to replicate these findings in a larger study group of depressed patients and to examine the associations between the IgA and IgM responses to gut commensals and staging of depression as well as the fatigue and somatic (F&S) symptoms of depression.


We measured serum concentrations of IgM and IgA against the LPS of gram-negative enterobacteria, i.e. Hafnia alvei, Pseudomonas aeruginosa, Morganella morganii, Pseudomonas putida, Citrobacter koseri, and Klebsiella pneumoniae in 112 depressed patients and 28 normal controls. The severity of F&S symptoms was measured using the Fibromyalgia and Chronic Fatigue Syndrome Rating Scale.


The prevalences and median values of serum IgM and IgA against LPS of these commensals were significantly higher in depressed patients than in controls. The IgM levels directed against the LPS of these commensal bacteria were significantly higher in patients with chronic depression than in those without. The immune responses directed against LPS were not associated with melancholia or recurrent depression. There was a significant correlation between the IgA response directed against LPS and gastro-intestinal symptoms.


The results indicate that increased bacterial translocation with immune responses to the LPS of commensal bacteria may play a role in the pathophysiology of depression, particularly chronic depression. Bacterial translocation may a) occur secondary to systemic inflammation in depression and intensify and perpetuate the primary inflammatory response once the commensals are translocated; or b) be a primary trigger factor associated with the onset of depression in some vulnerable individuals. The findings suggest that "translocated" gut commensal bacteria activate immune cells to elicit IgA and IgM responses and that this phenomenon may play a role in the pathophysiology of (chronic) depression by causing progressive amplifications of immune pathways.

Obesity may increase risk of MS in children and teens

 "Over the last 30 years, childhood obesity has tripled," said study author Annette Langer-Gould, MD, PhD, with the Kaiser Permanente Southern California Department of Research & Evaluation in Pasadena and a member of the American Academy of Neurology. "In our study, the risk of pediatric MS was highest among moderately and extremely obese teenage girls, suggesting that the rate of pediatric MS cases is likely to increase as the childhood obesity epidemic continues."

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Androgenic hormones could help treat multiple sclerosis, study finds

 "Testosterone and its derivatives could constitute an efficient treatment against myelin diseases such as multiple sclerosis, reveals a study by researchers from the Laboratoire d'Imagerie et de Neurosciences Cognitives. Myelin composes the sheaths that protect the nerve fibers and allow the speed of nerve impulses to be increased. A deficit in the production of myelin or its destruction cause serious illnesses for which there is no curative treatment. The researchers have shown that in mice brains whose nerve fibers have been demyelinated, testosterone and a synthetic analog induce the regeneration of oligodendrocytes, the cells responsible for myelination, and that they stimulate remyelination. This work is published on January in the journal Brain."

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Futurity.org – Rogue DNA busts out of aging cell ‘prison’

As cells age, they lose control over parasitic strands of mobile DNA that insert themselves into chromosomes, new research shows.The parasitic strands of genetic material called transposable elements—transposons—lurk in our chromosomes, poised to wreak genomic havoc. Cells have evolved ways to defend themselves, but in the new study, researchers describe how cells lose this ability as they age, possibly resulting in a decline in their function and health.
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The Antiaging Protein Klotho Enhances Oligodendrocyte Maturation and Myelination of the CNS

We have previously shown that myelin abnormalities characterize the normal aging process of the brain and that an age-associated reduction in Klotho is conserved across species. Predominantly generated in brain and kidney, Klotho overexpression extends life span, whereas loss of Klotho accelerates the development of aging-like phenotypes. Although the function of Klotho in brain is unknown, loss of Klotho expression leads to cognitive deficits. We found significant effects of Klotho on oligodendrocyte functions, including induced maturation of rat primary oligodendrocytic progenitor cells (OPCs) in vitro and myelination. Phosphoprotein analysis indicated that Klotho's downstream effects involve Akt and ERK signal pathways. Klotho increased OPC maturation, and inhibition of Akt or ERK function blocked this effect on OPCs. In vivo studies of Klotho knock-out mice and control littermates revealed that knock-out mice have a significant reduction in major myelin protein and gene expression. By immunohistochemistry, the number of total and mature oligodendrocytes was significantly lower in Klotho knock-out mice. Strikingly, at the ultrastructural level, Klotho knock-out mice exhibited significantly impaired myelination of the optic nerve and corpus callosum. These mice also displayed severe abnormalities at the nodes of Ranvier. To decipher the mechanisms by which Klotho affects oligodendrocytes, we used luciferase pathway reporters to identify the transcription factors involved. Together, these studies provide novel evidence for Klotho as a key player in myelin biology, which may thus be a useful therapeutic target in efforts to protect brain myelin against age-dependent changes and promote repair in multiple sclerosis.

Genome-wide study of association and interaction with maternal cytomegalovirus infection suggests new schizophrenia loci.

Genetic and environmental components as well as their interaction contribute to the risk of schizophrenia, making it highly relevant to include environmental factors in genetic studies of schizophrenia. This study comprises genome-wide association (GWA) and follow-up analyses of all individuals born in Denmark since 1981 and diagnosed with schizophrenia as well as controls from the same birth cohort. Furthermore, we present the first genome-wide interaction survey of single nucleotide polymorphisms (SNPs) and maternal cytomegalovirus (CMV) infection. The GWA analysis included 888 cases and 882 controls, and the follow-up investigation of the top GWA results was performed in independent Danish (1396 cases and 1803 controls) and German-Dutch (1169 cases, 3714 controls) samples. The SNPs most strongly associated in the single-marker analysis of the combined Danish samples were rs4757144 in ARNTL (P=3.78 × 10(-6)) and rs8057927 in CDH13 (P=1.39 × 10(-5)). Both genes have previously been linked to schizophrenia or other psychiatric disorders. The strongest associated SNP in the combined analysis, including Danish and German-Dutch samples, was rs12922317 in RUNDC2A (P=9.04 × 10(-7)). A region-based analysis summarizing independent signals in segments of 100 kb identified a new region-based genome-wide significant locus overlapping the gene ZEB1 (P=7.0 × 10(-7)). This signal was replicated in the follow-up analysis (P=2.3 × 10(-2)). Significant interaction with maternal CMV infection was found for rs7902091 (P(SNP × CMV)=7.3 × 10(-7)) in CTNNA3, a gene not previously implicated in schizophrenia, stressing the importance of including environmental factors in genetic studies.Molecular Psychiatry advance online publication, 29 January 2013; doi:10.1038/mp.2013.2.

