Brilliant. News is about rare events, especially bad things. Massive amounts of raw data is boring — but tells a completely different story.
If you follow the news closely, chances are your view of the state of the world is not super optimistic. From war in Ukraine to a warming planet to global poverty and hunger, there’s plenty to get upset about. But what if things are actually getting…better?
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This video covers digital immortality, its required technologies, processes of uploading a mind, its potential impact on society, and more. Watch this next video about the world in 2200: https://bit.ly/3htaWEr.
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CHAPTERS
00:00 Required Technologies.
01:42 The Processes of Uploading a Mind.
03:32 Positive Impacts On Society.
05:34 When Will It Become Possible?
05:53 Is Digital Immortality Potentially Dangerous?
SOURCES:
• The Singularity Is Near: When Humans Transcend Biology (Ray Kurzweil): https://amzn.to/3ftOhXI
• The Future of Humanity (Michio Kaku): https://amzn.to/3Gz8ffA
• https://www.scientificamerican.com/article/what-is-the-memory-capacity/
• https://www.anl.gov/article/researchers-image-an-entire-mous…first-time.
• https://interestingengineering.com/cheating-death-and-becomi…-uploading.
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For as long as we’ve been around, human beings have fought against the inevitability of death. This struggle has given rise to religions that have dominated human culture for millennia and has been central to philosophies that have shaped our civilizations.
But might it be the case that a scientific solution to immortality is finally in sight? In recent years, artificial intelligence (AI) has evolved to the stage where it looks set to revolutionize every aspect of our lives. It may just be possible that it’s going to change the way that we think about – and perhaps even experience – death, too.
Science fiction has given us several examples of situations – mostly horrific — where human minds can be uploaded to machines, effectively allowing us to outlast our mortal, fallible bodies.
Scientists have successfully used nanotechnology to develop a 3D scaffold that supports the growth of healthy retinal cells, a breakthrough that could revolutionize the treatment of age-related macular degeneration (AMD), a leading cause of blindness worldwide. Utilizing electrospinning technology, researchers created a scaffold that, when treated with the steroid fluocinolone acetonide, enhances the resilience and growth of retinal pigment epithelial cells, potentially aiding in the development of ocular tissue for transplantation.
Scientists have discovered a way to use nanotechnology to create a 3D ‘scaffold’ to grow cells from the retina. This breakthrough could lead to innovative approaches for treating a common source 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.
Cognitive decline is a growing public health concern that affects millions of people around the world. Amid an aging population, strategies that help prevent or mitigate cognitive deterioration become increasingly relevant to support healthy aging and maintaining independence for longer. Studies in the field of neuroscience applied to architecture (neuroarchitecture) have shown that the physical environment, both internal and external, public and private, plays a fundamental role in this aspect [1]. In this sense, architects and urban planners can direct their projects to create solutions that significantly contribute to this objective.
The human brain is a very plastic organ. In other words, it transforms functionally and structurally according to how it is stimulated. Although this plasticity is much more intense during the development period, it continues to exist throughout our lives [2,3]. Therefore, keeping the brain stimulated during adulthood and aging is key to keeping cognition functioning at its best. In this context, recent studies indicate that certain stimuli help in the development of a cognitive reserve [4]. This, in turn, is the brain’s resilience capacity, which helps it to remain functional even throughout aging and even when some neurodegenerative diseases arise [5].
Let’s say that it is a curse. The issue is he is also against life extension entirely. Maybe I want 200 years. Or 1,000. I have zero concern over a boredom problem as it is brain process which can eventually be controlled. And I am disgusted with the idea that I have to die because we might not progress very fast? Ugh.
Elon Musk has said a lot of potentially stupid stuff about aging and longevity, from saying that people shouldn’t live very long because society would ossify to advocating that we judge people based on their chronological age. Most recently, he’s taken to Twitter (aka X) to say “May you live forever is the worst possible curse once you understand deep time.” In this case though, he’s not wrong.
In this episode, we explore the diverse perspectives and heated debates triggered by Elon’s provocative statements on aging and the prospect of eternal life. We navigate through the complexities of deep time, the philosophical implications of living forever, and the importance of autonomy and control. Join host Ryan O’Shea as we examine arguments in favor of human’s being able to end their own lives, and explore how this played out in NBC’s The Good Place, starting Kristen Bell.
A team of mechanical engineers at Nanyang Technological University in Singapore has found a way to electronically control cockroaches without injuring them. In their paper published in the journal npj Flexible Electronics, the group describes the new technology they used to remotely control the cockroaches and the benefits of doing so.
Prior research teams have created a variety of cyborg cockroaches, but they all had one feature in common—they all involved attaching probes to the insect’s nervous system—procedures that led to damage to the insect, and likely some degree of pain.
In this new effort, the researchers noted that damaging cockroaches during attempts to control them results in a very short life expectancy, which then results in very little payoff for a lot of work. They also suggest such research is unethical because of the pain inflicted on the cockroaches. In this new effort, they have found a way to control cockroaches that does not involve cutting into them, resulting in a much longer lifespan.
Just about everyone may want to look and feel younger and healthier, but multimillion-dollar investments and broccoli smoothies are not for everyone. Still, that doesn’t mean the less hardcore among us are out of luck if we’re hoping to turn back the clock on our brain health.
New research by a team of psychologists uncovered a simple way just about anyone can get their brain working like it’s decades younger.
You probably don’t need science to tell you this, but people’s cognitive acuity generally starts to level off in their 30s and 40s before declining more markedly in their 60s. Most of us write our slower responses and memory lapses off to the unavoidable indignities of aging. But what if they were just the adult equivalent of the “summer slide” that affects kids, a pair of researchers wanted to know.
Though drug developers have achieved some progress in treating Alzheimer’s disease with medicines that reduce amyloid-beta protein, other problems of the disease, including inflammation, continue unchecked. In a new study, scientists at The Picower Institute for Learning and Memory at MIT describe a candidate drug that in human cell cultures and Alzheimer’s mouse models reduced inflammation and improved memory.
The target of the new “A11” molecule is a genetic transcription factor called PU.1. Prior research has shown that amid Alzheimer’s disease, PU.1 becomes an overzealous director of inflammatory gene expression in the brain’s microglia immune cells. A11 suppresses this problematic PU.1 activity, the new research shows, by recruiting other proteins that repress the inflammatory genes PU.1 works to express. But because A11 concentrates mostly in the brain and does not reduce PU.1 levels, it does not appear to disrupt PU.1’s other job, which is to ensure the production of a wide variety of blood cells.
“Inflammation is a major component of Alzheimer’s disease pathology that has been especially hard to treat,” says study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute and MIT’s Aging Brain Initiative. “This preclinical study demonstrates that A11 reduces inflammation in human microglia-like cells, as well as in multiple mouse models of Alzheimer’s disease, and significantly improves cognition in the mice. We believe A11 therefore merits further development and testing.”
