Italy’s supreme court has upheld a ruling that said there was a link between a business executive’s brain tumor and his heavy mobile phone usage, potentially opening the door to further legal claims.
The court’s decision flies in the face of much scientific opinion, which generally says there is not enough evidence to declare a link between mobile phone use and diseases such as cancer and some experts said the Italian ruling should not be used to draw wider conclusions about the subject.
“Great caution is needed before we jump to conclusions about mobile phones and brain tumors,” said Malcolm Sperrin, director of medical physics and clinical engineering at Britain’s Royal Berkshire Hospital.
Swedish researchers at Uppsala University have, together with Brazilian collaborators, discovered a new group of nerve cells that regulate processes of learning and memory. These cells act as gatekeepers and carry a receptor for nicotine, which can explain our ability to remember and sort information.
The discovery of the gatekeeper cells, which are part of a memory network together with several other nerve cells in the hippocampus, reveal new fundamental knowledge about learning and memory. The study is published today in Nature Neuroscience.
The hippocampus is an area of the brain that is important for consolidation of information into memories and helps us to learn new things. The newly discovered gatekeeper nerve cells, also called OLM-alpha2 cells, provide an explanation to how the flow of information is controlled in the hippocampus.
“It is known that nicotine improves cognitive processes including learning and memory, but this is the first time that an identified nerve cell population is linked to the effects of nicotine”, says Professor Klas Kullander at Scilifelab and Uppsala University.
Preliminary results from an ongoing, large-scale study by Yale School of Medicine researchers shows that oxytocin - a naturally occurring substance produced in the brain and throughout the body- increased brain function in regions that are known to process social information in children and adolescents with autism spectrum disorders (ASD).
A Yale Child Study Center research team that includes postdoctoral fellow Ilanit Gordon and Kevin Pelphrey, the Harris Associate Professor of Child Psychiatry and Psychology, will present the results on Saturday, May 19 at 3 p.m. at the International Meeting for Autism Research.
“Our findings provide the first, critical steps toward devising more effective treatments for the core social deficits in autism, which may involve a combination of clinical interventions with an administration of oxytocin,” said Gordon. “Such a treatment approach will fundamentally improve our understanding of autism and its treatment.”
Social-communicative dysfunctions are a core characteristic of autism, a neurodevelopmental disorder that can have an enormous emotional and financial burden on the affected individual, their families, and society.
An editorial authored by University of Cincinnati (UC) diabetes researchers to be published in the Feb. 7, 2012, issue of the journal Cell Metabolism sheds light on the biological factors contributing to rising rates of obesity and discusses strategies to reduce body weight.
According to the U.S. Centers for Disease Control, about one-third of U.S. adults are obese, a number that continues to climb.
“While we don’t usually think of it this way, body weight is regulated. How much we weigh is influenced by a number of biological systems, and this is part of what makes it so hard for people to lose weight and keep it off,” says Randy Seeley, PhD, Donald C. Harrison Endowed Chair, director of the Cincinnati Diabetes and Obesity Center and author on the paper along with Karen Ryan, PhD, an assistant professor in endocrinology, diabetes and metabolism at UC.
Scientists are one step closer to repairing the damage caused by brain metastasis, a major challenge in cancer treatment, according to data published in Cancer Research, a journal of the American Association for Cancer Research.
“We are making progress from the neck down in cancer treatment, but brain metastases are increasing and are often a primary reason patients with breast cancer do not survive,” said Patricia S. Steeg, Ph.D., head of the Women’s Cancers Section at the National Cancer Institute’s Center for Cancer Research.
Steeg, who is also a deputy editor of Clinical Cancer Research, another journal of the AACR, said very few drugs that are effective for the treatment of breast cancer break what scientists call the “blood–brain barrier” and treat disease established inside the brain.
Scientists are striving to understand the mechanisms and effects of brain cancer metastasis.
Scientists and educators alike have long known that cramming is not an effective way to remember things. With their latest findings, researchers at the RIKEN Brain Science Institute in Japan, studying eye movement response in trained mice, have elucidated the neurological mechanism explaining why this is so. Published in the Journal of Neuroscience, their results suggest that protein synthesis in the cerebellum plays a key role in memory consolidation, shedding light on the fundamental neurological processes governing how we remember.
