How can consciousness be addressed scientifically? The Tucson conference, founded in 1994 and celebrating its 20th anniversary in 2014, exemplifies the quest. What are the range of theories? Where do participants position themselves? Meet the founders, early visionaries, new scientists and thinkers. Progress is being made, but what does this really mean?
Fragile X syndrome is a genetic disorder caused by a mutation in a gene that lies at the tip of the X chromosome. It is linked to autism spectrum disorders.
People with fragile X experience a range of symptoms that include cognitive impairment, developmental and speech delays and hyperactivity. They may also have some physical features such as large ears and foreheads, flabby muscles and poor coordination.
Scientists have found a way to use nanotechnology to create a 3D “scaffold” to grow cells from the retina—paving the way for potential new ways of treating a common cause of blindness.
Researchers, led by Professor Barbara Pierscionek from Anglia Ruskin University (ARU), have been working on a way to successfully grow retinal pigment epithelial (RPE) cells that stay healthy and viable for up to 150 days. RPE cells sit just outside the neural part of the retina, and when damaged, can cause vision to deteriorate. Their work is published in Materials & Design.
It is the first time this technology, called “electrospinning,” has been used to create a scaffold on which the RPE cells could grow, and could revolutionize treatment for one of age-related macular degeneration, one of the world’s most common vision complaints.
For many people, depression turns out to be one of the most disabling illnesses that we have in society. Despite the treatments that we have available, many people are not responding that well. It’s a disorder that can be very disabling in society. It’s also a disorder that has medical consequences. By understand the neurobiology of depression we hope to be able more to find the right treatment for the patient suffering from this disease. The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially, presuming that one of three neurotransmitters in the brain is deficient or underactive. But the reality is, there are more than 100 neurotransmitters in the brain. And billions of connections between neurons. So we know that that’s a limited hypothesis. Neurotransmitters can be thought of as the chemical messengers within the brain, it’s what helps one cell in the brain communicate with another, to pass that message along from one brain region to another. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine. However, norepinephrine and serotonin did not seem to be able to account for this cause, or to cause the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. When you’re exposed to severe and chronic stress like people experience when they have depression, you lose some of the connections between the nerve cells. The communication in these circuits becomes inefficient and noisy, we think that the loss of these synaptic connections contributes to the biology of depression. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is, when you treat that depression effectively, the brain goes back to looking like a healthy brain, both at the cellular level and at a global scale. It’s critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses, and we can start to target treatments based on that. We are in a new era of psychiatry. This is a paradigm shift, away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ. All of the research is driven by the imperative to alleviate human suffering. Depression is one of the most substantial contributors to human suffering. The opportunity to make even a tiny dent in that is an incredible opportunity.
Can the fountain of youth come in the form a pill?
Imagine this: a cocktail of specialized chemicals that rejuvenates your whole body, from your eyes and brain to your kidneys and muscles—bringing you back to a more youthful version of yourself.
Adopting a curious mindset over a high-pressure one can enhance memory, according to recent research from Duke University. The study showed that participants who envisioned themselves as a thief planning a heist in a virtual art museum demonstrated better recall of the paintings they encountered than those who imagined executing the heist on the spot while playing the same computer game.
The slight variation in motivations — the urgent need to achieve immediate goals versus the curious exploration for future objectives — could have significant implications in real-life scenarios. These include incentivizing people to receive a vaccine, prompting action against climate change, and potentially providing new treatments for psychiatric conditions.
The findings were recently published in the Proceedings of the National Academy of Sciences.
Humans have a distinctive skeleton, and are the only bipedal great apes (the great ape species are bonobos, chimpanzees, gorillas, orangutans, and humans). While the evolution of the human skeleton enabled us to walk upright, it also led to the rise of musculoskeletal disease. It’s thought that cognitive development began to accelerate in humans once we started to move around, adapt to new environments, and make use of tools. Researchers have now used advanced computational tools and a trove of human genetic data in the UK Biobank to outline the genetic changes that occurred as primates started to walk upright for the first time.
These findings, which were reported in Science, have suggested that natural selection had a strong influence on the genetic changes that altered our anatomy, and gave early humans an evolutionary leg up.
An international team led by investigators at McLean Hospital has analyzed the genes expressed in approximately 575,000 individual cells from the brains of people with and without post-traumatic stress and major depressive disorders (PTSD and MDD), revealing new insights into the mechanisms behind the brain’s stress response in these conditions.
The findings, which are published in The American Journal of Psychiatry, could lead to novel markers of PTSD and MDD and well as new therapeutic targets.
Because studies have implicated the dorsolateral prefrontal cortex (DLPFC) region of the brain in PTSD and MDD, the scientists compared the genes expressed in cells in DLPFC samples collected postmortem from 11 individuals with PTSD, 10 with MDD, and 11 without either of these conditions with a replication dataset half the size. The researchers detected which genes were expressed by which cells—including eight different types of cells—through a technique called single-cell RNA sequencing.
Scientists at the University of Colorado Anschutz Medical Campus have discovered what they believe to be the central mechanism behind cognitive decline associated with normal aging.
“The mechanism involves the mis-regulation of a brain protein known as CaMKII which is crucial for memory and learning,” said the study’s co-senior author Ulli Bayer, PhD, professor of pharmacology at the University of Colorado School of Medicine. “This study directly suggests specific pharmacological treatment strategies.”
The study was published today in the journal ‘Science Signaling.’
