Do you remember learning to drive a car? You probably fumbled around for the controls, checked every mirror multiple times, made sure your foot was on the brake pedal, then ever-so-slowly rolled your car forward.
Fast forward to now and you’re probably driving places and thinking, “how did I even get here? I don’t remember the drive”. The task of driving, which used to take a lot of mental energy and concentration, has now become subconscious, automatic—habitual.
But how—and why—do you go from concentrating on a task to making it automatic?
Brains are like puzzles, requiring many nested and co-dependent pieces to function well. The brain is divided into areas, each containing many millions of neurons connected across thousands of synapses. These synapses, which enable communication between neurons, depend on even smaller structures: message-sending boutons (swollen bulbs at the branch-like tips of neurons), message-receiving dendrites (complementary branch-like structures for receiving bouton messages), and power-generating mitochondria. To create a cohesive brain, all these pieces must be accounted for.
However, in the aging brain, these pieces can get lost or altered, and no longer fit in the greater brain puzzle. A research team has now published a study in Frontiers in Aging Neuroscience on this topic.
“Fifty percent of people experience loss of working memory with old age, meaning their ability to hold and manipulate information in the short-term decreases,” says co-first author Courtney Glavis-Bloom, a senior staff scientist in Salk Institute Professor John Reynolds’s lab. “We set out to understand why some individuals maintain healthy working memory as they age, while others do not. In the process, we discovered a novel mechanism for the synaptic basis of cognitive impairment.”
Functional movement/conversion disorder (FMD), part of the spectrum of Functional Neurological Disorder (FND), is a neuropsychiatric condition marked by a range of neurological symptoms, including tremors, muscular spasms and cognitive difficulties. Despite being the second-most common cause of referrals to neurology outpatient clinics after headache, scientists have struggled to pin down the disorder’s root cause. Female sex and a history of childhood trauma are factors associated with higher risk of developing FMD, but it’s been unclear why.
A new study from investigators of the Brigham and Women’s Hospital, in collaboration with researchers at the National Institute of Neurological Disorders and Stroke, demonstrated that FMD is characterized by epigenetic changes, and that women and childhood abuse survivors with FMD have different epigenetic profiles linked to this condition. Their study, which examined the genomes of over 100 individuals and was recently published in Progress in Neuro-Psychopharmacology and Biological Psychiatry, is the first to demonstrate the occurrence of epigenetic changes in FMD.
“This study finally takes FMD out of a cloud of confusion and provides a neuroscientifically grounded explanation for why childhood trauma and female sex are associated with this disorder,” said lead author Primavera A. Spagnolo, MD, Ph.D., scientific director of the Mary Horrigan Connors Center for Women’s Health and Gender Biology and assistant professor of psychiatry at HMS.
Over a hundred years after the discovery of the neuron by neuroanatomist Santiago Ramón y Cajal, scientists continue to deepen their knowledge of the brain and its development.
In a publication in Science Advances on April 5, a team from the Institut Pasteur and the CNRS, in collaboration with Harvard University, revealed novel insights into how cells in the outer layers of the brain interact immediately after birth during formation of the cerebellum, the brain region towards the back of the skull.
The scientists demonstrated a novel type of connection between neural precursor cells via nanotubes, even before the formation of synapses, the conventional junctions between neurons.
You learn from your mistakes. At least, most of us have been told so. But science shows that we often fail to learn from past errors. Instead, we are likely to keep repeating the same mistakes.
What do I mean by mistakes here? I think we would all agree that we quickly learn that if we put our hand on a hot stove, for instance, we get burned, and so are unlikely to repeat this mistake again. That’s because our brains create a threat-response to the physically painful stimuli based on past experiences. But when it comes to thinking, behavioral patterns and decision making, we often repeat mistakes—such as being late for appointments, leaving tasks until the last moment or judging people based on first impressions.
The reason can be found in the way our brain processes information and creates templates that we refer to again and again. These templates are essentially shortcuts, which help us make decisions in the real world. But these shortcuts, known as heuristics, can also make us repeat our errors.
In a large study led by the MHH neurology department, researchers investigated the cognition of patients with the rare disease NMOSD. It was found that about 20 percent of those affected have limited cognitive abilities.
