A new statistical framework developed by researchers at the Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine, and Kaiser Permanente Northern California offers improved understanding of how genetics and environment contribute to autism risk.
Large-scale genetic studies have led to the development of genetic risk scores that estimate a person’s predisposition to diseases and health conditions based on their DNA profiles. The new framework allows researchers and clinicians to analyze these scores using family data and characterize the risk of conditions such as autism and other developmental conditions in children based on their own DNA, parental factors, and environmental influences such as maternal diet and lifestyle.
For their study published in Nature Genetics, the researchers analyzed more than 18,000 case-parent trios —autistic children and their parents—across diverse ancestral populations in the Simons Foundation Powering Autism Research for Knowledge consortium and the Genes and Environment Autism Research Study.
Spinal cord injuries can have devastating consequences for those affected. Nerve cells in the spinal cord rarely regenerate naturally, while scarring often prevents the regrowth of nerve fibers. Modern therapies attempt to influence implanted stem cells using electrical stimulation to promote the growth of new nerve cells. This approach has several drawbacks: it requires implanted electrodes, and the transplanted cells do not always survive or integrate properly into the existing tissue.
Researchers in Zurich are pursuing a new approach, which they have published in the journal Nature Materials. This involves combining therapeutic stem cells with magnetoelectric nanoparticles in such a way that the cells can be guided magnetically to the precise site of an injury and stimulate the stem cells to accelerate repair.
To achieve this, the researchers created a biohybrid microrobot, which combines living neural progenitor cells (NPCs) with a technical component in the form of specially engineered nanoparticles.
Every year, more than 2 million people in the United States are diagnosed with treatment-resistant depression.
Desperate for solutions, some brave patients are now volunteering to undergo surgery to place experimental ‘pacemakers’ into their brains.
These implanted electrodes are part of a treatment known as deep brain stimulation, which is currently used to address some cases of Parkinson’s disease and epilepsy.
In this groundbreaking conversation, Professor of Genetics and longevity scientist, Dr. David Sinclair, A.O., Ph.D., joins Sarah Grynberg to unpack the future of human aging, the science of longevity, and how we live today impacts how we age tomorrow.
From reversing blindness in mice to exploring treatments that could one day delay menopause and extend healthy human life, this episode will completely change the way you think about your body, your health, and your future.
But beyond the science, this is also a deeply human conversation about purpose, suffering, love, family, and what it truly means to live a great life.
In this episode, you will learn: Why aging may actually be reversible. The daily habits accelerating aging in your body right now. How stress, loneliness, and cortisol could impact longevity. The real science behind supplements like NMN, resveratrol, and NAD boosters. Why exercise, sleep, and relationships matter more than you think. What Dr. Sinclair believes is coming in the next 10 years of medicine. How scientists are working to reverse female infertility and delay menopause. The surprising reason your “biological age” may be younger or older than your real age. Why suffering through disease and decline should not be considered “normal aging” The philosophy and mindset Dr. Sinclair lives by every day.
00:00 — Introduction. 01:18 — Why David Sinclair Became Obsessed With Aging. 06:20 — The Childhood Conversation That Changed His Life. 10:18 — The Groundbreaking Discovery That Could Reverse Aging. 12:47 — Reversing Blindness In Mice. 13:33 — Human Trials Are About To Begin. 16:11 — What Accelerates Aging Faster Than Anything Else. 20:08 — Why Relationships & Loneliness Impact Longevity. 24:14 — The Truth About Sun Exposure & Aging. 28:59 — Alzheimer’s, Cancer & Diseases Of Aging. 35:28 — Will Humans Live Longer In The Next Decade? 38:34 — The Supplements David Sinclair Personally Takes. 46:50 — Menopause, Fertility & Reversing Ovarian Aging. 50:20 — What Humans Will Eventually Die From. 51:18 — The Difference Between His Mother & Father’s Aging. 55:37 — Skin Rejuvenation, Hair Growth & Looking Younger. 58:16 — Why He Became A “Struggling Vegan” 01:00:08 — David Sinclair’s Workout & Exercise Routine. 01:03:28 — The Lifespan Community & Podcast. 01:06:02 — The Best Advice He’s Ever Received. 01:08:09 — What A Life Of Greatness Means To David Sinclair.
