senior researcher at the Department of Medical Biochemistry and Biophysics. ut in recent years wee developed much more sensitive methods of analysis that allow us to see which genes are active in individual cells.
protect against infection and supply nerve cells with nutrients. With the help of this detailed map, the scientists were able to identify hitherto unknown cell types,
The new knowledge the project has generated can shed more light on diseases that affect the myelin
such as multiple sclerosis (MS). e could also confirm previous findings, such as that the pyramidal cells of the cerebral cortex are organised functionally in layers,
This gives science a new tool for studying these cell types in disease models and helps us to understand better how brain cell respond to disease and injury.
There are estimated to be 100 million cells in a mouse brain and 65 billion in a human brain.
The study was carried out by Sten Linnarsson and Jens Hjerling-Leffler research groups at the department of medical biochemistry and biophysics, in particular by Amit Zeisel and Ana Muños Manchado.
It also involved researchers from Karolinska Institutet Department of Oncology-Pathology, and Uppsala University. The study was financed with grants from several bodies,
including the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the EU Seventh Framework Programme, the Swedish Society of Medicine, the Swedish Brain Fund, Karolinska Institutet strategic programme for neuroscience (Stratneuro), the Human Frontier Science Program
, the Åke Wiberg Foundation and the Clas Groschinsky Memorial Fund s
#Molecular Inhibitor Breaks Cycle That Leads to Alzheimer's A molecular chaperone has been found to inhibit a key stage in the development of Alzheimer disease and break the toxic chain reaction that leads to the death of brain cells, a new study shows.
The research provides an effective basis for searching for candidate molecules that could be used to treat the condition.
A molecule that can block the progress of Alzheimer disease at a crucial stage in its development has been identified by researchers in a new study,
breaking the cycle of events that scientists believe leads to the disease. Specifically, the molecule, called Brichos, sticks to threads made up of malfunctioning proteins, called amyloid fibrils,
which are the hallmark of the disease. By doing so, it stops these threads from coming into contact with other proteins,
scientists have moved closer to identifying a substance that could eventually be used to treat the disease.
great deal of work in this field has gone into understanding which microscopic processes are important in the development of Alzheimer disease;
Alzheimer disease is one of a number of conditions caused by naturally occurring protein molecules folding into the wrong shape
however a second critical step in the disease development. After amyloid fibrils first form from misfolded proteins, they help other proteins
and are thought now to be responsible for the devastating effects of Alzheimer disease. This second stage, known as secondary nucleation, sets off a chain reaction which creates many more toxic oligomers
what happens during the progression of Alzheimer disease, but also what might happen if one stage in the process was switched somehow off. e had reached a stage where we knew what the data should look like
The research team then carried out further tests in which living mouse brain tissue was exposed to amyloid-beta, the specific protein that forms the amyloid fibrils in Alzheimer disease.
confirming that the molecule had suppressed the chain reaction from secondary nucleation that feeds the catastrophic production of oligomers leading to Alzheimer disease.
if these can be used as the starting point for developing a future therapy. e
#Tau Associated MAPT Gene Increases Risk for Alzheimer's disease A international team of scientists, led by researchers at the University of California,
San diego School of medicine, has identified the microtubule associated-protein protein tau (MAPT) gene as increasing the risk for developing Alzheimer disease (AD).
The MAPT gene encodes the tau protein, which is involved with a number of neurodegenerative disorders, including Parkinson disease (PD) and AD.
These findings provide novel insight into Alzheimer neurodegeneration, possibly opening the door for improved clinical diagnosis and treatment.
The findings are published in the February 18 online issue of Molecular Psychiatry. Alzheimer disease, which afflicts an estimated 5 million Americans,
is characterized typically by progressive decline in cognitive skills, such as memory and language and behavioral changes.
While some recent AD genome-wide association studies (GWAS), which search the entire human genome for small variations,
have suggested that MAPT is associated with increased risk for AD, other studies have found no association.