Translational Psychiatry - Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder

Autism spectrum disorder (ASD) has been associated with mitochondrial disease (MD). Interestingly, most individuals with ASD and MD do not have a specific genetic mutation to explain the MD, raising the possibility of that MD may be acquired, at least in a subgroup of children with ASD. Acquired MD has been demonstrated in a rodent ASD model in which propionic acid (PPA), an enteric bacterial fermentation product of ASD-associated gut bacteria, is infused intracerebroventricularly. This animal model shows validity as it demonstrates many behavioral, metabolic, neuropathologic and neurophysiologic abnormalities associated with ASD. This animal model also demonstrates a unique pattern of elevations in short-chain and long-chain acyl-carnitines suggesting abnormalities in fatty-acid metabolism. To determine if the same pattern of biomarkers of abnormal fatty-acid metabolism are present in children with ASD, the laboratory results from a large cohort of children with ASD (n=213) who underwent screening for metabolic disorders, including mitochondrial and fatty-acid oxidation disorders, in a medically based autism clinic were reviewed. Acyl-carnitine panels were determined to be abnormal if three or more individual acyl-carnitine species were abnormal in the panel and these abnormalities were verified by repeated testing. Overall, 17% of individuals with ASD demonstrated consistently abnormal acyl-carnitine panels. Next, it was determined if specific acyl-carnitine species were consistently elevated across the individuals with consistently abnormal acyl-carnitine panels. Significant elevations in short-chain and long-chain, but not medium-chain, acyl-carnitines were found in the ASD individuals with consistently abnormal acyl-carnitine panels—a pattern consistent with the PPA rodent ASD model. Examination of electron transport chain function in muscle and fibroblast culture, histological and electron microscopy examination of muscle and other biomarkers of mitochondrial metabolism revealed a pattern consistent with the notion that PPA could be interfering with mitochondrial metabolism at the level of the tricarboxylic-acid cycle (TCAC). The function of the fatty-acid oxidation pathway in fibroblast cultures and biomarkers for abnormalities in non-mitochondrial fatty-acid metabolism were not consistently abnormal across the subgroup of ASD children, consistent with the notion that the abnormalities in fatty-acid metabolism found in this subgroup of children with ASD were secondary to TCAC abnormalities. Glutathione metabolism was abnormal in the subset of ASD individuals with consistent acyl-carnitine panel abnormalities in a pattern similar to glutathione abnormalities found in the PPA rodent model of ASD. These data suggest that there are similar pathological processes between a subset of ASD children and an animal model of ASD with acquired mitochondrial dysfunction. Future studies need to identify additional parallels between the PPA rodent model of ASD and this subset of ASD individuals with this unique pattern of acyl-carnitine abnormalities. A better understanding of this animal model and subset of children with ASD should lead to better insight in mechanisms behind environmentally induced ASD pathophysiology and should provide guidance for developing preventive and symptomatic treatments.

Polymer Film That Gradually Releases DNA Coding For Viral Proteins Could Offer A Better Alternative To Traditional Vaccines

Vaccines usually consist of inactivated viruses that prompt the immune system to remember the invader and launch a strong defense if it later encounters the real thing. However, this approach can be too risky with certain viruses, including HIV

In recent years, many scientists have been exploring DNA as a potential alternative vaccine. About 20 years ago, DNA coding for viral proteins was found to induce strong immune responses in rodents, but so far, tests in humans have failed to duplicate that success. 

Obesity and its consequences spreading rapidly around the world

Clogged arteries and sedentary lifestyles have replaced germs as the world's leading killers. Where hunger once held much of the world in its grip, the 1.6 billion overweight and obese now outnumber the malnourished by nearly 2-to-1.

Read more at: http://medicalxpress.com/news/2013-01-obesity-consequences-rapidly-world.html#jCp

Toll-like receptor 4 stimulation with the detoxified ligand monophosphoryl lipid A improves Alzheimer’s disease-related pathology

Alzheimer’s disease (AD) is the most common cause of dementia worldwide. The pathogenesis of this neurodegenerative disease, currently without curative treatment, is associated with the accumulation of amyloid β (Aβ) in brain parenchyma and cerebral vasculature. AD patients are unable to clear this toxic peptide, leading to Aβ accumulation in their brains and, presumably, the pathology associated with this devastating disease. Compounds that stimulate the immune system to clear Aβ may therefore have great therapeutic potential in AD patients. Monophosphoryl lipid A (MPL) is an LPS-derived Toll-like receptor 4 agonist that exhibits unique immunomodulatory properties at doses that are nonpyrogenic. We show here that repeated systemic injections of MPL, but not LPS, significantly improved AD-related pathology in APPswe/PS1 mice. MPL treatment led to a significant reduction in Aβ load in the brain of these mice, as well as enhanced cognitive function. MPL induced a potent phagocytic response by microglia while triggering a moderate inflammatory reaction. Our data suggest that the Toll-like receptor 4 agonist MPL may be a treatment for AD.

Case History Database | From Biomed Central

Documenting a patient's case history to inform physicians how the patient has been evaluated and the subsequent progression of his or her disease is arguably the oldest method of communicating medical evidence. And in the 21st century case reports play an equally important role.

Since the launch of Journal of Medical Case Reports in 2007 and the more recent introduction of case reports to the broad-scope journal BMC Research NotesBioMed Central has acknowledged the value of case reports to the scientific record.  To strengthen this commitment we have developed a valuable new resource – Cases Database, a continuously-updated, freely-accessible database of thousands of medical case reports from multiple publishers, including Springer, BMJ and PubMed Central.
By aggregating case reports and facilitating comparison, Cases Database provides clinicians, researchers, regulators and patients a simple resource to explore content, and identify emerging trends.
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Radioactive in situ hybridization for Epstein–Barr virus–encoded small RNA supports presence of Epstein–Barr virus in the multiple sclerosis brain

ALS May Be Prevented By Eating Colorful Fruits And Vegetables

MNT: "Eating bright colored foods, especially those that are yellow, orange, and red, may prevent or slow the onset of amyotrophic lateral sclerosis (ALS).The study, published in the journal Annals of Neurology, confirmed that colorful carotenoids prevented the onset of ALS, while diets high in lycopene, beta-cryptoxanthin, and vitamin C did not decrease ALS risk."

