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Fields as Formal Causes, with David Bentley Hart

In this conversation, Rupert Sheldrake and David Bentley Hart delve into the concept of fields in physics, discussing their nature as non-material formative causes and their historical context in scientific thought. They explore the idea that fields, such as gravitational and electromagnetic, act as top-down causes, aligning with Aristotle’s formal and final causes, and argue for a re-evaluation of these ancient concepts in modern science.

Chapter List:

00:00 — Introduction.
01:14 — Exploring Fields as Causes in Nature.
02:08 — Magnetic Fields and Formative Processes.
04:19 — Gravitational Fields and Formative Effects.
06:10 — Aristotle’s Formal and Final Causes.
07:32 — Challenges in Understanding Fields.
09:09 — Fields as Top-Down Causes.
10:34 — Morphic Fields and Formative Causation.
12:23 — Information Theory vs. Form.
14:15 — Fields and Order in Physics.
17:15 — Semantic and Syntactic Information.
18:18 — Universal Gravitational Field.
19:44 — Strong and Weak Nuclear Fields.
21:18 — History of Field Theory and Ether.
23:14 — Gilbert’s Magnetic Theory.
24:46 — Mind-like Structure in Nature.
25:39 — Combination of Top-Down and Bottom-Up Theories.
27:07 — Mechanistic Models and Their Limitations.
28:52 — Recovering Aristotelian Causality.
31:39 — Conclusion and Reflection on Fields as Modern Souls.

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Dr Rupert Sheldrake, PhD, is a biologist and author best known for his hypothesis of morphic resonance. At Cambridge University, as a Fellow of Clare College, he was Director of Studies in biochemistry and cell biology. As the Rosenheim Research Fellow of the Royal Society, he carried out research on the development of plants and the ageing of cells, and together with Philip Rubery discovered the mechanism of polar auxin transport. In India, he was Principal Plant Physiologist at the International Crops Research Institute for the Semi-Arid Tropics, where he helped develop new cropping systems now widely used by farmers. He is the author of more than 100 papers in peer-reviewed journals and his research contributions have been widely recognized by the academic community, earning him a notable h-index for numerous citations. On ResearchGate his Research Interest Score puts him among the top 4% of scientists.

https://www.sheldrake.org

Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus

Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older.

Until now.

A landmark study from researchers at the Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

Led by Dr. Ashok Shetty, university distinguished professor and associate director of the Institute for Regenerative Medicine, along with senior research scientists Dr. Madhu Leelavathi Narayana and Dr. Maheedhar Kodali, the team developed a nasal spray that, with just two doses, dramatically reduced brain inflammation, restored the brain’s cellular power plants and significantly improved memory.

The most surprising part? It all happened within weeks and lasted for months.

The findings, published in the Journal of Extracellular Vesicles, could reshape the future of neurodegenerative therapies and may even change how scientists think about brain aging itself.

Continue reading “Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus” | >

Human Gene Editing Has Begun | George Church

We are already gene editing humans. You just haven’t noticed.

George Church, Harvard geneticist and Human Genome Project pioneer, explains why CRISPR wasn’t the real breakthrough, how multiplex gene editing unlocked organ transplants and de-extinction, and why aging will likely require rewriting many genes at once.

Hosted by Mgoes → https://twitter.com/m_goes_distance
Brought to you by SuperHuman Fund → https://superhuman.fund/

0:00 — Gene Editing Mammals → Humans
8:36 — Germline vs Somatic
14:56 — Modified Humans Are Already Here
18:50 — Enhancing Healthy Humans
25:00 — Aging Therapies vs Cognitive Enhancement
30:20 — Embryo Selection
38:10 — Is US Losing To UAE?
42:33 — Biotech Failures
49:31 — Next Dire Wolf Moment
54:21 — AI x Science
1:02:07 — Synthetizing Entire Genomes.

The Accelerate Bio Podcast explores the future of humanity in the age of Artificial Intelligence. Subscribe for deep-dive conversations with founders, scientists, and investors shaping AI, biotechnology, and human progress.

This episode discusses George Church, gene editing, CRISPR, human enhancement, longevity, aging, embryo selection, synthetic biology, multiplex editing, AI biotech.