In comparison, a number of studies have found a strong association between MAPT and other neurodegenerative disorders,
such as PD. hough a tremendous amount of work has been conducted showing the involvement of the tau protein in Alzheimer disease,
the role of the tau-associated MAPT gene is said still unclear Rahul S. Desikan, MD,
Phd, research fellow and radiology resident at the UC San diego School of medicine and the study first author.
Microscopic image depicting plaques and tangles characteristic of Alzheimer disease. Image credit: Tom Deerinck, NCMIR, UC San diego. In the new Molecular Psychiatry paper, conducted with collaborators across the country and world,
Desikan and colleagues narrowed their search. Rather than looking at all possible loci (specific gene locations),
and more likely to experience increased brain atrophy than non-carriers. his study demonstrates that tau deposits in the brains of Alzheimer disease subjects are not just a consequence of the disease,
and progression of the disease, said Gerard Schellenberg, Phd, professor of pathology and laboratory medicine at the University of Pennsylvania,
principal investigator of the Alzheimer Disease Genetics Consortium and a study co-author. n important aspect was the collaborative nature of this work.
Thanks to our collaborators from the Consortium, the International Parkinson Disease Genetics Consortium, the Genetic and Environmental Risk in Alzheimer Disease, the Cohorts for Heart and Aging research in Genomic Epidemiology, decode Genetics and the Demgene cohort,
professor of biological psychiatry at the University of Oslo and a senior co-author. Sudha Seshadri, MD, professor of neurology at the Boston University School of medicine, the principal investigator of the Neurology Working group within the Cohorts for Heart and Aging research in Genomic Epidemiology consortium and a study co-author added:
lthough it has been known since Alois Alzheimer time that both plaques (with amyloid) and tangles (of tau) are key features of Alzheimer pathology,
attempts to prevent or slow down clinical disease progression have focused on the amyloid pathway. Until this year no one had shown convincingly that the MAPT (tau) gene altered the risk of AD and this,
combined with the greater ease of imaging amyloid in life, lead some researchers to postulate that tau changes were secondary to amyloid changes.
These findings underscore the importance of using a multi-modal and multi-disciplinary approach to evaluating Alzheimer neurodegeneration. hese findings suggest that the combination of genetic,
and quantifying the biochemical effects of therapeutic interventions, said Anders M. Dale, Phd, professor of neurosciences and radiology and director of the Center for Translational Imaging and Precision Medicine at UC San diego and the study senior author e
#What Autism Can Teach Us About Brain Cancer Both disorders involve faults in the same protein.
Applying lessons learned from autism to brain cancer, researchers at The Johns hopkins university have discovered why elevated levels of the protein NHE9 add to the lethality of the most common and aggressive form of brain cancer, glioblastoma.
Their discovery suggests that drugs designed to target NHE9 could help to successfully fight the deadly disease.
A summary of their work in human tumor cells and mice will be published on Feb 9 in the journal Nature Communications. y laboratory research on cargo transport inside the cells of patients with autism has led to a new strategy
for treating a deadly brain cancer says Rajini Rao, Ph d, . a professor of physiology at the Johns hopkins university School of medicine. his is a great example of the unexpected good that can come from going wherever the science takes us.
All animal and human cells contain many argo packagessurrounded by membranes. These so-called endosomes carry newly minted proteins to specific destinations throughout the cell
and haul away old proteins for destruction. Key to their hipping speedis the level of acidity inside the endosomes.
Rao research group previously showed that autism-associated defects in the protein NHE9 are harmful
Teaming up with Alfredo Quinones-Hinojosa, M d.,a professor of neurosurgery at Johns Hopkins, the researchers examined NHE9 in tumor cells from several patients.
Cells with low levels of NHE9 grew the slowest, the team found, and those with the highest levels grew fastest.
And this was confirmed when the tumor cells, which were manipulated to have high or low NHE9, were transplanted into the brains of mice.