This episode is a powerful reminder that longevity is not just about living longer… it’s about living better.
I had Tom Benson, CEO of Mitrix on to discuss mitochondrial transplantation. We covered what mitochondria are, the discovery that your body is constantly delivering fresh mitochondria through your bloodstream (people didn’t know that mitochondria were transferred outside the cell until recently!), why we age, what kills mitochondria (stress, smoking, radiation, chemotherapy and certain antibiotics like fluoroquinolones, psych meds), why COVID destroys mitochondria and what that means for long COVID, the Alzheimer’s and Parkinson’s brain tissue regeneration research their company has already done in mice, what mitochondrial transplantation actually is and how it has already been used in pediatric heart surgery, what a bioreactor growing mitochondria for personal use might look like, and more.
Mice wearing specialized goggles reveal that the brain’s internal visual networks rewire themselves to match the exact patterns they see in the world. The study shows how visual feedback loops actively learn to predict our surroundings.
While E. Josie Clowney would never suggest that neuroscience is simple, a new study by her team at the University of Michigan could drastically reduce complexity in future studies. Their work focused on instinctual behaviors in fruit flies, but it has the potential to accelerate work to better understand the neurobiology that underlies behavior and decision-making in mammals, including humans.
The research establishes a new way to understand neurons, their connectivity and the behaviors they control. Within this new framework, the researchers can circumvent the conventional approach of considering each type of neuron individually and instead focus on groupings defined by shared structure and by two sets of regulatory genes. The work is published in the journal Nature.
While there are more than 8,000 kinds of neurons in the fruit fly cerebrum —the part of its brain where instinctual behaviors are hardwired—there are less than 200 major structural groups, or ground plans. Led by Najia Elkahlah, who recently defended her doctoral thesis in the Clowney lab, the team’s discoveries revealed how these ground plans get set up. There is a sort of order or hierarchy, where one set of genes coordinates the formation of the ground plan, and the other set produces small differences in shape and connectivity among neurons within each ground plan.
The human brain contains roughly 86 billion neurons. That number appears in almost every popular account of memory and intelligence, and it tends to carry an implicit argument: that the scale of human cognition follows from the scale of this cell count. What is less often mentioned is that the brain contains a roughly comparable number of a different cell type entirely, one that researchers have treated, for most of the history of neuroscience, as little more than biological scaffolding.
A paper published on 23 May in the Proceedings of the National Academy of Sciences puts forward a new hypothesis about what those cells, called astrocytes, might actually be doing. The work comes from a team at MIT: lead author Leo Kozachkov, Jean-Jacques Slotine, a professor of mechanical engineering and brain and cognitive sciences, and Dmitry Krotov of the MIT-IBM Watson AI Lab, who is the paper’s senior author. Their claim is not that astrocytes have been misunderstood in any dramatic sense; it is the more careful suggestion that they may be doing computational work that neurons, on their own, cannot account for.
This is a hypothesis supported by a mathematical model. The experimental work needed to test it has not yet been done.
A newly identified group of amygdala neurons appears to play a central role in anxiety and social behavior. Restoring normal activity in this tiny brain circuit reversed anxiety and social deficits in mice, revealing a promising new target for future treatments.
A new Yale study reveals that major organ systems in the body aren’t just passive structures operating on directions from command central—the brain—but instead are active participants in controlling their own functions.
Writing in the journal Nature, a team of researchers led by Yale’s Rui Chang demonstrates how organs develop and maintain their own neural circuitry, which in turn communicates with the brain in a sort of two-way conversation.
The findings provide a new understanding of how the body and brain communicate via networks of neurons embedded inside organs that constitute a mini-nervous system, called “organ intrinsic nervous systems,” which help control critical functions such as digestion, heart rhythm, breathing, insulin secretion, and immune responses, the researchers say.
