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It is quickly becoming a hot topic among machine learning experts and those concerned with AI safety.

One of us (Anders) has a background in computational neuroscience, and now works with groups such as the AI Objectives Institute, where we discuss how to avoid such problems with AI; the other (Thomas) studies history, and the various ways people have thought about both the future and the fate of civilization throughout the past. After striking up a conversation on the topic of wireheading, we both realized just how rich and interesting the history behind this topic is.

It is an idea that is very of the moment, but its roots go surprisingly deep. We are currently working together to research just how deep the roots go: a story that we hope to tell fully in a forthcoming book. The topic connects everything from the riddle of personal motivation, to the pitfalls of increasingly addictive social media, to the conundrum of hedonism and whether a life of stupefied bliss may be preferable to one of meaningful hardship. It may well influence the future of civilization itself.

“You may hit the tipping point when you’re 50; it may happen when you’re 80; it may never happen,” Schindler said. “But once you pass the tipping point, you’re going to accumulate high levels of amyloid that are likely to cause dementia. If we know how much amyloid someone has right now, we can calculate how long ago they hit the tipping point and estimate how much longer it will be until they are likely to develop symptoms.”


Summary: A new algorithm uses neuroimaging data of amyloid levels in the brain and takes into account a person’s age to determine when a person with genetic Alzheimer’s risk factors, and with no signs of cognitive decline, will develop the disease.

Source; WUSTL

Researchers at Washington University School of Medicine in St. Louis have developed an approach to estimating when a person who is likely to develop Alzheimer’s disease, but has no cognitive symptoms, will start showing signs of Alzheimer’s dementia.

In this podcast, I have invited Daniel Jue, one of the youngest Entrepreneurs of the field of AGI. Daniel is an Independent Artificial General Intelligence researcher at Cognami in the US. He has worked supporting the US Department of Defense, including Data Fusion and analytic development for DARPA, the Defense Advanced Research Projects Agency, whose mission is to prevent technological surprise by potential adversaries. In addition he worked with scientists and engineers at IronNet CyberSecurity, a startup with DARPA and NSA heritage who have recently gone public. In March of 2,021 Daniel took on full time AGI research, drawing upon the fields of Computer Science, Neuroscience, Philosophy and Psychology. Some of his major influences have been Jacques Pitrat’s CAIA (An Artificial AI Scientist) project, Jean Piaget’s childhood development theories and Spiking Neural Networks. He sees a generalizable substrate at the basis for AGI, where engineers design the “physics” in which intelligent behavior could emerge.

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Summary: A newly identified gene therapy pathway has the potential to protect us against dementia and cancer, researchers report.

Source: University of Sheffield.

Researchers from the University of Sheffield have discovered a new gene therapy pathway that has uncovered an important regulatory mechanism to keep our genome healthy. This pathway has the potential to protect us against serious life-limiting diseases such as cancer and dementia.

Summary: Researchers identified specific receptors for acetylcholine that reroute information flow through memory circuits in the hippocampus. The findings could have implications for the development of drugs to help enhance or protect memory from diseases associated with cognitive decline.

Source: University of Bristol.

Bristol-led research has identified specific drug targets within the neural circuits that encode memories, paving the way for significant advances in the treatment of a broad spectrum of brain disorders.

Watch the full documentary on Vimeo on demand: https://vimeo.com/ondemand/339083

The study of consciousness needs to be lifted out of the mysticism that has dominated it. Consciousness is not just a matter of philosophy or spirituality. It’s a matter of hard science. It’s a matter of understanding the brain and the mind — a pattern structure made out of information. It’s also a matter of engineering. If we can understand the functionality of the brain, its neural code, then we can build the same functionality into our computer systems. There’s no consensus on what produces consciousness, but everyone regardless of metaphysical views can agree what it is like to be conscious. Given that consciousness is subjectivity, what consciousness is like is what consciousness is.

‘Mind’ and ‘Consciousness’ are two different but somewhat overlapping terms related to the phenomenality of our experiential reality. Different species have a variety of their biological information processors which unsurprisingly results in qualia diversity. All species live in their own unique sensory universes. There is “something it is like to be” an organism. The human brain, our biological “wetware,” has a fractal structure on many genetic and abstract cognitive levels. Information is “modus operandi” of consciousness.