Based on their autism research, the team suspected that the boost NHE9 gave to glioblastomas was explained by abnormal endosome acidity.
Further studies revealed that, in contrast to autism, NHE9 is overactive in brain cancer, causing endosomes to leak too many protons
and become too alkaline. This slows down the hipping rateof cancer-promoting cargo and leaves them on the cell surface for too long.
Research from other laboratories suggested that one such cargo protein is EGFR, which maintains cancer-promoting signals at the cell surface
and helps tumors become more robust so they grow and move faster. It is also found at elevated levels in more than one-half of patients with glioblastomas.
Drugs targeting EGFR in these patients are sometimes effective. As they suspected, the team found that alkaline endosomes slow down the removal of EGFR from cell surfaces.
Lab-grown tumor cells were killed more readily when treated with both a drug countering NHE proteins
so that hopefully we can make this disease less aggressive and less devastating. About this genetics research Other authors of the report include Kalyan Kondapalli, Jose Llongueras, Vivian Capilla-Gonzalez, Hari Prasad, Anniesha Hack, Christopher Smith and Hugo Guerrero
This work was supported by grants from the National Institute of Neurological disorders and Stroke (NS070024), the National Institute of Diabetes and Digestive and Kidney diseases (DK054214
the National Institute of General Medical sciences (GM62142), the American Heart Association (11post7380034), the Johns Hopkins Post-Baccalaureate Research Education Program, the International Fulbright Science and Technology Award,
and Extra Copies of Disease Gene in Alzheimer s Brain cells The surprise discovery offers a new understanding of Alzheimer s disease.
Scientists at The Scripps Research Institute (TSRI) have found diverse genomic changes in single neurons from the brains of Alzheimer s patients pointing to an unexpected factor that may underpin the most common form of the disease.
and Alzheimer s disease#said Jerold Chun professor at TSRI and its Dorris Neuroscience Center and senior author of the new study.
Alzheimer s disease is an irreversible brain disease that tends to strike older people. It is progressive#impairing memory destroying motor skills and eventually causing death.
The U s. Centers for Disease Control and Prevention estimates 5. 3 million Americans currently have Alzheimer s disease
Researchers have known long about disease-related protein accumulations (called amyloid plaques) in the brains of Alzheimer s patients.
They#ve also known that chromosome 21 plays a role in the disease due to Alzheimer s-like symptoms in people with Down syndrome (with three copies of chromosome 21.
Remarkably the researchers found that more than 90 percent of sporadic Alzheimer s disease brains displayed highly significant DNA increases of hundreds of millions more DNA base-pairs compared with control samples showing that genomic mosaicism was altered in the Alzheimer s brain.
The tests showed that neurons from patients with sporadic Alzheimer s disease were four times as likely to contain more than the normal two copies of APP with some Alzheimer s neurons containing up to 12 copies of APP a phenomenon never seen in the controls.#
so to be able to connect it with a disease is really interesting#said Gwen Kaeser a graduate student studying in Chun#s lab and co-first author of the study with former graduate student Diane Bushman.
because the genomic signatures of sporadic Alzheimer s disease occur within individual brain cells. Indeed a majority of major brain diseases are also sporadic.
For example amyotrophic lateral sclerosis (ALS) can be linked to a gene in one to two percent of cases
Chun believes genomic mosaicism could possibly have a role in other brain diseases. Future studies in the Chun lab will investigate the relationship between mosaicism
and disease the causes of mosaicism and potential new disease drug targets present in the millions of extra base-pairs found in single Alzheimer s disease neurons.