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Glial cells assist in the repair of injured nerves

When a nerve is damaged, glial cells produce the protein neuregulin1 and thereby promote the regeneration of nerve tissue.

Read more at: http://medicalxpress.com/news/2013-01-glial-cells-nerves.html#jCp

Melanoma Genes Found In "Junk" DNA

US scientists have found two new mutations in non-coding (formerly dubbed "junk") DNA that occur in 71% of malignant melanomas. They say the highly recurrent mutations may be the most common in this deadliest form of skin cancer, more common than the already well-known protein-coding BRAF gene, and may well offer an alternative target for treatment. MNT

Meet the Scientist Webinars - March, 2013 | Depression and Schizophrenia "Brain & Behavior Research Foundation (Formerly NARSAD)

Meet the Scientist Webinar Series hosted by Brain & Behavior Research Foundation Acting President and CEO, Jeffrey Borenstein, M.D. Hear leading mental health researchers present the latest in new technologies, diagnostic tools, early intervention strategies and next generation therapies for mental illness.

Cholesterol Finding Offers New Way To Kill Lymphoma Without Chemotherapy

Medical News Today: How do you annihilate lymphoma without using any drugs? Starve it to death by depriving it of what appears to be a favorite food: HDLcholesterolNorthwestern Medicine® researchers discovered this with a new nanoparticle that acts like a secret double agent. It appears to the cancerous lymphoma cell like a preferred meal -- natural HDL. But when the particle engages the cell, it actually plugs it up and blocks cholesterol from entering. Deprived of an essential nutrient, the cell eventually dies. 
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Identification of Viral Pathogen Diversity in Sewage Sludge by Metagenome Analysis.

The large diversity of viruses that exist in human populations are potentially excreted into sewage collection systems and concentrated in sewage sludge. In the US, the primary fate of processed sewage sludge (class B biosolids) is application to agricultural land as a soil amendment. To characterize and understand infectious risks associated with land application, and to describe the diversity of viruses in human populations, shotgun viral metagenomics was applied to 10 sewage sludge samples from 5 wastewater treatment plants throughout the continental U.S, each serving between 100,000 and 1,000,000 people. Nearly 330 million DNA sequences were produced and assembled, and annotation resulted in identifying 43 (26 DNA, 17 RNA) different types of human viruses in sewage sludge. Novel insights include the high abundance of newly emerging viruses (e.g. Coronavirus HKU1, Klassevirus, and Cosavirus) the strong representation of respiratory viruses, and the relatively minor abundance and occurrence of Enteroviruses. Viral metagenome sequence annotations were reproducible and independent PCR-based identification of selected viruses suggests that viral metagenomes were a conservative estimate of the true viral occurrence and diversity. These results represent the most complete description of human virus diversity in any wastewater sample to date, provide engineers and environmental scientists with critical information on important viral agents and routes of infection from exposure to wastewater and sewage sludge, and represent a significant leap forward in understanding the pathogen content of class B biosolids.

Lupus: Peptide P140/LupuzorTM effectiveness confirmed

A clinical trial with 149 patients suffering from the very disabling autoimmune disease systemic lupus erythematosus, has shown the effectiveness of a synthetic peptide developed by a team of researchers led by CNRS biologist Slyviane Muller at the Institut de Biologie Moleculaire (IBMC) in Strasbourg, France."

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Chronic or late lyme neuroborreliosis: analysis of evidence compared to chronic or late neurosyphilis.

Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. Today, the same question is in the center of debate with respect to Lyme disease. The goal of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions would indicate that the spirochete is responsible for the neuropsychiatric manifestations of late/chronic Lyme neuroborreliosis. The substantial amounts of data available in the literature show that the major forms of late/chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed. Borrelia burgdorferi was detected in association with tertiary brain lesions and cultivated from the affected brain or cerebrospinal fluid. The accumulated data also indicate that Borrelia burgdorferi is able to evade from destruction by the host immune reactions, persist in host tissues and sustain chronic infection and inflammation. These observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis.Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing. Further pathological investigations and the detection of spirochetes in infected tissues and body fluids are strongly needed.

Synthetic corkscrew peptide kills antibiotic-resistant gram-negative bacteria

An engineered peptide provides a new prototype for killing an entire category of resistant bacteria by shredding and dissolving their double-layered membranes, which are thought to protect those microbes from antibiotics.

Scientists discover how epigenetic information could be inherited: Mechanism of epigenetic reprogramming revealed

New research reveals a potential way for how parents' experiences could be passed to their offspring's genes. The research was published January, 25 in the journal Science.

Antibodies Not Only Fend Off Pathogens, They Also Help To Convey Messages Between Immune Cells

"scientists at the Helmholtz Centre for Infection Research (HZI) and the Hannover Medical School (MHH) were able to show that antibodies are essential for dendritic cell maturation. The researchers' findings have been published in the renowned scientific journal, Proceedings of the National Academy of Sciences (PNAS). "

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Plastic products and jet fuel exposures raising incidences of 'epigenetic transgenerational inheritance'

Writing in the online journal PLOS ONE, scientists led by molecular biologist Michael Skinner document reproductive disease and obesity in the descendants of rats exposed to the plasticizer bisephenol-A, or BPA, as well DEHP and DBP, plastic compounds known as phthalates. In a separate article in the journal Reproductive Toxicology, they report the first observation of cross-generation disease from a widely used hydrocarbon mixture the military refers to as JP8.

Read more at: http://medicalxpress.com/news/2013-01-plastic-products-jet-fuel-exposures.html#jCp
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Scientists find cancer-causing virus in the brain, potential connection to epilepsy

Researchers at Shriner's Hospital Pediatric Research Center at the Temple University School of Medicine, and the University of Pennsylvania have evidence linking the human papillomavirus 16 (HPV16) – the most common cause of cervical cancer – to a common form of childhood epilepsy. They have shown for the first time that HPV16 may be present in the human brain, and found that when they added a viral protein to the brains of fetal mice, the mice all demonstrated the same developmental problems in the cerebral cortex associated with this type of epilepsy, called focal cortical dysplasia type IIB (FCDIIB). The findings suggest that the virus could play a role in the development of epilepsy.

