Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD
Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.
Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD
Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.
OpenAI says it trained a new AI model called GPT-4b micro with Retro Biosciences, a longevity science startup trying to extend the human lifespan by 10 years, according to the MIT Technology Review.
Retro, which is backed by Sam Altman, has been working with OpenAI for roughly a year on this research, according to the report. The GPT-4b micro model tries to re-engineer proteins — a specific set called the Yamanaka factors — that can turn human skin cells into young-seeming stem cells. Retro believes these proteins are a promising step toward building human organs and providing supplies of replacement cells.
The model differs slightly from Google’s Nobel prize-winning AlphaFold, which predicts the shape of proteins, but it appears to be OpenAI’s first model that is custom-built for biological research. OpenAI and Retro tell the MIT Technology Review they plan to release research on the model and its outputs.
Summary: A new study has identified three psychological profiles that influence brain health, cognitive decline, and dementia risk in aging adults. Profiles with high protective traits, like purpose and openness, show better cognition and brain integrity, while those with low protective traits or high negative traits face accelerated brain atrophy and mental health issues.
Researchers emphasize comprehensive psychological assessments to tailor interventions, like therapies that enhance life purpose or reduce distress symptoms. These findings pave the way for personalized strategies to prevent cognitive decline and support brain health in adulthood and aging.
Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD
Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.
+ Decoding the secrets of DNA, CRISPR gene editing allows scientists to target specific genes linked to aging. By modifying these genes, researchers aim to prevent conditions that come with aging. Envision a future where genetic risks for age-related diseases are minimized through precise DNA editing.
It is possible to regenerate cells using stem cells, which can turn into a variety of types. In recent trials, stem cells showed promise in regenerating aged tissues like cartilage. Scientists hope to develop therapies that might slow down physical decline and maintain vitality longer by using this potential.
Nanobots could someday be the future of healthcare by targeting damaged cells directly as they move through your bloodstream. Researchers are currently exploring how nanobots might repair cellular damage and improve overall health, potentially reversing some age-related effects at the cellular level.
Patients suffering from diseased and injured organs are often treated with transplanted organs, and this treatment has been in use for over 50 years. In 1955, the kidney became the first entire organ to be replaced in a human, when Murray transplanted this organ between identical twins. Several years later, Murray performed an allogeneic kidney transplant from a non-genetically identical patient into another. This transplant, which overcame the immunologic barrier, marked a new era in medicine and opened the door for use of transplantation as a means of therapy for different organ systems.
As modern medicine increases the human lifespan, the aging population grows, and the need for donor organs grows with it, because aging organs are generally more prone to failure. However, there is now a critical shortage of donor organs, and many patients in need of organs will die while waiting for transplants. In addition, even if an organ becomes available, rejection of organs is still a major problem in transplant patients despite improvements in the methods used for immunosuppression following the transplant procedure. Even if rejection does not occur, the need for lifelong use of immunosuppressive medications leads to a number of complications in these patients.
These problems have led physicians and scientists to look to new fields for alternatives to organ transplantation. In the 1960s, a natural evolution occurred in which researchers began to combine new devices and materials sciences with cell biology, and a new field that is now termed tissue engineering was born. As more scientists from different fields came together with the common goal of tissue replacement, the field of tissue engineering became more formally established. Tissue engineering is now defined as an interdisciplinary field which applies the principles of engineering and life sciences towards the development of biological substitutes that aim to maintain, restore or improve tissue function.
In recent years, biomedical devices have proven to be able to target also different neurological disorders. Given the rapid ageing of the population and the increase of invalidating diseases affecting the central nervous system, there is a growing demand for biomedical devices of immediate clinical use. However, to reach useful therapeutic results, these tools need a multidisciplinary approach and a continuous dialogue between neuroscience and engineering, a field that is named neuroengineering. This is because it is fundamental to understand how to read and perturb the neural code in order to produce a significant clinical outcome.
Researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have developed brain organoids — 3D, brain-like structures grown from human stem cells — that show organized waves of activity similar to those found in living human brains.
Then, while studying organoids grown from stem cells derived from patients with the neurological disorder Rett syndrome, the scientists were able to observe patterns of electrical activity resembling seizures, a hallmark of the condition.
The study, published today in the journal Nature Neuroscience, broadens the list of brain conditions that can be studied in organoids and further illustrates the value of these human cell–based models in investigating the underlying causes of diseases and testing potential therapies.
A new stroke-healing gel created by UCLA researchers helped regrow neurons and blood vessels in mice whose brains had been damaged by strokes. The finding is reported May 21 in Nature Materials.
“We tested this in laboratory mice to determine if it would repair the brain and lead to recovery in a model of stroke,” said Dr. S. Thomas Carmichael, professor of neurology at the David Geffen School of Medicine at UCLA and co-director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. “The study indicated that new brain tissue can be regenerated in what was previously just an inactive brain scar after stroke.”
The results suggest that such an approach could some day be used to treat people who have had a stroke, said Tatiana Segura, a former professor of chemical and biomolecular engineering at UCLA who collaborated on the research. Segura is now a professor at Duke University.
Brain cells receive sensory inputs from the outside world and send signals throughout the body telling organs and muscles what to do. Although neurons comprise only 10% of brain cells, their functional and genomic integrity must be maintained over a lifetime. Most dividing cells in the body have well-defined checkpoint mechanisms to sense and correct DNA damage during DNA replication.
Neurons, however, do not divide. For this reason, they are at greater risk of accumulating damage and must develop alternative repair pathways to avoid dysfunction. Scientists do not understand how neuronal DNA damage is controlled in the absence of replication checkpoints.
A recent study led by Cynthia McMurray and Aris Polyzos in Lawrence Berkeley National Laboratory’s (Berkeley Lab’s) Molecular Biophysics and Integrated Bioimaging Division addressed this knowledge gap, shedding light on how DNA damage and repair occur in the brain. Their results suggest that DNA damage itself serves as the checkpoint, limiting the accumulation of genomic errors in cells during natural aging.