In addition to Chun Kaeser and Bushman other authors of the study#Genomic mosaicism with increased amyloid precursor protein (APP) gene copy number in single neurons from sporadic Alzheimer s disease brains#were Jurgen
Full open access research for#Genomic mosaicism with increased amyloid precursor protein (APP) gene copy number in single neurons from sporadic Alzheimer s disease brains#by Diane M Bushman
In this study we report altered genomic mosaicism in single sporadic Alzheimer s disease (AD) neurons characterized by increases in DNA content and amyloid precursor protein (APP) gene copy number.
or understand how cancer cells are organized in a metastasizing tumor, or how immune cells are configured in an autoimmune attack,
other possible applications for this technique include studying tumor metastasis and angiogenesis (growth of blood vessels to nourish a tumor),
or visualizing how immune cells attack specific organs during autoimmune disease i
#Gene Breakthrough Sparks Fear of Homemade Morphine Scientists on Monday said they had unlocked a pathway for producing opiates from genetically engineered yeast
but feared the discovery could one day be a bonanza for drug lords. Other experts agreed, saying anyone with basic skills could use such a yeast to churn out morphine,
and exude opiates and other therapeutic drugs. The goal is to provide cheaper and possibly less addictive painkillers from a dependable source as compared to the poppy.
as opposed to a medical device, and therefore hasn undergone any testing, except those required by the Underwriter Laboratory to ensure its electrical safety.
and deliver medicines to specific locations. Yes, creepy but also undeniably cool. At the ICRA 2015 conference in Seattle, researchers from MIT and TU Munich presented just such a creation in a presentation titled (cleverly) n Untethered Miniature Origami Robot That Self-folds, Walks, Swims,
it could give future amputees a natural transplant option that doesn require immunosuppressive therapies. The rat limb was grown by a team from the Massachusetts General Hospital in Boston.
They used a technique called ecellularization, which basically strips the cellular materials from a limb of a dead rat,
of the MGH Department of Surgery and the Center for Regenerative medicine and senior author of the research paper,
#Facial recognition System Detects Pain It a dilemma that plagued doctors for centuries: When it comes to pain management,
Doctors typically rely on self-reporting, in which patients are asked to rate their pain on a scale of zero to ten.
In a study published this week in the journal Pediatrics, the researchers suggest that the technology can indeed help with accurate pain level assessment.
Nurses might only check on a pediatric patient every few hours whereas a facial recognition system could provide constant monitoring.
The device taking this fantastic electronic voyage may soon be able to zap tumors, repair damaged spinal cords or even connect parts of the brain like an artificial synapse.
and mesh combination is so small and bendy that it doesn cause any damage to the surrounding brain tissue, something that often plagues surgical procedures done with a needle, knife or other type of probe.
Could A Brain Implant Cure Depression? f one is thinking of trying to change the way one does long term brain implants,
it could be a really big deal, said Charles Lieber, chemistry professor at Harvard university and lead author on the new paper published in the journal Nature Nanotechnology. ou can promote a positive interaction
After an injection several centimeters into the brain of a laboratory mouse the scientists were able to monitor electronic brain signals.
Brain-Zapping Implant Could Aid Injured Soldiers The authors of the paper say next step is to use the mesh system to deliver living stem cells that may help repair damaged sections of the brain or perhaps a multifunction electronic device
and manipulate these fields, in a relatively blunt fashion, with implants and wires. But it like working with oven mitts on.
New findings published in the journal Future Medicine suggest that we may have another way forward.
A medical research team at Florida International University in Miami injected 20 billion nanoparticles into the brains of mice
#Brain-Sensing Headband Helps Users Manage Stress Technology and relaxation don always go hand in hand. However, a brain-sensing headband that reads brain waves
and manage stress. The Muse headband is lined with seven EEG sensors that detect the brain electrical activity
Users are asked then to participate in a three-minute guided exercise that aims to reduce stress, calm anxiety and increase focus and concentration.
Hospitals have been on a crisis footing and dedicated heatstroke treatment centres have been set up around the city to treat the tens of thousands affected by heatstroke
Pakistan largest welfare charity and a leading provider of emergency medical care in Karachi, told AFP.
According to figures collected by AFP from hospitals around the city, a total of 1, 079 people have died as a result of the heatwave.
Karachi hospitals have treated nearly 80,000 people for the effects of heatstroke and dehydration, according to medical officials.
