A Conversation between Robert Lawrence Kuhn and Àlex Gómez-Marín.
The conversation will explore “a landscape of consciousness”, toward a taxonomy of explanations and implications.
In 2024, Àlex will curate and host conversations to address The Future Mind, seeking to gain clarity and insight into important contemporary matters that require both urgent action as well as deep reflection.
Recorded January 31, 2024
As brain tumors grow, they must do one of two things: push against the brain or use finger-like extensions to invade and destroy surrounding tissue.
Previous research found that tumors that push—or put mechanical force on the brain—cause more neurological dysfunction than tumors that destroy tissue. But what else can these different tactics of tumor growth tell us?
Now, the same team of researchers from the University of Notre Dame, Harvard Medical School/Massachusetts General Hospital, and Boston University has developed a technique for measuring a brain tumor’s mechanical force and a new model to estimate how much brain tissue a patient has lost. Published in Clinical Cancer Research, the study explains how these measurements may help inform patient care and be adopted into surgeons’ daily workflow.
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer’s disease.
Alzheimer’s is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It’s not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen.
Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it’s only been regarded as an energy backup for the liver and the muscles.
Alzheimer’s disease (AD) is a common, debilitating neurodegenerative disease affecting about 10% of people over the age of 65 and one third of people aged 85 and above. Besides environmental factors, the genes have a strong influence on whether or not a person develops AD during their lifetime.
Through genome sequencing of DNA from large groups of healthy people and people with AD, some naturally occurring small changes in the DNA, known as genetic variants, were found to be more frequent in AD patients than in healthy people.
As more and more of these AD-associated genetic “risk” variants are discovered, it is now possible to calculate a person’s individual polygenic risk score (PRS), meaning the likelihood of the person developing AD, with high accuracy.
Christof’s idea that split brain patients have split consciousness doesn’t really make sense and doesn’t correspond to the evidence. Consciousness is metaphysically simple — that is, my thoughts and sense of self can’t be split with a knife like the brain or a material thing can be split. What would it mean to say that I have “split” consciousness? Instead of Mike, there would be Mike and Joe, which wouldn’t be “split,” it would just be two people.
A category error
‘Split consciousness’ is an oxymoron, a category error. Consciousness is not the kind of thing that can be split, and there’s no evidence that one person can ever become two people. It’s science fiction, not science.
Smarter people don’t just crunch numbers better—they actually see the future more clearly. Examining thousands of over-50s, Bath researchers found the brightest minds made life-expectancy forecasts more than twice as accurate as those with the lowest IQs. By tying cognitive tests and genetic markers to real-world predictions, the study shows how sharp probability skills translate into wiser decisions about everything from crossing the road to planning retirement—and hints that clearer risk information could help everyone close the gap.
Every year, tens of thousands of people with signs of Parkinson’s disease go unnoticed until the incurable neurodegenerative condition has already progressed.
Motor symptoms, such as tremors or rigidity, often emerge only after significant neurological damage has occurred. By the time patients are diagnosed, more than half of their dopamine-producing neurons may already be lost. This kind of diagnostic delay can limit treatment options and slow progress on early-stage interventions.
While there are existing tests to detect biomarkers of Parkinson’s, including cell loss in the brain and inflammatory markers in blood, they typically require access to specialists and costly equipment at major medical centers, which may be out of reach for many.