The “spacing effect”, first discovered over a century ago, describes the observation that humans and animals are able to remember things more effectively if learning is distributed over a long period of time rather than performed all at once. The effect is believed to be closely connected to the process of memory consolidation, whereby short-term memories are stabilized into long-term ones, yet the underlying neural mechanism involved has long remained unclear.
To clarify this mechanism, the researchers developed a technique based around the phenomenon of horizontal optokinetic response (HOKR), a compensatory eye movement which can be used to quantify the effects of motor learning. Studying HOKR in mice, they found that the long-term effects of learning are strongly dependent on whether training is performed all at once (“massed training”), or in spaced intervals (“spaced training”): whereas gains incurred in massed training disappeared within 24 hours, those gained in spaced training were sustained longer.
A new treatment that treats a subset of stroke patients by combining minimally invasive surgery, an imaging technique likened to “GPS for the brain,” and the clot-busting drug t-PA appears to be safe and effective, according to a multicenter clinical trial led by Johns Hopkins researchers.
The novel treatment, detailed for the first time at this week’s European Stroke Conference in Hamburg, Germany, was developed for patients with intracerebral hemorrhage (ICH), a bleed in the brain that causes a clot to form within brain tissue. This clot builds up pressure and leaches inflammatory chemicals that can cause irreversible brain damage, often leading to death or extreme disability. The usual treatments for ICH - either general supportive care such as blood pressure control and ventilation, which is considered the current standard of care, or invasive surgeries that involve taking off portions of the skull to remove the clot - have similar mortality rates, ranging from 30 to 80 percent depending on the size of the clot.
Seeking to improve these mortality rates and surviving ICH patients’ quality of life, Daniel Hanley, M.D., professor of neurology at the Johns Hopkins University School of Medicine, and his colleagues developed and tested the new treatment on 60 patients at 12 hospitals in the United States, Canada, the United Kingdom and Germany. They compared their results to those of 11 patients who received only supportive care.
Lapses in memory occur more frequently with age, yet the reasons for this increasing forgetfulness have not always been clear. According to new research from Concordia University, older individuals have reduced learning and memory because their minds tend to be cluttered with irrelevant information when performing tasks. Published in The Quarterly Journal of Experimental Psychology, these findings offer new insights into why ageing is associated with a decline in memory and may lead to practical solutions.
“The first step of our study was to test the working memory of a younger and older population and compare the results,” says Mervin Blair, first author and a PhD student in Concordia’s Department of Psychology and a member at the Centre for Research in Human Development. “In our study, working memory refers to the ability of both retaining and processing information.”
Some 60 participants took part in the study: half were an average of 23 years old, while the other half was about 67 years old. Each participant was asked to perform a working memory task, which included recalling and processing different pieces of information.
The population of aged persons worldwide is expanding rapidly, and it is becoming increasingly clear that there are many different diseases that affect the minds of these individuals. Researchers at the University of Kentucky are breaking new ground in the ongoing project of identifying and defining those diseases most likely to affect an aged population. Dr. Peter Nelson of the University of Kentucky Sanders-Brown Center on Aging is the lead author on a paper soon to be published in the journal BRAIN; the paper deals with the little-understood but serious condition hippocampal sclerosis (HS-AGING). He is also the recipient of a newly approved grant from the National Institutes of Health (NIH) to conduct a study of HS-AGING genetics.
Many different diseases may produce symptoms of dementia - defined as cognitive decline and impaired memory - in aged persons. Although Alzheimer’s disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in older adults. In those who live to a very advanced age (beyond the age of 95) HS-AGING is roughly as prevalent as Alzheimer’s.
It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline.
Research is trying to determine whether Alzheimer’s disease might be slowed or prevented with nutritional approaches, but a new study suggests those efforts could be improved by use of nutrient “biomarkers” to objectively assess the nutrient status of elderly people at risk for dementia.
The traditional approach, which primarily relies on self-reported dietary surveys, asks people to remember what they have eaten. Such surveys don’t consider two common problems in elderly populations – the effect that memory impairment has on recall of their diet, or digestive issues that could affect the absorption of nutrients.
This issue is of particular concern, experts say, because age is the primary risk factor for Alzheimer’s disease, and the upcoming wave of baby boomers and people 85 years and older will soon place many more people at risk for dementia.