Doctor Qaiser Sajjad of the Pakistan Medical Association in Karachi said that a lack of understanding of heatstroke among the public how to spot symptoms
edible barcodes that can be planted right onto medicine to verify that the pills and tablets you might consume are the real deal.
According to Wuh, a medical doctor, this kind of wider recognition is an indication that these bite-size barcodes could play a role in a tech revolution sweeping through medicine. t (Trutag) is really a game-changer
think about public health it impacts all of those areas. We think of this technology as a tremendous way to sort of improve the system. he company ags,
according to statistics from the American Society of Consultant Pharmacists. ay mom is in the hospital
and the nurse comes in with a cup that has seven pills in it. They are out of the package in the cup and there all of these morning pills together,
who also has a Masters of Public health degree from Harvard university, a big component of this company is to empower consumers to understand what they are putting into their bodies,
Imagine someone being treated for diabetes. You want to make sure they have the right medication. n an interconnected world where smartphones
which is used to treat hepatitis. The law enforcement has to ship it by express mail to a lab that then has to process the drug and run a series of tests.
#'Dog Nose'Light Sniffs Out Disease Here a riddle: What kind of light can smell? Answer:
breath for disease. Gold nanoparticles Could Detect Disease: Discovery Newsprevious studies have shown that diseases such as lung and esophageal cancer,
asthma and diabetes can be all be detected in the breath. Using light to smell might be a little counterintuitive,
but stick with us for a moment. Anstie and his team shine the laser onto a sample of gas.
Since each molecule in the universe absorbs light at different optical frequencies, an odor has its own unique signature. ather than sniffing out a variety of smells as a dog would,
Disease Detection Goes Mobilee now have a robust system to be able to detect the presence and concentrations of molecules in a sample,
Dr. Bruce Conklin, a stem cell biologist at the Gladstone Institute of Cardiovascular disease in San francisco, along with colleagues developed these tiny hearts using stem cells derived from skin tissue.
#Lab on a chip turns smart phones into mobile disease clinics Smart phones can pay our bills,
Soon they may become a leading weapon in the global fight against disease. Researchers have designed a cheap,
easy-to-use smart phone attachment (shown above) that can test patients for multiple deadly infectious diseases in 15 minutes.
several detection zones snag any antibodies in the blood that reveal the presence of a particular disease.
The researchers conducted a field test of the device at three Rwandan community clinics, where health care workers rapidly screened 96 patients for HIV
and active and latent forms of syphilis. Compared with gold standard laboratory tests, the dongle was 96%as accurate in detecting infections,
missing just one case of latent syphilis, the team reports online today in Science Translational Medicine.
Despite a 14%false alarm rate, the researchers say the device high sensitivity and ease of use make it a powerful tool for diagnosing these deadly diseases in the field,
particularly among pregnant women. The researchers are now preparing a larger scale trial for the $34 device,
which they hope will let mobile clinics and health workers provide rapid and reliable disease screening in the remotest areas of the world r
#Microbe found in grassy field contains powerful antibiotic For much of the last decade, a team of researchers in Boston has exhumed eagerly
and reburied dirt. It part of a strategy to access an untapped source of new antibioticshe estimated 99%of microbes in the environment that refuse to grow in laboratories.
a previously unknown bacterium that makes a compound with infection-killing abilities. What more, the team claims in a report out today,
it would be needed a much weapon against several increasingly hard-to-treat infections. Many existing antibiotics, including penicillin,
the team let each of them duel in a lab dish with Staphylococcus aureus, a cause of serious skin and respiratory infections.
including many human pathogens. Moreover, these pathogens failed to develop resistance to the compound: There were no surviving individuals that had evolved to withstand its attack.
Resistance usually develops when a small percentage of microbes escape an antibiotic because of a mutation
In mice infected with MRSA, injections of teixobactin led to a 100%survival rate at lower doses than vancomycin.
increasingly feared in hospitals for their resistance to existing drugs. But the authors suggest it could be of great value to people fighting MRSA, tuberculosis,
and infections with rare-but-nasty Enterococcus bacterial strains that aren responding to available drugs.
