Showing posts with label nerds. Show all posts
Showing posts with label nerds. Show all posts
Sep 16, 2026
Sep 11, 2026
Jul 24, 2026
Jul 21, 2026
Jun 13, 2026
May 19, 2026
Apr 29, 2026
Dr Ben
Some more good nerdy stuff.
My oldest is really good at math, and my fatherly guidance was for him to get into Materials Science or Battery Tech.
He didn't.
And this is how we come to blame our kids for our problems instead of looking to our own bad selves for not taking our own advice.
Or something.
Apr 28, 2026
Wild Thoughts
I hate thinking I'm falling into a stream of thought that follows a pattern that may well be valid, but may certainly be just a product of several thousand generations of evolutionary training to look for those patterns, and to assume they're the real deal.
Here's a story of the Chaco Canyon civilization which concludes that high-handed theocratic rulers will become literal cannibals in order to impose their will on the people they rule.
And also maybe too - the leaders ate people thinking they could absorb the essence of their victims so they can extend their own lives as well as the power they hold over their subjects. (Nothing new about that, BTW)
At the end of this piece, try not to think about the grisly possibility that American plutocrats may actually have butchered young children, and eaten parts of them, or used parts of them to concoct some stupidly contrived tonic - or serum - or some goddamned thing.
Apr 27, 2026
Apr 23, 2026
Apr 17, 2026
Today's Nerd Thing
This kinda Star Trek shit makes my head buzz.
OK, so first it makes my head hurt, but that goes away after a bit, and then I get the buzz.
Happy now?
Look, it's good to get a Physics For Dummies explanation, but I'm the guy who struggles with a credit card statement, so all the math and science stuff always ends in "it's wonderment".
I'm just glad to know there are people in the world who are working on it for me.
Thank you, nerds.
Dec 30, 2025
Today's Nerdy Thing
We have to have this kinda thing going on. I don't know if there was much government funding, but it's McGill University in Montreal, so yeah, probably. Canadians are still pretty normal, in that they're willing to do it right, letting the nerds do what they need to do to get us good and useful stuff.
Oct 10, 2025
Oct 9, 2025
Sep 25, 2025
Quote
I am far less interested in the weight and convolutions of Einstein's brain than I am in the near certainty that people of equal talent have lived and died in cotton fields and sweatshops.
--Stephen Jay Gould
Sep 9, 2025
Almost Half A Century
Voyager 1
Quite possibly the last time anything built
in USAmerica Inc was still working
after 48 years of continuous use.
Aug 7, 2025
Calling Dr Kennedy
Quick - somebody get hold of BKjr and tell him those evil science nerds are trying to inject heavy metals directly into our brains!
Research on reversing Alzheimer’s reveals lithium as potential key
Years of investigation by scientists at Harvard has revealed that lithium is deeply involved in Alzheimer’s disease, a finding that could lead to new treatments.
Seven years of investigation by scientists at Harvard Medical School has revealed that the loss of the metal lithium plays a powerful role in Alzheimer’s disease, a finding that could lead to earlier detection, new treatments and a broader understanding of how the brain ages.
Researchers led by Bruce A. Yankner, a professor of genetics and neurology at Harvard Medical School, reported that they were able to reverse the disease in mice and restore brain function with small amounts of the compound lithium orotate, enough to mimic the metal’s natural level in the brain. Their study appeared Wednesday in the journal Nature.
“The obvious impact is that because lithium orotate is dirt cheap, hopefully we will get rigorous, randomized trials testing this very, very quickly,” said Matt Kaeberlein, former director of the Healthy Aging and Longevity Research Institute at the University of Washington, who did not participate in the study. “And I would say that it will be an embarrassment to the Alzheimer’s clinical community if that doesn’t happen right away.”
Yankner, who is also the co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard, said: “I do not recommend that people take lithium at this point, because it has not been validated as a treatment in humans. We always have to be cautious because things can change as you go from mice to humans.” He added that the findings still need to be validated by other labs.