Read more at: http://medicalxpress.com/news/2013-01-scientists-cancer-causing-virus-brain-potential.html#jCp

PLOS Genetics: Gene Copy-Number Polymorphism Caused by Retrotransposition in Humans

The era of whole-genome sequencing has revealed that gene copy-number changes caused by duplication and deletion events have important evolutionary, functional, and phenotypic consequences. Recent studies have therefore focused on revealing the extent of variation in copy-number within natural populations of humans and other species. These studies have found a large number of copy-number variants (CNVs) in humans, many of which have been shown to have clinical or evolutionary importance. For the most part, these studies have failed to detect an important class of gene copy-number polymorphism: gene duplications caused by retrotransposition, which result in a new intron-less copy of the parental gene being inserted into a random location in the genome. Here we describe a computational approach leveraging next-generation sequence data to detect gene copy-number variants caused by retrotransposition (retroCNVs), and we report the first genome-wide analysis of these variants in humans. We find that retroCNVs account for a substantial fraction of gene copy-number differences between any two individuals. Moreover, we show that these variants may often result in expressed chimeric transcripts, underscoring their potential for the evolution of novel gene functions. By locating the insertion sites of these duplicates, we are able to show that retroCNVs have had an important role in recent human adaptation, and we also uncover evidence that positive selection may currently be driving multiple retroCNVs toward fixation. Together these findings imply that retroCNVs are an especially important class of polymorphism, and that future studies of copy-number variation should search for these variants in order to illuminate their potential evolutionary and functional relevance.

Parasites: evolution’s neurobiologists

For millions of years, parasites have altered the behaviour of their hosts. Parasites can affect host behaviour by: (1) interfering with the host’s normal immune–neural communication, (2) secreting substances that directly alter neuronal activity via non-genomic mechanisms and (3) inducing genomic- and/or proteomic-based changes in the brain of the host. Changes in host behaviour are often restricted to particular behaviours, with many other behaviours remaining unaffected. Neuroscientists can produce this degree of selectivity by targeting specific brain areas. Parasites, however, do not selectively attack discrete brain areas. Parasites typically induce a variety of effects in several parts of the brain. Parasitic manipulation of host behaviour evolved within the context of the manipulation of other host physiological systems (especially the immune system) that was required for a parasite’s survival. This starting point, coupled with the fortuitous nature of evolutionary innovation and evolutionary pressures to minimize the costs of parasitic manipulation, likely contributed to the complex and indirect nature of the mechanisms involved in host behavioural control. Because parasites and neuroscientists use different tactics to control behaviour, studying the methods used by parasites can provide novel insights into how nervous systems generate and regulate behaviour. Studying how parasites influence host behaviour will also help us integrate genomic, proteomic and neurophysiological perspectives on behaviour.

Prenatal inflammation linked to autism risk, News Release - National Institutes of Health (NIH)

Maternal inflammation during early pregnancy may be related to an increased risk of autism in children, according to new findings supported by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health.  Researchers found this in children of mothers with elevated C-reactive protein (CRP), a well-established marker of systemic inflammation.
The risk of autism among children in the study was increased by 43 percent among mothers with CRP levels in the top 20th percentile, and by 80 percent for maternal CRP in the top 10th percentile. The findings appear in the journal Molecular Psychiatry and add to mounting evidence that an overactive immune response can alter the development of the central nervous system in the fetus.

Molecular Psychiatry - Increased inflammatory markers identified in the dorsolateral prefrontal cortex of individuals with schizophrenia

Upregulation of the immune response may be involved in the pathogenesis of schizophrenia with changes occurring in both peripheral blood and brain tissue. To date, microarray technology has provided a limited view of specific inflammatory transcripts in brain perhaps due to sensitivity issues. Here we used SOLiD Next Generation Sequencing to quantify neuroimmune mRNA expression levels in the dorsolateral prefrontal cortex of 20 individuals with schizophrenia and their matched controls. We detected 798 differentially regulated transcripts present in people with schizophrenia compared with controls. Ingenuity pathway analysis identified the inflammatory response as a key change. Using quantitative real-time PCR we confirmed the changes in candidate cytokines and immune modulators, including interleukin (IL)-6, IL-8, IL-1β and SERPINA3. The density of major histocompatibility complex-II-positive cells morphologically resembling microglia was significantly increased in schizophrenia and correlated with IL-1β expression. A group of individuals, most of whom had schizophrenia, were found to have increased inflammatory mRNA expression. In summary, we have demonstrated changes in an inflammatory response pathway that are present in ~40% of people diagnosed with schizophrenia. This suggests that therapies aimed at immune system attenuation in schizophrenia may be of direct benefit in the brain.

From Molecular Entities to Competent Agents: Viral Infection-Derived Consortia Act as Natural Genetic Engineers - Springer

Endogenous viruses and defectives, transposons, retrotransposons, long terminal repeats, non-long terminal repeats, long interspersed nuclear elements, short interspersed nuclear elements, group I introns, group II introns, phages and plasmids are currently investigated examples that use genomic DNA as their ­preferred live habitat. This means that DNA is not solely a genetic storage medium that serves as an evolutionary protocol, but it is also a species-specific ecological niche. A great variety of such mobile genetic elements have been identified during the last 40 years as obligate inhabitants of all genomes, either prokaryotic or eukaryotic. They infect, insert, delete, some cut and paste, others copy and paste and spread within the genome. They change host genetic identities either by insertion, recombination or the epigenetic (re)regulation of genetic content, and co-evolve with the host and interact in a module-like manner. In this respect they play vital roles in evolutionary and developmental processes. In contrast to accidental point ­mutations, integration at various preferred sites is not a randomly occurring process but is coherent with the genetic content of the host; otherwise, important protein coding regions would be damaged, causing disease or even lethal consequences for the host organism. In contrast to “elements”, “entities” and “systems”, biological agents are capable of identifying sequence-specific loci of genetic text. They are masters of the shared technique of coherently identifying and combining nucleotides according contextual needs. This natural genetic engineering competence is absent in ­inanimate nature, and therefore represents a core capability of life.
From : An ebook: 


ISBN: 978-94-007-4898-9 (Print) 978-94-007-4899-6 (Online)

Viruses: Essential Agents of Life

Immune cell death defects linked to autoimmune diseases

Melbourne researchers have discovered that the death of immune system cells is an important safeguard against the development of diseases such as type 1 diabetes, rheumatoid arthritis and lupus, which occur when the immune system attacks the body's own tissues."