Continue reading “Human Gene Editing Has Begun | George Church” | >

This nasal spray rewinds the aging brain, restoring memory and reversing inflammation in preclinical models

Picture this: your brain is a high-performance engine. Over decades, it doesn’t just wear down, it also starts to run hot. Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older. Until now.

A landmark study by researchers at Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

A simple shot shows promise to reverse osteoarthritis within weeks

A research team including scientists and engineers from University of Colorado Boulder, CU Anschutz and Colorado State University has developed a suite of new therapies that prompt aging or damaged joints to repair themselves within weeks, according to animal studies.

The new osteoarthritis treatments include a single, regenerative injection to a joint and a biomaterial repair kit that recruits the body’s own cells to patch holes in damaged cartilage.

To expedite the research, the federal Advanced Research Projects Agency for Health (ARPA-H) announced this week that the multidisciplinary team will advance to the next phase of the project.

Integrative approaches to aging: Mechanisms, antiaging strategies, and emerging biomedical interventions

This imbalance results in dermal thinning, wrinkle formation, and loss of skin elasticity. Both intrinsic aging (chronological) and extrinsic aging (photoaging) contribute to collagen depletion. Studies have shown that UV-induced ROS accelerate collagen breakdown and inhibit new collagen synthesis, exacerbating visible signs of aging. [20]

Collagen is vital for skin firmness and elasticity. Aging, both intrinsic and extrinsic, leads to reduced collagen production and increased enzymatic degradation. Antiaging interventions such as retinoids, marine peptides, and nanoformulations aim to restore collagen levels and improve skin structure.

Understanding these cellular and molecular mechanisms provides the foundation for developing targeted antiaging interventions, ranging from holistic lifestyle modifications to advanced biomedical therapies.

APOE4, the Alzheimer’s risk gene, silently undermines bone quality in women

Scientists at the Buck Institute for Research on Aging, along with collaborators at UC San Francisco, have discovered that APOE4, the most common genetic risk factor for Alzheimer’s disease, causes bone quality deficits specifically in female mice, through a mechanism that is invisible to standard imaging and can emerge as early as midlife. The findings, published in Advanced Science, reveal an unexpected biological link between Alzheimer’s risk and skeletal health, and identify a new molecular pathway that could one day inform earlier diagnosis of cognitive decline or guide treatment for bone quality loss in women who carry the APOE4 gene.

“What makes this finding so striking is that bone quality is being compromised at a molecular level that a standard bone scan simply will not catch,” says Buck professor Birgit Schilling, Ph.D., a senior author of the study. “APOE4 is quietly disrupting the very cells responsible for keeping bone strong, and it is doing this specifically in females, which mirrors what we see with Alzheimer’s disease risk.”

Physicians have long observed that people with Alzheimer’s disease suffer bone fractures at higher rates, and that a diagnosis of osteoporosis in women is actually the earliest known predictor of Alzheimer’s. But the underlying mechanism connecting brain and bone health has remained elusive.

Single-nucleus multiome analysis in the human prefrontal cortex identifies gene expression and cis-regulatory elements associated with aging

Catching et al. use single-nucleus ATAC plus gene expression to profile 357 neurologically unaffected postmortem human prefrontal cortices and characterize the molecular effects of aging on different cell types. Analysis of each cell type identifies genes and chromatin regions associated with aging in the human prefrontal cortex.

TgFbox1-TgNAC2-TgWIN1 module regulates petal senescence by fine-tuning cuticular wax biosynthesis in tulip

Fine-tuning petal senescence is crucial for the manipulation of flower longevity and genetic improvement. Yang et al. propose a TgFbox1-TgNAC2-TgWIN1 regulatory cascade that integrates ABA and ethylene signaling pathways with cuticular wax biosynthesis to govern petal senescence in a developmentally stage-dependent manner.

Single-cell epigenomics uncovers heterochromatin instability and transcription factor dysfunction during mouse brain aging

Amaral et al. present a single-cell atlas of brain aging, revealing coordinated chromatin and gene expression changes across multiple regions from young to old mice. Their analyses show that aging involves loss of progenitor cells, dysregulation of master transcription factors, and destabilization of heterochromatin, driving a gradual erosion of cellular identity.

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