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Research by Dr. Silvia de Santis and Dr. Santiago Canals, both from the Institute of Neurosciences UMH-CSIC (Alicante, Spain), has made it possible to visualize for the first time and in great detail brain inflammation using diffusion-weighted Magnetic Resonance Imaging. This detailed “X-ray” of inflammation cannot be obtained with conventional MRI, but requires data acquisition sequences and special mathematical models. Once the method was developed, the researchers were able to quantify the alterations in the morphology of the different cell populations involved in the inflammatory process in the brain.

An innovative strategy developed by the researchers has made possible this important breakthrough, which is published today in the journal Science Advances and which may be crucial to change the course of the study and treatment of neurodegenerative diseases.

The research demonstrates that diffusion-weighted MRI can noninvasively and differentially detect the activation of microglia and astrocytes, two types of cells that are at the basis of neuroinflammation and its progression.

The Stem Cell Reports paper demonstrated the capability to grow and differentiate cortical neurons — known to be responsible for a majority of higher brain function — into fully mature and functional cells.

These neurons were then incorporated into a circuit functioning as a simulated system, where the researchers were able to induce long-term potentiation (LTP). LTP — which allows for memory formation — is a key phenomenon in the study of cognition, and one that has mostly evaded direct observation in human models.


A UCF researcher’s work to create a “brain-on-a-chip” aims to improve neurological disorder research by speeding up drug discovery and providing an alternative to animal testing.

James Hickman — professor of chemistry, biomolecular sciences and electrical engineering — recently published some of his latest findings in the journals Stem Cell Reports and Advanced Therapeutics.

These studies explain advancements in his research group’s efforts to develop the functional neural model otherwise known as a “brain-on-a-chip.” Such a model could revolutionize neurological research by replicating the pathologies of neurological disorders and rare autoimmune neuropathies, without the need for testing on human or animal subjects.

In the early 2000s, scientists from the Human Genome Project announced a breakthrough: they had sequenced the complete human reference genome, including all three billion DNA letter, a scientific undertaking likened at the time to landing astronauts on the Moon.

While the reference genome has come under question as of late, with scientists adding more than two million additional variants, it still doesn’t take a whole lot of space to store the entire sequence on a traditional computer.

And now, Tesla and SpaceX CEO Elon Musk is once again weighing in on an issue outside his expertise, arguing that one could “fit the DNA sequences of all humans alive today in a fairly small data storage system” — a vaguely terrifying thought coming from the richest man in the world, as if he didn’t already have enough fires to put out and problems to solve.

By 2025, the World Economic Forum estimates that 97 million new jobs may emerge as artificial intelligence (AI) changes the nature of work and influences the new division of labor between humans, machines and algorithms. Specifically in banking, a recent McKinsey survey found that AI technologies could deliver up to $1 trillion of additional value each year. AI is continuing its steady rise and starting to have a sweeping impact on the financial services industry, but its potential is still far from fully realized.

The transformative power of AI is already impacting a range of functions in financial services including risk management, personalization, fraud detection and ESG analytics. The problem is that advances in AI are slowed down by a global shortage of workers with the skills and experience in areas such as deep learning, natural language processing and robotic process automation. So with AI technology opening new opportunities, financial services workers are eager to gain the skills they need in order to leverage AI tools and advance their careers.

Today, 87% of employees consider retraining and upskilling options at workplaces very important, and at the same time, more companies ranked upskilling their workforce as a top-5 business priority now than pre-pandemic. Companies that don’t focus on powering AI training will fall behind in a tight hiring market. Below are some key takeaways for business leaders looking to prioritize reskilling efforts at their organization.

Most treatments for strokes aim to help reduce or repair damage to affected neurons. But a new study in mice has shown that a drug already in use to treat certain neurological disorders could help patients recover from strokes by getting undamaged neurons to pick up the slack.

An ischemic stroke occurs when a blood vessel blockage interrupts blood flow to the brain, causing neurons to die off. Survivors can suffer impaired fine motor control and speech, and other disabilities, for which long-term rehabilitation is often required.

Logically, many treatment options in development focus on minimizing or reversing damage to neurons, using things like stem cells, anti-inflammatory drugs, injectable hydrogels, or molecules that convert neighboring cells into neurons.

Most people carry the fungus Candida albicans on their bodies without it causing many problems. However, a systemic infection with this fungus is dangerous and difficult to treat. Few antimicrobials are effective, and drug resistance is increasing. An international group of scientists, including Albert Guskov, associate professor at the University of Groningen, have used single-particle cryogenic electron microscopy to determine the structure of the fungal ribosome. Their results, which were published in Science Advances on 25 May, reveal a potential target for new drugs.

