Lifeboat Foundation

Scientists at Weill Cornell Medicine discovered a previously unknown link between two key pathways that regulate the immune system in mammals — a finding that impacts our understanding of chronic inflammatory bowel diseases (IBD). This family of disorders severely impacts the health and quality of life of more than 2 million people in the United States.

The immune system has many pathways to protect the body from infection, but sometimes an overactive immune response results in autoimmune diseases including IBD, psoriasis, rheumatoid arthritis and multiple sclerosis. Interleukin-23 (IL-23) is one such immune factor that fights infections but is also implicated in many of these inflammatory diseases. However, it was unknown why IL-23 is sometimes beneficial, and other times becomes a driver of chronic disease.

In the study, published June 12 in Nature, the team found that IL-23 acts on group 3 innate lymphoid cells (ILC3s), a family of immune cells that are a first line of defense in mucosal tissues such as the intestines and lungs. In response, ILC3s increase activity of CTLA-4, a key regulatory factor that prevents the immune system from attacking the body and beneficial gut microbiota. This interaction critically balances the pro-inflammatory effects IL-23 to maintain gut health, but is impaired in IBD.

Common treatments for Parkinson’s disease can address short-term symptoms, but can also cause extensive problems for patients in the long run. Namely, treatments can cause dyskinesia, a form of uncontrollable movements and postures.

In a recent study published in The Journal of Neuroscience, researchers at the University of Alabama at Birmingham took a different approach to dyskinesia and treated it like a “bad motor memory.” They found that blocking a protein called Activin A could halt dyskinesia symptoms and effectively erase the brain’s “bad memory” response to certain Parkinson’s treatments.

“Instead of looking for a completely alternative treatment, we wanted to see if there was a way to prevent dyskinesia from developing in the first place,” said David Figge, M.D., Ph.D., lead study author and assistant professor in the UAB Department of Pathology. “If dyskinesia does not occur, then patients could potentially stay on their Parkinson’s treatment for longer.”

The ability to recognize and respond to emotionally-charged situations is essential to a species’ evolutionary success. A new study published in Nature Communications advances our understanding of how the brain responds to emotionally charged objects and scenes.

The research, led by Trinity College Dublin neuroscientist Prof. Sonia Bishop, and Google researcher Samy Abdel-Ghaffar while he was a Ph.D. student in Prof. Bishop’s lab at UC Berkeley, has identified how the brain represents different categories of emotional stimuli in a way that allows for more than a simple “approach/avoid” dichotomy when guiding behavioral responses.

Sonia Bishop, now Chair of Psychology in Trinity’s School of Psychology, and senior author of the paper, explains, It is hugely important for all species to be able to recognize and respond appropriately to emotionally salient stimuli, whether that means not eating rotten food, running from a bear, approaching an attractive person in a bar or comforting a tearful child.

Recent fossil finds suggest that big brains weren’t an evolutionary asset to our ancestors but evolved by accident – and are likely to shrink again in the near future.

By Colin Barras

This Perspective explores the potential of organic electrochemical neurons, which are based on organic electrochemical transistors, in the development of adaptable and biointegrable neuromorphic event-based sensing applications.

Scientists have connected two organoids together with an axon bundle, to study how brain areas communicate. They sent signals back and forth and responded to external stimulation. This could be a step toward biocomputing.

Learn about: axons, white matter, re-entry, optogenetics, myelination, entrainment, short-term potentiation.

Continue reading “Brain Organoids Communicate: A Step Toward ‘Organoid Intelligence’” »

Eexxeccellent.

Human brains outperform computers in many forms of processing and are far more energy efficient. What if we could harness their power in a new form of biological computing?

Continue reading “Thomas Hartung and colleagues | The future of organoid intelligence | Frontiers Forum Deep Dive 2023” »

“Machine-Learning Assisted Directed Evolution of Viral Vectors and Microbial Opsins for Minimally Invasive Neuroscience.” AI-4-Science Workshop, October 25, 2019 at Bechtel Residence Dining Hall, Caltech. Learn more about: — AI-4-science: https://www.ist.caltech.edu/ai4science/ — Events: https://www.ist.caltech.edu/events/ Produced in association with Caltech Academic Media Technologies. ©2019 California Institute of Technology.

Summary: Researchers have discovered how glial cells can be reprogrammed into neurons through epigenetic modifications, offering hope for treating neurological disorders. This reprogramming involves complex molecular mechanisms, including the transcription factor Neurogenin2 and the newly identified protein YingYang1, which opens chromatin for reprogramming.

The study reveals how coordinated epigenome changes drive this process, potentially leading to new therapies for brain injury and neurodegenerative diseases.