We have a great opportunity in front of us. The Review of Federal Support for Fundamental Science (Naylor report), gives a very clear assessment of the funding situation in this country and presents thoughtful recommendations. It is now time to Support the Report, and implement its recommendations. Visit SupportTheReport.ca to see how you can get involved.
One example of the latter recently came from the joint laboratory of Freda Miller and David Kaplan, at the Hospital for Sick Children in Toronto. They found that a type of cell known for transmitting information between nerve cells also plays another vital role. It instructs stem cells that build the brain to make another type of cell called an oligodendrocyte. This cell is crucial for making sure communication and information transmission in the brain happen at the right time in the right place. The results were published in the journal, Neuron, http://www.cell.com/neuron/fulltext/S0896-6273(17)30344-6.
There is no denying autism spectrum disorders, commonly known as ASD, have become some of the world’s greatest health concerns. But what most people do not know is the incredible complexity of these conditions. As researchers have found, the problems are not singular in nature. Rather, they are a consequence of several changes in the way the cells of the brain function. This reality has forced ASD researchers to head deep into the molecular level of the brain in the hope of understanding what is happening in those affected.
No one can argue against exercise being good for you. Decades of research have revealed how getting our bodies in motion can offer a wealth of health benefits. Our muscles, metabolism, and immunity all improve as well as our brains. Our ability to learn and remember gets better and we may be able to ward off diseases such as Alzheimer’s disease and multiple sclerosis .
Scientists at The Hospital for Sick Children (SickKids) have used the gene-editing tool CRISPR to correct a disease-causing mutation in mice with a form of congenital muscular dystrophy, MDC1A. The findings, published in the July 17 online edition of Nature Medicine, show significant improvement in muscle strength and function among the mice treated with CRISPR, with no remaining signs of paralysis.
MDC1A is a rare neuromuscular disease affecting one in 150,000 worldwide. It is caused by a mutation in a gene called laminin alpha 2 and is characterized at birth by muscle weakness and low muscle tone, as well as brain abnormalities. Babies born with this condition eventually lose all muscle function and live an average of 30 years.
Researchers train brains to use different regions for same task
Practice might not always make perfect, but it’s essential for learning a sport or a musical instrument. It’s also the basis of brain training, an approach that holds potential as a non-invasive therapy to overcome disabilities caused by neurological disease or trauma.
Research at the Montreal Neurological Institute and Hospital of McGill University (The Neuro) has shown just how adaptive the brain can be, knowledge that could one day be applied to recovery from conditions such as stroke.
When trying to memorize information, it is better to relate it to something meaningful rather than repeat it again and again to make it stick, according to a recent Baycrest study published in NeuroImage.
“When we are learning new information, our brain has two different ways to remember the material for a short period of time, either by mentally rehearsing the sounds of the words or thinking about the meaning of the words,” says Dr. Jed Meltzer
Non-dependent users also experience dopamine release in response to drug cues
Even among non-dependent cocaine users, cues associated with consumption of the drug lead to dopamine release in an area of the brain thought to promote compulsive use, according to researchers at McGill University.
The findings, published in Scientific Reports, suggest that people who consider themselves recreational users could be further along the road to addiction than they might have realized.