Although there have been recent breakthroughs in the treatment of Alzheimer’s, no medication has succeeded in stopping or reversing the disease that afflicts more than 7 million Americans, a number projected to reach almost 13 million by 2050, according to the Alzheimer’s Association.
Pathology images from the brain of an Alzheimer's mouse model. The images show that when the mice are treated with a very low dose of lithium orotate, it almost completely eradicates the amyloid plaques and the tau tangle-like structures. (Harvard)
Lithium is widely prescribed for patients with bipolar disorder, and previous research indicated that it held potential as an Alzheimer’s treatment and an antiaging medication. A 2017 study in Denmark suggested the presence of lithium in drinking water might be associated with a lower incidence of dementia.
However, the new work is the first to describe the specific roles that lithium plays in the brain, its influence on all of the brain’s major cell types and the effect that its deficiency later in life has on aging.
Results of the study by Yankner’s lab and researchers at Boston Children’s Hospital and the Rush Alzheimer’s Disease Center in Chicago also suggest that measuring lithium levels might help doctors screen people for signs of Alzheimer’s years before the first symptoms begin to appear. Yankner said doctors might be able to measure lithium levels in the cerebrospinal fluid or blood, or through brain imaging.
How our brains use lithium
Alzheimer’s treatments mostly help to manage symptoms and slow the decline it causes in thinking and functioning. Aducanumab, lecanemab, and donanemab, all lab-made antibodies, bind to the harmful amyloid plaques and help remove them.
Donepezil, rivastigmine and galantamine ― all in the class of medications known as cholinesterase inhibitors ― work by replenishing a chemical messenger called acetylcholine, which is diminished in Alzheimer’s. Acetylcholine plays an important role in memory, muscle movement and attention.
Yankner and his team found that when they gave otherwise healthy mice a reduced-lithium diet, the mice lost brain synapses and began to lose memory. “We found that when we administered lithium orotate to aging mice [that had] started losing their memory, the lithium orotate actually reverted their memory to the young adult, six-month level,” he said.
Lithium orotate helped the mice reduce production of the amyloid plaques and tau tangles, and allowed the microglial cells to remove the plaques much more effectively.
Yankner said one factor that might help lithium orotate reach clinical trials sooner is the small amount of the treatment needed, which could greatly reduce the risk of harmful side effects, such as kidney dysfunction and thyroid toxicity.
Aside from its potential in treating Alzheimer’s, Yankner said lithium orotate might also have implications for the treatment of Parkinson’s disease, an area his lab is investigating.
“That needs to be rigorously examined,” he said. “But we’re looking at a whole slew of disorders.”
Years of investigation by scientists at Harvard has revealed that lithium is deeply involved in Alzheimer’s disease, a finding that could lead to new treatments.
Seven years of investigation by scientists at Harvard Medical School has revealed that the loss of the metal lithium plays a powerful role in Alzheimer’s disease, a finding that could lead to earlier detection, new treatments and a broader understanding of how the brain ages.
Researchers led by Bruce A. Yankner, a professor of genetics and neurology at Harvard Medical School, reported that they were able to reverse the disease in mice and restore brain function with small amounts of the compound lithium orotate, enough to mimic the metal’s natural level in the brain. Their study appeared Wednesday in the journal Nature.
“The obvious impact is that because lithium orotate is dirt cheap, hopefully we will get rigorous, randomized trials testing this very, very quickly,” said Matt Kaeberlein, former director of the Healthy Aging and Longevity Research Institute at the University of Washington, who did not participate in the study. “And I would say that it will be an embarrassment to the Alzheimer’s clinical community if that doesn’t happen right away.”
Cue the private equity assholes to buy up all the lithium rights - can't have affordable healthcare now can we.
