Startups are combining AI and genetics to make more food for less money
Why do cells age—and why do we lose our energy and vitality as we get older? This question is one of the central challenges of modern biomedicine. The focus is particularly on mitochondria—tiny cellular organelles long known as the cell’s powerhouses but now understood as dynamic control centers that not only produce energy, but also coordinate cellular communication, adaptation, and many of the processes essential for life.
They supply us with the energy that our body needs for movement, growth, and repair processes. But as we age, these powerhouses begin to slow down. It has long been known that their function declines with age. But until now, the mechanisms driving this gradual decline have been poorly understood.
Focus on membrane lipids For a long time, it was assumed that genetic damage within the mitochondria themselves was primarily responsible. A study now published in Nature Communications by an international research team led by Dr. Maria Ermolaeva of the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena provides a surprising answer to this question: A key factor appears to be the imbalance in the structure of the mitochondrial network, which is caused by the absence of a major lipid in the membrane composition.
Northwestern Medicine scientists have developed a novel synthetic biomolecular condensate that can degrade intracellular disease-causing proteins, providing a framework for new therapeutic approaches for a wide range of diseases, as detailed in a recent study published in Nature Communications.
Shana Kelley, Ph.D., the Neena B. Schwartz Professor of Chemistry, Biomedical Engineering, and Biochemistry and Molecular Genetics and the president of the Chan Zuckerberg Biohub Chicago, was senior author of the study.
Targeted protein degradation is an emerging therapeutic strategy that harnesses cells’ own degradation machinery to clear disease-causing proteins. However, achieving this degradation process across different cell types has remained a challenge due to subtle variations in protein structure.
An international collaboration of genetic researchers has identified more than 90 genetic regions associated with the risk of Alzheimer’s disease and related dementias. The large-scale meta-analysis reveals new biological insights into the disease, highlighting the important roles of immune processes, beta-amyloid and tau biology, and lipid metabolism.
Alzheimer’s disease is the most common cause of dementia worldwide, and its development is influenced by a complex interplay of genetic and environmental factors. Understanding the genetic architecture of the disease is essential for improving diagnosis, risk prediction, and the development of targeted therapies.
In this study, researchers combined genome-wide association data from nearly a million individuals of European ancestry, including over 128,000 Alzheimer’s disease cases and nearly 850,000 controls.
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.
On April 21, the Munk Debates convened a special debate about gene editing in Deerfield, Massachusetts for 650 students at Deerfield Academy.
Motion: Be it Resolved, let’s engineer better human beings.
About the Debate:
New powerful engineering technology is already being used to edit human embryos, curing diseases and repairing defective genes before a child is even born. Some welcome this new science as a powerful tool to enhance human intelligence, memory, appearance and physical health. Why wouldn’t we embrace a science that allows people to live longer, healthier, and happier lives? Others warn that this new technology will be used to create designer babies and a new class of genetically “enhanced” elites. It will undermine human dignity and autonomy, and risk unleashing new diseases into the human gene pool. Playing G-d with human nature, critics argue, will result in a dystopian nightmare of our own making.
About the Debaters:
Arguing in favour of the motion was the biophysicist, best-selling author, biotechnology entrepreneur, and the former director of the Program on Medicine, Technology and Society at UCLA School of Medicine, Gregory Stock. His debate partner was the internationally acclaimed strategic philosopher and pioneering transhumanist Max More. Arguing against the motion was the prominent American bioethicist Ezekiel Emanuel, Special Advisor to the Director General of the WHO and a former founding chair of the Department of Bioethics at the NIH. His debate partner was the award-winning educator, author, and Professor of Reproductive Science at University College London, Joyce Harper.
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.