These results offer hope that other promising agents await discovery in the soil, says Helen Zgurskaya, a biochemist at the University of Oklahoma, Norman,
#'Superspreading event'triggers MERS explosion in South korea SEOULUTHORITIES in South korea are scrambling to contain an outbreak of the deadly Middle Eastern respiratory syndrome (MERS.
Scientists are wondering how a single imported case could have led to so many secondary infections. The outbreak started
He was treated at several clinics before being diagnosed with MERS on 20 may. Several countries have seen such imported cases
but the disease has never spread to more than a few other people, and the general consensus has been that MERS does not spread easily from human to human
But the Korean patient appears to have infected at least 22 family members, health care workers, and fellow patients at a hospital where he was treated from 15 may to 17 may.
The hospital's name has not been revealed. No special precautions were taken during that time, because the patient had not yet been diagnosed.
The early phase of the disease, just after hospitalization and when symptoms are getting worse,
is the time when patients tend to secrete the most virus, says Christian Drosten, a virologist at the University of Bonn in Germany. e know from Saudi arabia that the virus can be transmitted during this time
Yet in similar situations, hundreds of exposed contacts did not develop the disease, says Peter Ben Embarek, the point person on MERS at the World health organization (WHO).
is a lapse in infection control measures at the hospital, Ben Embarek says. The SARS virus,
which is distantly related to MERS, is known to have spread widely in 2003 when tubes were placed in patients'airways for mechanical ventilation,
or Koreans may be more susceptible to the disease than other populations, Ben Embarek says. One important piece of evidence will be the genetic sequence of the virus. Ben Embarek says Korea has agreed to share samples with several labs working on MERS,
and placed him in isolation in Huizhou Municipal Central Hospital on 27 may. He tested positive for MERS on 29 may.
and 27"other contacts"are under medical surveillance. None of those quarantined or under surveillance in Hong kong and China have showed any signs of illness so far.
With reporting by Dennis Normile in Tokyo o
#New test could reveal every virus that's ever infected you Can remember every viral infection youe ever had?
Don worry, your blood can. A new test surveys the antibodies present in a person bloodstream to reveal a history of the viruses theye been infected with throughout their life.
but for developing vaccines and studying links between viruses and chronic disease. his is really a technical tour de force,
But others point out that it's unclear how many past infections the new technology misses. Now
researchers wondering whether a patient has a particular viral infectionrom herpes and flu to the AIDS virusest blood samples for one pathogen at a time.
Many tests look for antibodies, proteins the immune system produces to recognize invaders, while others hunt for the virus own genetic material.
or absence of longer-lasting antibodies that can linger for decades after an infection. Researchers led by biologist Stephen Elledge of Brigham
and Women's Hospital in Boston and Harvard Medical school wanted to develop a test that could look at every current or past infection in one fell swoop.
and old or those with a disease and those withoutnd see whether there a difference in their viral histories.
whether viral infections can trigger diabetes or chronic fatigue syndrome. Elledge and colleagues used Virscan on more than 500 people from the United states
most people had antibodies for about 10 previous viral infections, although those with HIV and who lived outside the United states averaged more.
Surprisingly, many people had generated the exact same antibodies to infections; researchers believed people's immune responses to be more diverse,
That observation could inform future vaccine development, he says. Whether the test really catches everything is up for debate,
which cause large numbers of intestinal infections. This could be because antibodies for these viruses don stick around for
or pathogens youe fought in your lifetime and what signatures of those infections remain, the results of this paper wouldn be a surprise."
"The technology's real value lies in the new questions scientists can answer, he says."
but Elledge hopes it won't cost much more than existing tests that only look at one pathogen at a time.
if you have any new infections, he says. This could help diagnose viruses like hepatitis C
which people often don know they have u
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