Yankner, who is also the co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard, said: “I do not recommend that people take lithium at this point, because it has not been validated as a treatment in humans. We always have to be cautious because things can change as you go from mice to humans.” He added that the findings still need to be validated by other labs.
Although there have been recent breakthroughs in the treatment of Alzheimer’s, no medication has succeeded in stopping or reversing the disease that afflicts more than 7 million Americans, a number projected to reach almost 13 million by 2050, according to the Alzheimer’s Association.
Pathology images from the brain of an Alzheimer's mouse model. The images show that when the mice are treated with a very low dose of lithium orotate, it almost completely eradicates the amyloid plaques and the tau tangle-like structures. (Harvard)
Lithium is widely prescribed for patients with bipolar disorder, and previous research indicated that it held potential as an Alzheimer’s treatment and an antiaging medication. A 2017 study in Denmark suggested the presence of lithium in drinking water might be associated with a lower incidence of dementia.
However, the new work is the first to describe the specific roles that lithium plays in the brain, its influence on all of the brain’s major cell types and the effect that its deficiency later in life has on aging.
Results of the study by Yankner’s lab and researchers at Boston Children’s Hospital and the Rush Alzheimer’s Disease Center in Chicago also suggest that measuring lithium levels might help doctors screen people for signs of Alzheimer’s years before the first symptoms begin to appear. Yankner said doctors might be able to measure lithium levels in the cerebrospinal fluid or blood, or through brain imaging.
How our brains use lithium
In a healthy brain, lithium maintains the connections and communication lines that allow neurons to talk with one another. The metal also helps form the myelin that coats and insulates the communication lines and helps microglial cells clear cellular debris that can impede brain function.
“In normal aging mice,” Yankner said, “lithium promotes good memory function. In normal aging humans,” higher lithium levels also correspond to better memory function.
The depletion of lithium in the brain plays a role in most of the deterioration in several mouse models of Alzheimer’s disease.
Loss of lithium accelerates the development of harmful clumps of the protein amyloid beta and tangles of the protein tau that resemble the structures found in people with Alzheimer’s. Amyloid plaques and tau tangles disrupt communication between nerve cells.
The plaques in turn undermine lithium by trapping it, weakening its ability to help the brain function.
Lithium depletion is involved in other destructive processes of Alzheimer’s: decay of brain synapses, damage to the myelin that protects nerve fibers and reduced capacity of microglial cells to break down amyloid plaques.
Lithium’s pervasive role comes despite the fact that our brains contain only a small amount of it. After examining more than 500 human brains from Rush and other brain banks, Yankner’s team discovered the naturally occurring lithium in the brain is 1,000 times less than the lithium provided in medications to treat bipolar disorder.
Li-Huei Tsai, director of the Picower Institute for Learning and Memory at Massachusetts Institute of Technology and who was not involved in the study, called it “very exciting,” especially when many in the field, including her own lab, have focused on genetic risk factors for Alzheimer’s.
“But clearly genetic risk factors are not the only things,” said Tsai, who is also Picower professor of neuroscience. “There are a lot of people walking around carrying these risk genes, but they are not affected by Alzheimer’s disease. I feel this study provides a very important piece of the puzzle.”
Pathways for treatment
“In normal aging mice,” Yankner said, “lithium promotes good memory function. In normal aging humans,” higher lithium levels also correspond to better memory function.
The depletion of lithium in the brain plays a role in most of the deterioration in several mouse models of Alzheimer’s disease.
Loss of lithium accelerates the development of harmful clumps of the protein amyloid beta and tangles of the protein tau that resemble the structures found in people with Alzheimer’s. Amyloid plaques and tau tangles disrupt communication between nerve cells.
The plaques in turn undermine lithium by trapping it, weakening its ability to help the brain function.
Lithium depletion is involved in other destructive processes of Alzheimer’s: decay of brain synapses, damage to the myelin that protects nerve fibers and reduced capacity of microglial cells to break down amyloid plaques.
