Regeneron’s AAV gene therapy for congenital deafness has been approved by the FDA — a clinical victory for helping patients and an exciting milestone for gene therapy in general!
Approved Thursday via the FDA’s Commissioner’s National Priority Voucher program, Otarmeni is the first gene therapy for hearing loss—and the first treatment to target an underlying cause of the condition.
Stanford published a paper in Science showing they regrew joint cartilage in aging mice — and in human tissue samples taken from knee-replacement patients — by blocking a single enzyme called 15-PGDH. It’s being hyped as the end of knee and hip replacement surgery. The science is real. The hype is getting ahead of what the paper actually says.
This episode walks through the study itself — the three experiments, the surprising mechanism (which doesn’t involve stem cells at all), and the actual clinical timeline.
Bottom line: the mechanism is a genuinely new paradigm for tissue regeneration. The human osteoarthritis trial? \.
Technology promised simplicity. It delivered complexity.
AI promised resolution. It is delivering acceleration.
The paradox is not a bug. It is the feature. And the question is what we choose to do about it.
This week I published a new essay, It is the argument I have been circling for a decade, finally in one place.
The short version: as AI’s capabilities grow, so do the risks. They are not separate variables. They climb the same curve. A more powerful model can cure more diseases and design more weapons. A smarter agent can book your travel and drain your bank account. Capability is leverage. Leverage is indifferent to ethics.
Every time we raise the ceiling of what AI can do, we raise the floor of what can go wrong.
We still have the how. We are drowning in the what. What we have neglected, almost completely, is the why.
Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder that primarily affects persons aged 65 years and above. It causes dementia with memory loss and deterioration in thinking and language skills. AD is characterized by specific pathology resulting from the accumulation in the brain of extracellular plaques of amyloid-β and intracellular tangles of phosphorylated tau. The importance of mitochondrial dysfunction in AD pathogenesis, while previously underrecognized, is now more and more appreciated. Mitochondria are an essential organelle involved in cellular bioenergetics and signaling pathways. Mitochondrial processes crucial for synaptic activity such as mitophagy, mitochondrial trafficking, mitochondrial fission, and mitochondrial fusion are dysregulated in the AD brain. Excess fission and fragmentation yield mitochondria with low energy production.