Many have argued that free will is in illusion, but science does not support that. We should be grateful that free will exists.

Circa 2007 face_with_colon_three
The World Wide Brain—a hybrid human–digital intelligent network, spanning the globe and carrying out information processing different in extent and nature from anything that has come before—is as yet little more than a dream and a little less than a reality. It is coming into being, bit by bit, each year. This process of emergence is, as all Net-aholics know, a wonder to behold, and growing more wondrous all the time. This is an exploration in which human psychology and sociology interact in a fascinating way, with the psychology of an emerging, nonhuman organism. It is an exploration in which mundane technical issues such as groupware and server–server communication software rub up against concepts from transpersonal psychology, such as the Collective Unconscious and the Hierarchy of Being. It is, therefore, an exploration that not only transcends disciplinary boundaries but pushes the boundaries of human thought itself. The increasing integration of human activity with World Wide Brain operations may ultimately occur via body-modifying or body-obsolescing technologies a la Moravec, or it may occur without them, through the advent of more sophisticated noninvasive interfaces. One way or another, it will fuse the global Web.
At first glance, the human body looks symmetrical: two arms, two legs, two eyes, two ears, even the nose and mouth appear to be mirrored on an imaginary axis dividing the faces of most people. And finally, the brain: it is divided into two halves that are roughly the same size, and the furrows and bulges also follow a similar pattern.
But the first impression is deceptive: the different brain regions have subtle yet functionally relevant differences between the left and right sides. The two hemispheres are specialized for different functions. Spatial attention, for example, is predominantly processed in the right hemisphere in most people, while language is largely processed in the left. This way, work can be distributed more effectively to both halves and thus the range of tasks is expanded overall.
But this so-called lateralization, the tendency for brain regions to process certain functions more in the left or right hemisphere, varies from person to person. And not only in the minority whose brains are specialized mirror-inverted compared to the majority. Even people with classically arranged brains differ in how pronounced their asymmetry is.
Daniel Dennett explores the first steps towards a unified theory of information, through common threads in the convergence of evolution, learning, and engineering.
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The concept of information is fundamental to all areas of science, and ubiquitous in daily life in the Internet Age. However, it is still not well understood despite being recognised for more than 40 years. In this talk, Daniel Dennett explores steps towards a unified theory of information, through common threads in evolution, learning, and engineering.
This event was the first in a series on the theme of ‘Convergence’, exploring the links between neuroscience, philosophy and artificial intelligence. If you’re in London, look out for more events later in the year: http://rigb.org/whats-on.
We are grateful for the help of the Real Time Club in organising this event.
Daniel Dennett is known as one the most important philosophers of our time, with controversial and thought-provoking arguments about human consciousness, free will, and human evolution.
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A team of scientists is using the tools offered by the HBP’s digital research infrastructure EBRAINS to address one of the oldest enigmas in neuroscience: the dichotomy of brain structure and function.
Every human brain is different. But even with structural differences, individual brains function in a similar way. In other words, there are functional brains based on completely different configurations. At the same time, a structural change may cause loss of function in one brain, but have no consequences in another individual. Or a drug cocktail may be efficient for one patient, and have no effects for another.
The study population comprised 6,245,282 older adults (age ≥65 years) who had medical encounters with healthcare organizations between 2/2/2020–5/30/2021 and had no prior diagnosis of Alzheimer’s disease. The population was divided into two cohorts: 1) COVID-19 cohort (n = 410,748)— contracted COVID-19 between 2/2/2020–5/30/2021; 2) non-COVID-19 cohort (n = 5,834,534)— had no documented COVID-19 but had medical encounters with healthcare organizations between 2/2/2020–5/30/2021. The status of Alzheimer’s disease and COVID-19 were based on the International Classification of Diseases (ICD-10) diagnosis codes and laboratory tests (details in the Supplementary Material).
We examined risks for new diagnosis of Alzheimer’s disease in COVID-19 and non-COVID-19 cohorts in all older adults, three age groups (65–74, 75–84, ≥85), and three racial/ethnic groups (Black, White, and Hispanic). Cohorts were propensity-score matched (1:1 using a nearest neighbor greedy matching) for demographics, adverse socioeconomical determinants of health including problems with education, occupational exposure, physical, social and psychosocial environment, and known risk factors for Alzheimer’s disease [13] (details in the Supplementary Material). Kaplan-Meier analysis was used to estimate the probability of new diagnosis of Alzheimer’s disease within 360 days after the COVID-19 diagnosis. Cox’s proportional hazards model was used to compare matched cohorts using hazard ratios and 95% confidence intervals. All statistical tests were conducted within the TriNetX Advanced Analytics Platform at significance set at p < 0.05 (2-sided).
(Medical Xpress)—A team of researchers at the Max Planck Institute has found what they believe is the DNA mutation that led to a change in function of a gene in humans that sparked the growth of a larger neocortex. In their paper published in the journal Science Advances, the team describes how they engineered a gene found only in humans, Denisovans and Neanderthals to look like a precursor to reveal its neuroproliferative effect.
A year ago, another team of researchers found the human gene that most in the field believe was a major factor in allowing the human brain to grow bigger, allowing for more complex processing. In this new effort, the researchers have found what they believe was the DNA change that arose in that gene.
To pinpoint that change, the researchers engineered the unique ARHGAP11B gene to make it more similar to the ARHGAP11A gene, which researchers believe was a predecessor gene—they swapped a single nucleotide (out of 55 possibilities) for another and in so doing, found the ARHGAP11B gene lost its neuroproliferative abilities. This, the team claims, shows that it was a single mutation that allowed humans to grow bigger brains. Such a mutation, they note, was not likely due to natural selection, but was more likely a simple mistake that occurred as a brain cell was splitting. Because it conferred an advantage (the ability to grow higher than normal amounts of brain cells) the mutation was retained through subsequent generations. They also point out that such a mutation would have resulted specifically in a larger neocortex—a portion of the cortex that has been associated with hearing and sight.