Lithium’s pervasive role comes despite the fact that our brains contain only a small amount of it. After examining more than 500 human brains from Rush and other brain banks, Yankner’s team discovered the naturally occurring lithium in the brain is 1,000 times less than the lithium provided in medications to treat bipolar disorder.
Li-Huei Tsai, director of the Picower Institute for Learning and Memory at Massachusetts Institute of Technology and who was not involved in the study, called it “very exciting,” especially when many in the field, including her own lab, have focused on genetic risk factors for Alzheimer’s.
“But clearly genetic risk factors are not the only things,” said Tsai, who is also Picower professor of neuroscience. “There are a lot of people walking around carrying these risk genes, but they are not affected by Alzheimer’s disease. I feel this study provides a very important piece of the puzzle.”
Pathways for treatment
Alzheimer’s treatments mostly help to manage symptoms and slow the decline it causes in thinking and functioning. Aducanumab, lecanemab, and donanemab, all lab-made antibodies, bind to the harmful amyloid plaques and help remove them.
Donepezil, rivastigmine and galantamine ― all in the class of medications known as cholinesterase inhibitors ― work by replenishing a chemical messenger called acetylcholine, which is diminished in Alzheimer’s. Acetylcholine plays an important role in memory, muscle movement and attention.
Yankner and his team found that when they gave otherwise healthy mice a reduced-lithium diet, the mice lost brain synapses and began to lose memory. “We found that when we administered lithium orotate to aging mice [that had] started losing their memory, the lithium orotate actually reverted their memory to the young adult, six-month level,” he said.
Lithium orotate helped the mice reduce production of the amyloid plaques and tau tangles, and allowed the microglial cells to remove the plaques much more effectively.
Yankner said one factor that might help lithium orotate reach clinical trials sooner is the small amount of the treatment needed, which could greatly reduce the risk of harmful side effects, such as kidney dysfunction and thyroid toxicity.
Aside from its potential in treating Alzheimer’s, Yankner said lithium orotate might also have implications for the treatment of Parkinson’s disease, an area his lab is investigating.
“That needs to be rigorously examined,” he said. “But we’re looking at a whole slew of disorders.”
Jul 27, 2025
Jul 20, 2025
Get Ready To Be Amazed
The nerds have spent millennia doing impressive things by taking small steps to get better analogous/mechanical fixes.
Now they're about to take a giant leap forward by going digital.
This could be truly outstanding.
We can only hope we don't let the politicians and the rubes fuck things up to the point where we foreclose on a future that promises real greatness, instead of settling for some phony sloganeering shit that fits on a hat.
Go get 'em, nerds.
Jul 10, 2025
Today's Nerds
Elizabeth Lee Hazen Rachel Fuller Brown
They weren’t famous professors.
They didn’t work in fancy labs.
In fact, Rachel Fuller Brown, a chemist in Albany, and Elizabeth Lee Hazen, a microbiologist in New York City, never even worked in the same room.
But what they did share was persistence, trust, and a common mission — to find a cure hidden in the most overlooked places: the soil beneath our feet.
Elizabeth would collect microbes from dirt samples across the country and mail them to Rachel. Rachel would test them — one by one — for any antifungal properties. Over time, hundreds of tiny vials traveled through the U.S. postal system in what became a groundbreaking long-distance collaboration.
Then, one humble sample from Virginia changed everything.
They discovered nystatin — the first safe and effective antifungal drug for humans.
It treated infections like candidiasis, athlete’s foot, and life-threatening fungal diseases that had no cure until then.
But nystatin did more than heal people.
It also protected ancient manuscripts, paintings, trees, and priceless works of art from fungal decay. It became a silent guardian not just in hospitals — but in museums and libraries too.
And the fortune they could’ve made?
They donated all of it.
With the royalties from their discovery, Brown and Hazen created a fund to support future scientists — especially young ones, just starting out. No headlines. No awards. Just a lasting legacy.
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