A breakthrough drug for pancreatic cancer, organ recovery, weight loss drugs that preserve muscle, a whole-cell simulation, how plants make nicotine, semaglutide fails for Alzheimer’s, and more.
Thanks for this roundup. I'm particularly intrigued by myostatin inhibitors like bimagrumab, and think in addition to being useful for body composition during weight loss and preventing sarcopenia in the elderly, they could replace anabolics as the recreational steroid of choice.
The semaglutide–Alzheimer result deserves more weight than it will probably receive in the science communication cycle.
Observational data suggested a possible benefit. The mechanistic story was plausible: cardiovascular protection, reduced vascular burden, anti-inflammatory effects, perhaps even direct neurological action. The extrapolation felt reasonable. Then two large phase three trials, involving about 3,800 patients with early Alzheimer's disease, found no meaningful slowing of cognitive or functional decline.
That is not science failing. It is science doing its job. But it shows a recurring pattern in medicine: a real therapeutic substrate, GLP-1 drugs genuinely helping with weight, diabetes, cardiovascular risk, and kidney outcomes, gets quietly stretched into a broader promise that the evidence has not yet earned. Biological plausibility fills the space between what we know and what we hope.
The clinical danger is that this gap-filling often happens before definitive trials arrive. Patients ask whether a drug might help their memory. Clinicians, aware of observational signals and plausible mechanisms, offer cautious optimism. By the time the randomized evidence returns negative, a half-truth may already have entered the background noise of practice.
The organ recovery story offers a useful contrast. Donation after circulatory death rose from 2% of deceased donors in 2000 to 49% in 2025, largely through procedural and infrastructure advances such as normothermic regional perfusion and improved preservation systems.
That is what durable biomedical progress often looks like: less glamorous than a sweeping mechanism, but more reliable, better tools, better systems, and careful application without asking the evidence to carry more meaning than it can bear.
I may have misunderstood, but I think it meant, out of people who volunteered to donate ('donors') and died from circulatory death, only 2% could actually donate their organs.
Great newsletter!
What an amazing article! I have learned much even though there's much I didn't understand. It was the big picture that awed me. Thank you! Anna
Thanks for this roundup. I'm particularly intrigued by myostatin inhibitors like bimagrumab, and think in addition to being useful for body composition during weight loss and preventing sarcopenia in the elderly, they could replace anabolics as the recreational steroid of choice.
The semaglutide–Alzheimer result deserves more weight than it will probably receive in the science communication cycle.
Observational data suggested a possible benefit. The mechanistic story was plausible: cardiovascular protection, reduced vascular burden, anti-inflammatory effects, perhaps even direct neurological action. The extrapolation felt reasonable. Then two large phase three trials, involving about 3,800 patients with early Alzheimer's disease, found no meaningful slowing of cognitive or functional decline.
That is not science failing. It is science doing its job. But it shows a recurring pattern in medicine: a real therapeutic substrate, GLP-1 drugs genuinely helping with weight, diabetes, cardiovascular risk, and kidney outcomes, gets quietly stretched into a broader promise that the evidence has not yet earned. Biological plausibility fills the space between what we know and what we hope.
The clinical danger is that this gap-filling often happens before definitive trials arrive. Patients ask whether a drug might help their memory. Clinicians, aware of observational signals and plausible mechanisms, offer cautious optimism. By the time the randomized evidence returns negative, a half-truth may already have entered the background noise of practice.
The organ recovery story offers a useful contrast. Donation after circulatory death rose from 2% of deceased donors in 2000 to 49% in 2025, largely through procedural and infrastructure advances such as normothermic regional perfusion and improved preservation systems.
That is what durable biomedical progress often looks like: less glamorous than a sweeping mechanism, but more reliable, better tools, better systems, and careful application without asking the evidence to carry more meaning than it can bear.
"In 2000, around 2 percent of donors who died from circulatory death were able to donate their organs; that figure rose to 49 percent in 2025."
100% of individuals who donate their organs are donors.
What the figure shows is that 2% of donors used to die from circulatory death, now it is evenly split with brain death at circa 50/50.
I may have misunderstood, but I think it meant, out of people who volunteered to donate ('donors') and died from circulatory death, only 2% could actually donate their organs.