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Fast food linked to asthma and eczema

A large international study led from The University of Auckland has shown that an increased risk of severe asthma, eczema and rhinitis in adolescents and children is associated with eating fast food three or more times a week."

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Futurity.org – From genes to brain: Schizophrenia untangled

The genomic pathway, Integrative Nuclear FGFR 1 Signaling (INFS), is a central intersection point for multiple pathways of as many as 160 different genes believed to be involved in the disorder.

Circadian rhythms can be modified for potential treatment of disorders | UCIrvine News

UC Irvine-led studies have revealed the cellular mechanism by which circadian rhythms – also known as the body clock – modify energy metabolism and also have identified novel compounds that control this action. The findings point to potential treatments for disorders triggered by circadian rhythm dysfunction, ranging from insomnia and obesity to diabetes and cancer.

Eczema in infants linked to gut bacteria

Children with eczema have a more diverse set of bacteria in their guts than non affected children, finds a new study in BioMed Central's open access journal BMC Microbiology. The types of bacteria present were also more typical of adult gut microbes than for toddlers without eczema.
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Viral reactivation a likely link between stress and heart disease

COLUMBUS, Ohio – A new study could provide the link that scientists have been looking for to confirm that reactivation of a latent herpes virus is a cause of some heart problems.
Looking at blood samples from 299 heart patients, researchers at Ohio State University found that those who had suffered a heart attack were the most likely to have inflammatory proteins circulating in their blood compared to patients with less acute symptoms. And having more of one of these proteins in the blood was linked to the presence of antibodies that signal a latent Epstein-Barr virus (EBV) reactivation.
To date, these relationships have been hard to find because scientists have been unable to detect evidence of a virus in diseased areas of the cardiovascular system.
In this study, however, the researchers instead looked for antibodies against a protein that can be produced even when only partial or incomplete reactivation of Epstein-Barr EBV occurs. And when this antibody was detected, it was associated with immune system malfunctions connected to inflammation – a known risk factor for heart disease.

Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases |Webinar: The New York Academy of Sciences

As life expectancy increases, the prevalence of age-related diseases will also increase. Efforts to develop therapies for age-related neurodegenerative diseases have yet to succeed in impacting disease pathogenesis; current treatments target only the symptoms, not the causes. To develop disease-modifying agents, some researchers aim to identify common features of neurodegenerative diseases that might provide clues to potential drug targets. On November 29, 2012, researchers investigating Alzheimer's, Parkinson's, and Huntington's diseases met at the New York Academy of Sciences to discuss one such feature—the effect of metals in neurodegenerative diseases—and to highlight clinical achievements using metal-binding compounds to influence disease progression. The symposium, Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases, was presented by the Academy's Brain Dysfunction Discussion Group.

The ISME Journal - Abstract of article: Gut microbiome composition is linked to whole grain-induced immunological improvements

The involvement of the gut microbiota in metabolic disorders, and the ability of whole grains to affect both host metabolism and gut microbial ecology, suggest that some benefits of whole grains are mediated through their effects on the gut microbiome. Nutritional studies that assess the effect of whole grains on both the gut microbiome and human physiology are needed. We conducted a randomized cross-over trial with four-week treatments in which 28 healthy humans consumed a daily dose of 60g of whole-grain barley (WGB), brown rice (BR), or an equal mixture of the two (BR+WGB), and characterized their impact on fecal microbial ecology and blood markers of inflammation, glucose and lipid metabolism. All treatments increased microbial diversity, the Firmicutes/Bacteroidetes ratio, and the abundance of the genus Blautia in fecal samples. The inclusion of WGB enriched the genera RoseburiaBifidobacterium andDialister, and the species Eubacterium rectaleRoseburia faecis andRoseburia intestinalis. Whole grains, and especially the BR+WGB treatment, reduced plasma interleukin-6 (IL-6) and peak postprandial glucose. Shifts in the abundance of Eubacterium rectale were associated with changes in the glucose and insulin postprandial response. Interestingly, subjects with greater improvements in IL-6 levels harbored significantly higher proportions of Dialister and lower abundance of Coriobacteriaceae. In conclusion, this study revealed that a short-term intake of whole grains induced compositional alterations of the gut microbiota that coincided with improvements in host physiological measures related to metabolic dysfunctions in humans.

The ISME Journal - An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice

Lipopolysaccharide endotoxin is the only known bacterial product which, when subcutaneously infused into mice in its purified form, can induce obesity and insulin resistance via an inflammation-mediated pathway. Here we show that one endotoxin-producing bacterium isolated from a morbidly obese human’s gut induced obesity and insulin resistance in germfree mice. The endotoxin-producing Enterobacter decreased in relative abundance from 35% of the volunteer’s gut bacteria to non-detectable, during which time the volunteer lost 51.4kg of 174.8kg initial weight and recovered from hyperglycemia and hypertension after 23 weeks on a diet of whole grains, traditional Chinese medicinal foods and prebiotics. A decreased abundance of endotoxin biosynthetic genes in the gut of the volunteer was correlated with a decreased circulating endotoxin load and alleviated inflammation. Mono-association of germfree C57BL/6J mice with strain Enterobacter cloacae B29 isolated from the volunteer’s gut induced fully developed obesity and insulin resistance on a high-fat diet but not on normal chow diet, whereas the germfree control mice on a high-fat diet did not exhibit the same disease phenotypes. The Enterobacter-induced obese mice showed increased serum endotoxin load and aggravated inflammatory conditions. The obesity-inducing capacity of this human-derived endotoxin producer in gnotobiotic mice suggests that it may causatively contribute to the development of obesity in its human host.
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Researchers show how cells' DNA repair machinery can destroy viruses

A team of researchers based at Johns Hopkins has decoded a system that makes certain types of immune cells impervious to HIV infection. The system's two vital components are high levels of a molecule that becomes embedded in viral DNA like a code written in invisible ink, and an enzyme that, when it reads the code, switches from repairing the DNA to chopping it up into unusable pieces. The researchers, who report the find in the Jan. 21 early edition of the Proceedings of the National Academy of Sciences, say the discovery points toward a new approach to eradicating HIV from the body."