For patients with low-grade gliomas, or slow growing brain tumors, a shot in the arm might soon lead to a new treatment therapy. A groundbreaking, first in humans vaccine will be tested in an early phase clinical trial that will soon begin at Wake Forest University Baptist Medical Center. Eighteen patients will be the first in the world to receive it.
“This study is looking at a very new form of treatment called a preventative brain tumor vaccine. The idea is to treat the low-grade glioma and to prevent it from growing back,” said Edward Shaw, M.D., a radiation oncologist. “In this early phase study, we are looking to see whether the patient develops an immune response against this kind of brain tumor, a necessary step for the vaccine to work.”
The trial is a bi-institutional pilot study, funded by the National Cancer Institute, and shared with the University of Pittsburgh (UP). Wake Forest Baptist and UP will enroll nine patients each. The vaccine will be administered to adult patients who have been diagnosed and had surgery for the removal of a low-grade brain tumor. They will receive the vaccine every three weeks for six months. A simple blood test will determine whether an immune response has developed.
Scientists at the Gladstone Institute of Neurological Disease (GIND) in San Francisco have discovered a new strategy to prevent memory deficits in a mouse model of Alzheimer’s disease (AD). Humans with AD and mice genetically engineered to simulate the disease have abnormally low levels of an enzyme called EphB2 in memory centers of the brain. Improving EphB2 levels in such mice by gene therapy completely fixed their memory problems. The findings will be published in the November 28 issue of the journal Nature.
In both humans and mice, learning and memory requires effective communication between brain cells called neurons. This communication involves the release of chemicals from neurons that stimulate cell surface receptors on other neurons. This important process, called neurotransmission, is impaired by amyloid proteins, which build up to abnormally high levels in brains of AD patients and are widely thought to cause the disease. But how exactly these poisonous proteins disrupt neurotransmission is unknown.
“EphB2 is a really cool molecule that acts as both a receptor and an enzyme,” said Moustapha Cisse, PhD, lead author of the study. “We thought it might be involved in memory problems of AD because it is a master regulator of neurotransmission and its brain levels are decreased in the disease.”
Research has suggested that families affected by melanoma skin cancer may also have a higher-than-average rate of Parkinson’s disease—but a large new study found no evidence of such a link.
This doesn’t mean no genetic link exists, the authors of the new study say. But it does suggest that such a link might not have very important effects.
Melanoma is the least common, but most serious, form of skin cancer. The disease sometimes runs in families, and people with two or more close relatives who have had melanoma are considered to be at higher-than-average risk.
Stroke is the leading cause of adult disability, due to the brain’s limited capacity for recovery. Physical rehabilitation is the only current treatment following a stroke, and there are no medications available to help promote neurological recovery.
Now, a new UCLA study published in the Nov. 11 issue of the journal Nature offers insights into a major limitation in the brain’s ability to recover function after a stroke and identifies a promising medical therapy to help overcome this limitation.
Researchers interested in how the brain repairs itself already know that when the brain suffers a stroke, it becomes excitable, firing off an excessive amount of brain cells, which die off. The UCLA researchers found that a rise in a chemical system known as “tonic inhibition” immediately after a stroke causes a reduction in this level of excitability.
While the blood-brain barrier (BBB) protects the brain from harmful chemicals occurring naturally in the blood, it also obstructs the transport of drugs to the brain. In an article in Nature scientists at the Swedish medical university Karolinska Institutet now present a potential solution to the problem. The key to the BBB is a cell-type in the blood vessel walls called pericytes, and the researchers hope that their findings will one day contribute to new therapies for diseases like Alzheimer’s and stroke.
“Our new results show that the blood-brain barrier is regulated by pericytes, and can be opened in a way that allows the passage of molecules of different sizes while keeping the brain’s basic functions operating properly,” says Christer Betsholtz, professor of vascular biology at the Department of Medical Biochemistry, who has led the study.
The blood-brain barrier is a term denoting the separation of blood from tissue by blood vessels that are extremely tight? Impermeable?. In other organs, the capillary walls let certain substances carried by the blood, such as the plasma proteins albumin and immunoglobulin, out into the surrounding tissue. In the brain, however, this pathway is closed off. This is essential for many reasons, one being that the plasma proteins are harmful to nerve cells.