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Category: neuroscience – Page 628

Daniel Schmachtenberger is a philosopher and founding member of The Consilience Project. Please support this podcast by checking out our sponsors:
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1:31 — Aliens and UFOs.
20:15 — Collective intelligence of human civilization.
28:12 — Consciousness.
39:33 — How much computation does the human brain perform?
43:12 — Humans vs ants.
50:30 — Humans are apex predators.
57:34 — Girard’s Mimetic Theory of Desire.
1:17:31 — We can never completely understand reality.
1:20:54 — Self-terminating systems.
1:31:18 — Catastrophic risk.
2:01:30 — Adding more love to the world.
2:28:55 — How to build a better world.
2:46:07 — Meaning of life.
2:53:49 — Death.
2:59:29 — The role of government in society.
3:16:54 — Exponential growth of technology.
4:02:35 — Lessons from my father.
4:08:11 — Even suffering is filled with beauty.

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Circa 2010

In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

The adult brain contains neural stem cells (NSCs) that self-renew, proliferate and give rise to neural progenitor cells (NPC) that exhibit partial lineage-commitment. Following several cycles of proliferation, NPC differentiate into new neurons and glia. NSCs are increasingly acknowledged to be of functional significance and harbor potential for repair of the diseased or injured brain. The dramatic decline in neurogenesis with age is thought to underlie impairments in learning and memory, at least in part. Aging is also the greatest risk factor for Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive loss of memory and cognitive decline. Alterations in neurogenesis have been described extensively in animal models of AD, and key proteins involved in AD pathogenesis are shown to regulate neurogenesis.

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Many people with rheumatoid arthritis, or RA, report having trouble thinking clearly, problems with memory, and difficulty concentrating.

These symptoms, known as brain fog, are widespread in people with chronic inflammatory conditions, including RA, Sjogren’s syndrome, and multiple sclerosis.

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If you want to learn, then you have to break some things.

Summary: Brain cells snap DNA in more places and in more cell types than previously realized in order to express genes for learning and memory.

Source: Picower Institute for Learning and Memory

The urgency to remember a dangerous experience requires the brain to make a series of potentially dangerous moves: Neurons and other brain cells snap open their DNA in numerous locations—more than previously realized, according to a new study—to provide quick access to genetic instructions for the mechanisms of memory storage.

The extent of these DNA double-strand breaks (DSBs) in multiple key brain regions is surprising and concerning, said study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute for Learning and Memory, because while the breaks are routinely repaired, that process may become more flawed and fragile with age. Tsai’s lab has shown that lingering DSBs are associated with neurodegeneration and cognitive decline and that repair mechanisms can falter.

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Summary: Axonal swelling in the Purkinje cells of mice had no detrimental impact on firing rate or the speed at which axons transmit signals. At peak firing rate, axons with swellings were less likely to fail than those without.

Source: McGill University.

Researchers at McGill University have shown that a brain cell structure previously thought to be pathological in fact enhances cells’ ability to transmit information and correlates with better learning on certain tasks.

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Humans are integrating with technology. Not in the future – now. With the emergence of custom prosthetics that make us stronger and faster, neural implants that change how our brains work, and new senses and abilities that you’ve never dreamed of having, it’s time to start imagining what a better version of you might look like.

From reality-enhancing implants to brain-controlled exoskeletons, breakthroughs in bio-tech have fuelled a new fusion of machinery and organic matter.

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A rare group of humans known as “superagers” can grow up without their minds growing old.

Even in their 60s, 70s, and 80s, a lucky few maintain incredibly youthful memories, recalling new experiences, events, and situations just as well as people decades younger.

New research now suggests that’s because their brains have somehow resisted the march of time.

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Math about black holes:

If you’ve been following the arXiv, or keeping abreast of developments in high-energy theory more broadly, you may have noticed that the longstanding black hole information paradox seems to have entered a new phase, instigated by a pair of papers [1, 2] that appeared simultaneously in the summer of 2019. Over 200 subsequent papers have since appeared on the subject of “islands”—subleading saddles in the gravitational path integral that enable one to compute the Page curve, the signature of unitary black hole evaporation. Due to my skepticism towards certain aspects of these constructions (which I’ll come to below), my brain has largely rebelled against boarding this particular hype train. However, I was recently asked to explain them at the HET group seminar here at Nordita, which provided the opportunity (read: forced me) to prepare a general overview of what it’s all about. Given the wide interest and positive response to the talk, I’ve converted it into the present post to make it publicly available.

Well, most of it: during the talk I spent some time introducing black hole thermodynamics and the information paradox. Since I’ve written about these topics at length already, I’ll simply refer you to those posts for more background information. If you’re not already familiar with firewalls, I suggest reading them first before continuing. It’s ok, I’ll wait.

Done? Great; let me summarize the pre-island state of affairs with the following two images, which I took from the post-island review [3] (also worth a read):

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Using CRISPR-Cas9, the researchers subsequently removed the one copy of the Ndn gene from the 15q dup mouse model to generate mice with a normalized genomic copy number for this gene (15q dupΔNdn mouse). Using this model, they demonstrated that the abnormalities observed in 15q dup mice (abnormal spine turnover rate and decreased inhibitory synaptic input) could be ameliorated.

A research group including Kobe University’s Professor TAKUMI Toru (also a Senior Visiting Scientist at RIKEN Center for Biosystems Dynamics Research) and Assistant Professor TAMADA Kota, both of the Physiology Division in the Graduate School of Medicine, has revealed a causal gene (Necdin, NDN) in autism model mice that have the chromosomal abnormality called copy number variation.

The researchers hope to illuminate the NDN gene’s molecular mechanism in order to contribute towards the creation of new treatment strategies for developmental disorders including autism.

These research results were published in Nature Communications on July 1, 2021.

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