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More ADHD Diagnoses Over The Last Ten Years: Up 24%

Rates of ADHD (attention deficit hyperactivity disorder) have risen by 24% over the last ten years, researchers from the Kaiser Permanente Southern California Medical Group reported in JAMA Pediatrics.

Overlooked ugly cholesterol causes heart disease | BreakThrough Digest Medical News

The risk of ischaemic heart disease , a disease affecting some 150,000 Danes , is three times higher in persons with high levels of the so-called ‘ugly’ cholesterol. This is the finding of a new study of 73,000 Danes, which is shedding light on a long debate on this topic. The results have just been published in theJournal of the American College of CardiologyMost Danes are aware that high cholesterol is life-threatening. But very few know which type of cholesterol is the most frequent killer. Cholesterol is divided into ‘the good’ HDL cholesterol, ‘the bad’ LDL cholesterol and ‘the ugly’ cholesterol. It is the so-called ‘ugly cholesterol’ ? also called ‘remnant-like particle cholesterol’ ? that is the really bad guy.

Australian scientists may have found ‘potential cure for Aids’ Microbe World

A FORM of gene therapy developed by researchers at the Queensland Institute of Medical Research may provide hope to sufferers of HIV, preventing the virus from crippling the immune system by manipulating its genetic structure and turning HIV into a weapon against itself.

A Closer Look At The 'Borderline Personality disorder' Brain: MNT

The work shows that brain regions that process negative emotions (for example, anger and sadness) are overactive in people with Borderline Personality disorder,   while brain regions that would normally help damp down negative emotions are underactive. Medical News Today
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Epigenetics explains rheumatism? Genes and their regulatory 'tags' conspire to promote rheumatoid arthritis

In one of the first genome-wide studies to hunt for both genes and their regulatory "tags" in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments.

Plasma-Based Circulating MicroRNA Biomarkers for Parkinson's Disease - Journal of Parkinson's Disease

The current “gold-standard” for Parkinson's disease (PD) diagnosis is based primarily on subjective clinical rating scales related with motor features. Molecular biomarkers that are objective and quantifiable remain attractive as clinical tools to detect PD prior to its motor onsets. Objective: Here, we aimed to identify, develop, and validate plasma-based circulating microRNA (miRNAs) as biomarkers for PD. Methods: Global miRNA expressions were acquired from a discovery set of 32 PD/32 controls using microarrays. k-Top Scoring Pairs (k-TSP) algorithm and significance analysis of microarrays (SAM) were applied to obtain comprehensive panels of PD-predictive biomarkers. TaqMan miRNA-specific real-time PCR assays were performed to validate the microarray data and to evaluate the biomarker performance using a new replication set of 42 PD/30 controls. Data was analyzed in a paired PD-control fashion. The validation set was composed of 30 PD, 5 progressive supranuclear palsy, and 4 multiple system atrophy samples from a new clinical site. Results: We identified 9 pairs of PD-predictive classifiers using k-TSP analysis and 13 most differentially-expressed miRNAs by SAM. A combination of both data sets produced a panel of PD-predictive biomarkers: k-TSP1 (miR-1826/miR-450b-3p), miR-626, and miR-505, and achieved the highest predictive power of 91% sensitivity, 100% specificity, 100% positive predicted value, and 88% negative predicted value in the replication set. However, low predictive values were shown in the validation set. Conclusions: This proof-of-concept study demonstrates the feasibility of using plasma-based circulating miRNAs as biomarkers for neurodegenerative disorders such as PD and shows the challenges of molecular biomarker research using samples from multiple clinical sites.

BBC News - 'Quadruple helix' DNA seen in human cells

Does Helicobacter pylori Infection Increase Incidence of Dementia? The Personnes Agées QUID Study - Roubaud Baudron - 2012 - Journal of the American Geriatrics Society - Wiley Online Library

At baseline, 391 (64.8%) subjects (348 women, mean age 73.9 ± 6.5) were seropositive for H. pylori. Dementia prevalence was higher in the infected group (5.4% vs 1.4%, = .02). After 20 years of follow-up, 148 incident cases of dementia were diagnosed. After controlling for age, sex, educational level, apolipoprotein E4 status, cardiovascular risk factors, and Mini-Mental State Examination score, H. pyloriinfection was determined to be a risk factor for developing dementia (hazard ratio = 1.46, = .04).


This longitudinal population-based study provides additional epidemiological support to the hypothesis of an association between dementia and H. pylori infection, which may enhance neurodegeneration.

Sex Differences in the Gut Microbiome Drive Hormone-Dependent Regulation of Autoimmunity.

Microbial exposures and sex hormones exert potent effects on autoimmune diseases, many of which are more prevalent in women. Here, we demonstrate a direct interaction between sex hormones and early life microbial exposures on the control of autoimmunity in the non-obese diabetic (NOD) mouse model of type 1 diabetes (T1D). Colonization by commensal microbes elevated serum testosterone and protected NOD males from T1D. Transfer of gut microbiota from adult males to immature females altered the recipient's microbiota, resulting in elevated testosterone and metabolomic changes, reduced islet inflammation and autoantibody production, and robust T1D protection. These effects were dependent on androgen receptor activity. Thus, the commensal microbial community alters sex hormone levels and regulates autoimmune disease fate in individuals with high genetic risk.

Evidence for an enterovirus as the cause of encephalitis lethargica.

The epidemic of encephalitis lethargica (EL), called classical EL, was rampant throughout the world during 1917-1926, affecting half a million persons. The acute phase was lethal for many victims. Post-encephalitic parkinsonism (PEP) affected patients for decades. Our purpose was to investigate the cause of classical EL by studying the few available brain specimens. Cases of PEP and modern EL were also studied. Transmission electron microscopy (TEM) and immunohistochemistry were employed to examine brain from four classical EL cases, two modern EL cases and one PEP case.


Standard methods for TEM, immunohistochemistry and RTPCR were applied.