If we are to reason for the non-dual picture of the world then quantum physics is directly linked to consciousness. The human brain is a physical organ that transmits and interprets electrochemical signals. Its biochemistry is certainly governed by quantum physical laws, and consciousness — which is clearly related to the functioning of the brain — must therefore be related to the quantum physical processes going on within the brain and in the cosmos at large. Research has shown that consciousness is non-local, a scientific way of alluding to a connection within a higher dimensional order. Matter has also been shown to be non-local, which hints that matter might be an expression of consciousness, emerging from the ‘Unified Field’ — the quantum layer of pure potentiality — the code layer beneath all dimensions where time and space are information.

A new Rutgers study will examine how COVID-19 is affecting individuals in a number of cognitive-related areas, including memory loss, “brain fog,” and dementia.

“Many people who recover from mild or moderate COVID-19 notice slowed thinking or memory loss, and this motivated us to leverage our experience in studying cognitive issues related to Alzheimer’s disease, multiple sclerosis, and HIV to examine this phenomenon,” said Dr. William T. Hu, associate professor and chief of cognitive neurology at Rutgers Robert Wood Johnson Medical School and the Institute for Health, Health Care Policy, and Aging Research.

A leading cognitive neurologist and neuroscientist, Dr. Hu is spearheading the characterization of cognitive impairment following mild-to-moderate COVID-19 at Rutgers.

“We then go on to show that dopamine is not a reward molecule at all. It instead helps encode information about all types of important and relevant events and drive adaptive behavior—regardless of whether it is positive or negative.”


Summary: A new study finds dopamine increases responses to stressful stimuli, not just pleasurable ones. The findings could have implications for the treatment of mental health disorders and addiction.

Source: Vanderbilt University

Pioneering research shows that dopamine levels increase in response to stressful stimuli, and not just pleasurable ones, potentially rewriting facts about the “feel-good” hormone—a critical mediator of many psychiatric diseases. This discovery is cause to rethink treatment for psychiatric disease and addiction.

That fossil wasn’t enough to confirm Africa as our homeland. Since that discovery, paleoanthropologists have amassed many thousands of fossils, and the evidence over and over again has pointed to Africa as our place of origin. Genetic studies reinforce that story. African apes are indeed our closest living relatives, with chimpanzees more closely related to us than to gorillas. In fact, many scientists now include great apes in the hominid family, using the narrower term “hominin” to refer to humans and our extinct cousins.

In a field with a reputation for bitter feuds and rivalries, the notion of humankind’s African origins unifies human evolution researchers. “I think everybody agrees and understands that Africa was very pivotal in the evolution of our species,” says Charles Musiba, a paleoanthropologist at the University of Colorado Denver.

Paleoanthropologists have sketched a rough timeline of how that evolution played out. Sometime between 9 million and 6 million years ago, the first hominins evolved. Walking upright on two legs distinguished our ancestors from other apes; our ancestors also had smaller canine teeth, perhaps a sign of less aggression and a change in social interactions. Between about 3.5 million and 3 million years ago, humankind’s forerunners ventured beyond wooded areas. Africa was growing drier, and grasslands spread across the continent. Hominins were also crafting stone tools by this time. The human genus, Homo, arrived between 2.5 million and 2 million years ago, maybe earlier, with larger brains than their predecessors. By at least 2 million years ago, Homo members started traveling from Africa to Eurasia. By about 300,000 years ago, Homo sapiens, our species, emerged.

Dementia has many faces, and because of the wide range of ways in which it can develop and affect patients, it can be very challenging to treat. Now, however, using supercomputer analysis of big data, researchers from Japan were able to predict that a single protein is a key factor in the damage caused by two very common forms of dementia.

In a study published this month in Communications Biology, researchers from Tokyo Medical and Dental University (TMDU) have revealed that the HMGB1 is a key player in both frontotemporal lobar and Alzheimer , two of the most common causes of dementia.

Frontotemporal lobar degeneration can be caused by mutation of a variety of genes, which means that no one treatment will be right for all patients. However, there are some similarities between frontotemporal lobar degeneration and Alzheimer disease, which led the researchers at Tokyo Medical and Dental University (TMDU) to explore whether these two conditions cause damage to the brain in the same way.