People with the rare neuromyelitis optica spectrum disease (NMOSD) have severe physical and psychological impairments. But do they also suffer from limitations in their cognitive abilities? Neurologists investigated this in the CogniNMO study. A total of 17 treatment centers specialized in the disease in Germany took part. Professor Dr. Corinna Trebst and Dr. Martin Hümmert from the Department of Neurology at the Hannover Medical School (MHH) led the study. The results were published in the Multiple Sclerosis Journal.
There are a few thousand people with NMOSD in Germany. This is a rare autoimmune disease that causes relapsing inflammations of the central nervous system. Those affected suffer from limitations such as impaired vision, paralysis, incontinence and pain. “Whether their cognitive abilities are also reduced has not been clear until now. Studies had delivered different and partly contradictory results on this,” Professor Trebst says.
The function of the human brain is exceptional, driving all aspects of our thoughts and creativity. Yet the part of the human brain—the neocortex—responsible for such cognitive functions has a similar overall structure to other mammals.
Through close collaboration between The University of Queensland (UQ), The Mater Hospital and the Royal Brisbane and Women’s Hospital, researchers have discovered the human brain’s enhanced processing power may stem from differences in the structure and function of our neurons.
The results of this study have been published in Cell Reports as “High-fidelity dendritic sodium spike generation in human layer 2/3 neocortical pyramidal neurons.”
Biodegradable devices that generate energy from the same effect behind most static electricity could help power transient electronic implants that dissolve in the body, researchers say.
However, when standard electronic implants run out of power, they need to be removed lest they eventually become sites of infection. But their surgical removal can result in potentially dangerous complications. Scientists are developing transient implantable electronics that dissolve once they are no longer needed, but these mostly rely on external sources of power, limiting their applications.
A study published in the journal Stem Cell Reports on March 23, led by Dr. Ryosuke Tsuchimochi and Professor Jun Takahashi, examined the effects of combining cell transplantation and gene therapy for axonal outgrowth in the central nervous system. The authors demonstrated the potential of this combinatorial therapy for promoting axonal regeneration in patients with central nervous system injuries.
Stroke and traumatic brain/spinal cord injuries often damage the corticospinal tract (CST), composed of descending axonal tracts from the motor cortex down the spinal cord, that innervates motor neurons to activate skeletal muscles for controlling voluntary movements. Pharmacological and surgical interventions, in conjunction with rehabilitation, can maintain some lost motor functions, but patients with such acute neural injuries often suffer from lifelong severe motor impairment.
Cell replacement therapy—the implantation of new neurons into damaged brain regions —is viewed as a last hope that could help patients recover sufficient motor functions to live a normal life. The research team previously demonstrated that brain tissues transplanted into injured mouse brains could find their way to the CST and spinal cord but believed that further optimization of the host environment was necessary to promote CST reconstruction and functional recovery.
Help us welcome Anders Sandberg to the Foresight family! As a Senior Research Fellow in Philosophy, we are proud that he will be joining a fantastic group of Foresight Senior Research Fellows: https://foresight.org/about-us/senior-research-fellows/
Anders will present a cherry-picked selection of his epic Grand Futures book project: What is available in the “nearer-term” for life if our immature civilization can make it past the tech/insight/coordination hurdles? We’ll focus on post-scarcity civilizations to get a sense of what is possible just past current human horizons in the hope it may inspire us to double down on solving humanity’s current challenges to unlock this next level.
Based on our Zoom polls, cognitive enhancement features as high interest for many of you and is also one of Anders’ main research interests. Let’s add a brief tour through different cognitive enhancement scenarios, their ethical considerations, and how to make progress in the right directions. Join us with your questions and comments and let’s give Anders a warm welcome into the Foresight community!
About Anders: Anders Sandberg is a Foresight Senior Fellow and a Research Associate at the Future of Humanity Institute from the University of Oxford. Anders Sandberg’s research at FHI centers on management of low-probability high-impact risks, estimating the capabilities of future technologies, and very long-range futures. Topics of particular interest include global catastrophic risk, cognitive biases, cognitive enhancement, collective intelligence, neuroethics, and public policy.
Anders is a Senior Research Fellow on the ERC UnPrEDICT Programme. He is a research associate to the Oxford Uehiro Centre for Practical Ethics, and the Oxford Centre for Neuroethics. He is on the advisory boards of a number of organizations and often debates science and ethics in international media.