27 nm virus-like particles (VLP) were observed in the cytoplasm and nuclei of midbrain neurons in all classical EL cases studied. Large (50 nm) VLP and 27 nm intranuclear VLP were observed in the modern EL cases and the PEP case. Influenza virus particles were not found. VLP were not observed in the control cases. TEM of cell cultures inoculated with coxsackievirus B4 and poliovirus revealed both small and large intranuclear virus particles and small cytoplasmic particles, similar to the VLP in EL neurons. In the EL brains, nascent VLP were embedded in putative virus factories and on endoplasmic reticulum (ER). The VLP in the cases of classical EL survived, whereas ribosomes underwent autolysis due to the lack of refrigeration and slow formaldehyde fixation of whole brain. The VLP were larger than ribosomes from well preserved brain. Immunohistochemistry of classical EL cases using anti-poliovirus and anti-coxsackievirus B polyclonal antibodies showed significant staining of cytoplasm and nuclei of neurons as well as microglia and neuropil. Purkinje cells were strongly stained.A 97-bp RNA fragment of a unique virus was isolated from brain tissue from acute EL case #91558. Sequence analysis revealed up to 95% identity to multiple human Enteroviruses. Additional cases had Enterovirus positive reactions by real time PCR.


The data presented here support the hypothesis that the VLP observed in EL tissue is an Enterovirus.
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Good bacteria in the intestine prevent diabetes, study finds

 "All humans have enormous numbers of bacteria and other micro-organisms (10 to 14) in the lower intestine. In fact our bodies contain about ten times more bacteria than our own cells and these tiny passengers are extremely important for our health. They help us digest our food and provide us with energy and vitamins. These "friendly" commensal bacteria in the intestine help to stop the "bad guys" such as Salmonella that cause infections, taking hold. Even the biochemical reactions that build up and maintain our bodies come from our intestinal bacteria as well as our own cells. "

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Repeated aggressions trigger social aversion in mice

One of the mechanisms involved in the onset of stress-induced depression has been highlighted in mice by researchers from CNRS, Inserm and UPMC.

Read more at: http://medicalxpress.com/news/2013-01-aggressions-trigger-social-aversion-mice.html#jCp

Bacteria Can Morph Host Cells Into Stem Cells

MNT "Bacteria have the ability to convert the host tissue cells that they infect to become like stem cells that can then differentiate into virtually any other type of cell, thereby enabling the bugs to spread to other parts of the body. "

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Endolysosome involvement in LDL cholesterol-induced Alzheimer's disease-like pathology in primary cultured neurons.

Elevated levels of circulating cholesterol are extrinsic factors contributing to the pathogenesis of sporadic Alzheimer's disease (AD). We showed previously that rabbits fed a cholesterol-enriched diet exhibited blood-brain barrier (BBB) dysfunction, increased accumulation of apolipoprotein B (ApoB) in brain neurons, and endolysosomes in brain had disturbed structures and functions. These effects were linked to increased amyloid beta (Aβ) production, increased tau-pathology, and disrupted synaptic integrity. Because pathological changes to endolysosomes represent a very early event in sporadic AD, we determined here the extent to which ApoB-containing LDL cholesterol altered the structure and function of endolysosomes and contributed to the development of AD-like pathology in primary cultured neurons.


Cholesterol distribution and endolysosome morphology were determined histologically. Endolysosome pH was measured ratio-metrically with LysoSensor dye. Endolysosome enzyme activity was measured for acid phosphatase, cathepsins B and D, and beta-site APP cleaving enzyme 1 (BACE-1). AD-like pathologies, including increased production of Aβ, increased tau-pathology, and disrupted synaptic integrity were determined using ELISA, immunoblotting, and immunostaining techniques.


Treatment of neurons with ApoB-containing LDL cholesterol increased endolysosome accumulation of cholesterol, enlarged endolysosomes, and elevated endolysosome pH. In addition, ApoB-containing LDL cholesterol increased endolysosome accumulation of BACE-1, enhanced BACE-1 activity, increased Aβ levels, increased levels of phosphorylated tau, and decreased levels of synaptophysin.


Our findings suggest strongly that alterations in the structure and function of endolysosomes play a key role in the exhibition of pathological features of AD that result from neuronal exposure to ApoB-containing LDL cholesterol.

Low Levels Of Common Flame-Retardant Chemical Damages Brain Cells

Finding may have implications for autism

A common ingredient in flame retardants, BDE-49 accumulates in human blood, fat and breast milk. Despite these concentrations, little research has been done on the chemical's potential health risks. However, a study by scientists at the UC Davis MIND Institute is shedding new light on BDE-49's potential danger to brain health. The study showed that even tiny amounts of the compound damage neural mitochondria, the energy plants that power our cells. The chemical, quite literally, reduces brain power. 

Cornell Chronicle: Viruses discovered in marine zooplankton

Cornell Chronicle: Viruses discovered in marine zooplankton:

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CNS response to a second pro-inflammatory event depends on whether the primary demyelinating lesion is active or resolved.

Interleukin-1β (IL-1β) is considered to be one of the most important mediators in the pathogenesis of inflammatory diseases, particularly in neurodegenerative diseases such as multiple sclerosis (MS). MS is a chronic inflammatory disease characterized by demyelination and remyelination events, with unpredictable relapsing and remitting episodes that seldom worsen MS lesions. We proposed to study the effect of a unique component of the inflammatory process, IL-1β, and evaluate its effect in repeated episodes, similar to the relapsing-remitting MS pathology. Using adenoviral vectors, we developed a model of focal demyelination/remyelination triggered by the chronic expression of IL-1β. The long-term expression of IL-1β in the striatum produced blood-brain barrier (BBB) breakdown, demyelination, microglial/macrophage activation, and neutrophil infiltration but no overt neuronal degeneration. This demyelinating process was followed by complete remyelination of the area. This simple model allows us to study demyelination and remyelination independently of the autoimmune and adaptive immune components. Re-exposure to this cytokine when the first inflammatory response was still unresolved generated a lesion with decreased neuroinflammation, demyelination, axonal injury and glial response. However, a second long-term expression of IL-1β when the first lesion was resolved could not be differentiated from the first event. In this study, we demonstrated that the response to a second inflammatory stimulus varies depending on whether the initial lesion is still active or has been resolved. Considering that anti-inflammatory treatments have shown little improvement in MS patients, studies about the behavior of specific components of the inflammatory process should be taken into account to develop new therapeutic tools.

