Abstract. Ageing and age-related diseases are the result of complex biological processes that progressively cause deterioration of cellular and tissue func
Category: biotech/medical – Page 10
Role of Dopamine in Pain
Dopamine is a member of a class of molecules called the catecholamines, which serve as neurotransmitters and hormones. In the brain, dopamine serves as a neurotransmitter and is released from nerve cells to send signals to other nerves. Outside of the nervous system, it acts as a local chemical messenger in several parts of the body.
Image Copyright: Meletios, Image ID: 71,648,629 via shutterstock.com
A number of important neurodegenerative diseases are associated with abnormal function of the dopamine system and some of the main medications used to treat those illnesses work by changing the effects of dopamine. The condition Parkinson’s disease is caused by a loss of dopamine secreting cells in a brain area called the substantia nigra.
Grant supports research into how microglia may spread toxic tau in Alzheimer’s
A paper describing Hopp’s upcoming study published on the CureAlz website, titled, “How Do Microglia Contribute to the Spread of Tau Pathology in Alzheimer’s Disease?”, says that while tau aggregates are a defining feature of Alzheimer’s disease and closely track with brain cell loss, memory problems and cognitive decline, much still isn’t known about how it spreads or what role the brain’s immune system plays in the process.
There is evidence, it says, that toxic forms of tau, which have become “misfolded” or dysfunctional, act like a “bad influence.”
“When they encounter nearby healthy tau proteins, they cause them to misfold as well, triggering a chain reaction that spreads from one brain region to another,” according to the paper. “Microglia … are among the first to encounter these toxic tau ‘seeds.’ Normally, microglia protect the brain by clearing debris and helping repair damage. But growing evidence suggests that microglia may also contribute to tau’s spread by engulfing misfolded tau and inadvertently releasing it, thereby amplifying its harmful effects.”
A researcher with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio has received a two-year, $402,500 grant award from the Cure Alzheimer’s Fund to study how microglia, the brain’s resident immune cells, paradoxically might contribute to the spread of toxic forms of tau protein in the disease.
Sarah C. Hopp, PhD, associate professor of pharmacology with the Biggs Institute and the South Texas Alzheimer’s Disease Research Center, along with her lab have been instrumental in uncovering the behavior of microglia. UT Health San Antonio is the academic health center of The University of Texas at San Antonio.
Starting this month, Hopp’s lab will test the hypothesis that microglial uptake of tau is a key mechanism driving its spread through the brain, and that specific molecular pathways determine whether this process protects or harms neurons. The Cure Alzheimer’s Fund, also known as CureAlz, is a nonprofit organization that funds research “with the highest probability of preventing, slowing or reversing Alzheimer’s disease.”
DeepRare AI helps shorten the rare disease diagnostic journey with evidence-linked predictions
Researchers developed DeepRare, an LLM-driven multi-agent diagnostic system that integrates clinical descriptions, phenotype data, and genomic information to improve rare disease identification. Across thousands of cases, the system showed higher diagnostic recall than existing AI tools and clinicians in benchmark testing, while providing traceable reasoning linked to medical evidence.
By 2050 we could get “10,000 years of technological progress”
Every major AI company has the same safety plan: when AI gets crazy powerful and really dangerous, they’ll use the AI itself to figure out how to make AI safe and beneficial. It sounds circular, almost satirical. But is it actually a bad plan? Today’s guest, Ajeya Cotra, recently placed 3rd out of 413 participants forecasting AI developments and is among the most thoughtful and respected commentators on where the technology is going.
She thinks there’s a meaningful chance we’ll see as much change in the next 23 years as humanity faced in the last 10,000, thanks to the arrival of artificial general intelligence. Ajeya doesn’t reach this conclusion lightly: she’s had a ring-side seat to the growth of all the major AI companies for 10 years — first as a researcher and grantmaker for technical AI safety at Coefficient Giving (formerly known as Open Philanthropy), and now as a member of technical staff at METR.
So host Rob Wiblin asked her: is this plan to use AI to save us from AI a reasonable one?
Ajeya agrees that humanity has repeatedly used technologies that create new problems to help solve those problems. After all:
• Cars enabled carjackings and drive-by shootings, but also faster police pursuits.
• Microbiology enabled bioweapons, but also faster vaccine development.
• The internet allowed lies to disseminate faster, but had exactly the same impact for fact checks.
But she also thinks this will be a much harder case. In her view, the window between AI automating AI research and the arrival of uncontrollably powerful superintelligence could be quite brief — perhaps a year or less. In that narrow window, we’d need to redirect enormous amounts of AI labour away from making AI smarter and towards alignment research, biodefence, cyberdefence, adapting our political structures, and improving our collective decision-making.
The plan might fail just because the idea is flawed at conception: it does sound a bit crazy to use an AI you don’t trust to make sure that same AI benefits humanity.
Key alterations discovered in the cerebral cortex of people with psychosis
Researchers at the University of Seville have analyzed alterations in the cerebral cortex in people suffering from psychosis. Their findings show that psychosis does not follow a single trajectory, but rather its evolution depends on a complex interaction between brain development, symptoms, cognition and treatment. The authors therefore emphasize the need to adopt more personalized approaches that take individual differences into account in order to better understand the disease and optimize long-term therapeutic strategies.
Psychosis is a set of symptoms—such as hallucinations and delusions—that are common in schizophrenia and involve a loss of contact with reality. From their first manifestation, known as the first psychotic episode, these symptoms can appear and evolve in very different ways between individuals, thus making schizophrenia a particularly complex disorder.
The results of the study show that, at the time of the first episode, people with psychosis present a reduction in cortical volume, which is particularly marked in regions with a high density of serotonin and dopamine receptors, key neurotransmitters in both the pathophysiology of psychosis and the mechanism of action of antipsychotics. The data also suggest that both neurons and other brain cells involved in inflammatory and immunological processes may play an important role in the disease.
One stem cell generates 14 million tumor-killing NK cells in major cancer breakthrough
Scientists in China have unveiled a breakthrough way to mass-produce powerful cancer-fighting immune cells in the lab. By engineering early-stage stem cells from cord blood—rather than trying to modify mature natural killer (NK) cells—they created a streamlined process that generates enormous numbers of highly potent NK cells, including CAR-equipped versions designed to hunt specific cancers.
Symbiotic bacteria in planthoppers break record for smallest non-organelle genome ever found
Many insects rely on heritable bacterial endosymbionts for essential nutrients that they cannot get through their diet. A new study, published in Nature Communications, indicates that the genomes of these symbiotic bacteria often shrink over time. Some of these bacteria, which live inside certain insect cells, have lost so many genes that they have broken the record for the tiniest genome ever found—almost blurring the lines between organelle and bacteria.
Endosymbiotic relationships are common in many insects, and in sap-sucking insects, like planthoppers and cicadas, they are essential for the insect’s survival. Because the sap of plants does not typically contain certain amino acids or vitamins, the insect must get them another way. Over hundreds of millions of years, these insects have co-evolved with bacteria that provide these additional nutrients.
Sulcia and Vidania are two examples of bacterial endosymbionts, which have co-evolved with planthoppers for more than 260 million years. These bacteria live in specialized cells within the planthopper abdomen. The new study has found that, along with their hosts, these endosymbionts have evolved—or devolved—in some unexpected ways.