A Genome-Wide Integrative Genomic Study Localizes Genetic Factors Influencing Antibodies against Epstein-Barr Virus Nuclear Antigen 1 (EBNA-1).

Infection with Epstein-Barr virus (EBV) is highly prevalent worldwide, and it has been associated with infectious mononucleosis and severe diseases including Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal lymphoma, and lymphoproliferative disorders. Although EBV has been the focus of extensive research, much still remains unknown concerning what makes some individuals more sensitive to infection and to adverse outcomes as a result of infection. Here we use an integrative genomics approach in order to localize genetic factors influencing levels of Epstein Barr virus (EBV) nuclear antigen-1 (EBNA-1) IgG antibodies, as a measure of history of infection with this pathogen, in large Mexican American families. Genome-wide evidence of both significant linkage and association was obtained on chromosome 6 in the human leukocyte antigen (HLA) region and replicated in an independent Mexican American sample of large families (minimum p-value in combined analysis of both datasets is 1.4×10(-15) for SNPs rs477515 and rs2516049). Conditional association analyses indicate the presence of at least two separate loci within MHC class II, and along with lymphocyte expression data suggest genes HLA-DRB1 and HLA-DQB1 as the best candidates. The association signals are specific to EBV and are not found with IgG antibodies to 12 other pathogens examined, and therefore do not simply reveal a general HLA effect. We investigated whether SNPs significantly associated with diseases in which EBV is known or suspected to play a role (namely nasopharyngeal lymphoma, Hodgkin lymphoma, systemic lupus erythematosus, and multiple sclerosis) also show evidence of associated with EBNA-1 antibody levels, finding an overlap only for the HLA locus, but none elsewhere in the genome. The significance of this work is that a major locus related to EBV infection has been identified, which may ultimately reveal the underlying mechanisms by which the immune system regulates infection with this pathogen.

Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study.

This study undertakes a systematic and comprehensive analysis of brain gene expression profiles of immune/inflammation-related genes in aging and Alzheimer's disease (AD).


In a well-powered microarray study of young (20 to 59 years), aged (60 to 99 years), and AD (74 to 95 years) cases, gene responses were assessed in the hippocampus, entorhinal cortex, superior frontal gyrus, and post-central gyrus.


Several novel concepts emerge. First, immune/inflammation-related genes showed major changes in gene expression over the course of cognitively normal aging, with the extent of gene response far greater in aging than in AD. Of the 759 immune-related probesets interrogated on the microarray, approximately 40% were significantly altered in the SFG, PCG and HC with increasing age, with the majority upregulated (64 to 86%). In contrast, far fewer immune/inflammation genes were significantly changed in the transition to AD (approximately 6% of immune-related probesets), with gene responses primarily restricted to the SFG and HC. Second, relatively few significant changes in immune/inflammation genes were detected in the EC either in aging or AD, although many genes in the EC showed similar trends in responses as in the other brain regions. Third, immune/inflammation genes undergo gender-specific patterns of response in aging and AD, with the most pronounced differences emerging in aging. Finally, there was widespread upregulation of genes reflecting activation of microglia and perivascular macrophages in the aging brain, coupled with a downregulation of select factors (TOLLIP, fractalkine) that when present curtail microglial/macrophage activation. Notably, essentially all pathways of the innate immune system were upregulated in aging, including numerous complement components, genes involved in toll-like receptor signaling and inflammasome signaling, as well as genes coding for immunoglobulin (Fc) receptors and human leukocyte antigens I and II.


Unexpectedly, the extent of innate immune gene upregulation in AD was modest relative to the robust response apparent in the aged brain, consistent with the emerging idea of a critical involvement of inflammation in the earliest stages, perhaps even in the preclinical stage, of AD. Ultimately, our data suggest that an important strategy to maintain cognitive health and resilience involves reducing chronic innate immune activation that should be initiated in late midlife.

Top 10 Killers in Your Kitchen | Medical News and Health Information

(Ivanhoe Newswire) -- Calories, fat, sugar, (fructose) and salt. They are four food landmines that add pounds and add to your risk of diabetes, heart disease and death. Add to this, the bisphenol (BPA)  in tins. 

An atlas of the Epstein-Barr virus transcriptome and epigenome reveals host-virus regulatory interactions.

Epstein-Barr virus (EBV), which is associated with multiple human tumors, persists as a minichromosome in the nucleus of B lymphocytes and induces malignancies through incompletely understood mechanisms. Here, we present a large-scale functional genomic analysis of EBV. Our experimentally generated nucleosome positioning maps and viral protein binding data were integrated with over 700 publicly available high-throughput sequencing data sets for human lymphoblastoid cell lines mapped to the EBV genome. We found that viral lytic genes are coexpressed with cellular cancer-associated pathways, suggesting that the lytic cycle may play an unexpected role in virus-mediated oncogenesis. Host regulators of viral oncogene expression and chromosome structure were identified and validated, revealing a role for the B cell-specific protein Pax5 in viral gene regulation and the cohesin complex in regulating higher order chromatin structure. Our findings provide a deeper understanding of latent viral persistence in oncogenesis and establish a valuable viral genomics resource for future exploration

GI tract bacteria may protect against autoimmune disease

Early life exposure to normal bacteria of the GI tract (gut microbes) protects against autoimmune disease in mice, according to research published on-line in the January 17 edition of Science. The study may also have uncovered reasons why females are at greater risk of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and lupus compared to males."

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Case study IDs Borrelia miyamotoi as cause of meningoencephalitis

The spirochete, Borrelia miyamotoi, may be an underrecognized cause of meningoencephalitis, according to a case study published in the Jan. 17 issue of the New England Journal of Medicine."

The new age of proteomics: An integrative vision of the cellular world

"The enormous complexity of biological processes requires the use of high­performance technologies —also known as '­omics'—, that are capable of carrying out complete integrated analyses of the thousands of molecules that cells are made up of, and of studying their role in illnesses. In the post-genomic age we find ourselves in, the comprehensive study of cellular proteins —prote-omics— acquires a new dimension, as proteins are the molecular executors of genes and, therefore, the most important pieces of the puzzle if we wish to understand more completely how cells work."