Candida albicans usually causes no problems, or just an itchy skin infection that is easily treated. However, in rare cases, it may cause systemic infections that can be fatal. Existing antifungal drugs cause a lot of side effects and are expensive. Furthermore, C. albicans is becoming more drug-resistant, so there is a real need for new drug targets. “We noted that no antifungal drugs are targeting protein synthesis, while half of the antibacterial drugs interfere with this system,” says Guskov. A reason for this is that fungal ribosomes, the cellular machineries that translate the genetic code into proteins, are very similar in humans and fungi. “So, you would need a very selective drug to avoid killing our own cells.”

In a paper appearing in Nature today, an international group of scientists report a new way to kill hard-to-treat cancers. These tumors resist current immunotherapies, including those using Nobel Prize-winning checkpoint-blocking antibodies.

The approach exploits Z-DNA. Rather than twisting to the right like B-DNA, Z-DNA has a left-handed twist. One role for Z-DNA is to regulate the to viruses. The response involves AADR1 and ZBP1, two proteins that specifically recognize Z-DNA. They do so through a Zα domain that binds to the Z-DNA structure with high affinity.

The Zα domain was originally discovered by Dr. Alan Herbert of InsideOutBio, a communicating author on the paper. The ADAR1 Zα domain turns off the , while the other ZBP1 Zα turns on pathways that kill virally infected , as previously shown by Dr. Sid Balachandran, the other communicating author on the paper. The interactions between ADAR1 and ZBP1 determine whether a cell lives or dies.

𝙏𝙝𝙚 𝙘𝙤𝙣𝙙𝙞𝙩𝙞𝙤𝙣𝙨 𝙘𝙖𝙣 𝙖𝙡𝙡 𝙖𝙛𝙛𝙚𝙘𝙩 𝙩𝙝𝙚 𝙗𝙧𝙖𝙞𝙣, 𝙙𝙖𝙢𝙖𝙜𝙞𝙣𝙜 𝙗𝙡𝙤𝙤𝙙 𝙫𝙚𝙨𝙨𝙚𝙡𝙨 𝙖𝙣𝙙 𝙡𝙚𝙖𝙙𝙞𝙣𝙜 𝙩𝙤 𝙨𝙩𝙧𝙤𝙠𝙚𝙨. 𝘽𝙪𝙩 𝙩𝙝𝙚 𝙘𝙤𝙣𝙣𝙚𝙘𝙩𝙞𝙤𝙣 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 𝙫𝙖𝙨𝙘𝙪𝙡𝙖𝙧 𝙙𝙞𝙨𝙚𝙖𝙨𝙚 𝙞𝙣 𝙩𝙝𝙚 𝙗𝙧𝙖𝙞𝙣 𝙖𝙣𝙙 𝘼𝙡𝙯𝙝𝙚𝙞𝙢𝙚𝙧’𝙨 𝙝𝙖𝙨 𝙧𝙚𝙢𝙖𝙞𝙣𝙚𝙙 𝙪𝙣𝙚𝙭𝙥𝙡𝙖𝙞𝙣𝙚𝙙 𝙙𝙚𝙨𝙥𝙞𝙩𝙚 𝙩𝙝𝙚 𝙞𝙣𝙩𝙚𝙣𝙨𝙚 𝙚𝙛𝙛𝙤𝙧𝙩𝙨 𝙤𝙛 … See more.

The Neuro-Network.

𝐑𝐞𝐬𝐞𝐚𝐫𝐜𝐡𝐞𝐫𝐬 𝐦𝐚𝐲 𝐡𝐚𝐯𝐞 𝐟𝐨𝐮𝐧𝐝 𝐭𝐡𝐞 𝐦𝐢𝐬𝐬𝐢𝐧𝐠 𝐥𝐢𝐧𝐤 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐀𝐥𝐳𝐡𝐞𝐢𝐦𝐞𝐫’𝐬 𝐚𝐧𝐝 𝐯𝐚𝐬𝐜𝐮𝐥𝐚𝐫 𝐝𝐢𝐬𝐞𝐚𝐬𝐞

𝙁𝙤𝙧 𝙢𝙤𝙧𝙚 𝙩𝙝𝙖𝙣 20 𝙮𝙚𝙖𝙧𝙨, 𝙨𝙘𝙞𝙚𝙣𝙩𝙞𝙨𝙩𝙨 𝙝𝙖𝙫𝙚 𝙠𝙣𝙤𝙬𝙣 𝙩𝙝𝙖𝙩 𝙥𝙚𝙤𝙥𝙡𝙚 𝙬𝙞𝙩𝙝 𝙝𝙮𝙥𝙚𝙧𝙩𝙚𝙣𝙨𝙞𝙤𝙣… See more.


For more than 20 years, scientists have known that people with hypertension, diabetes, high cholesterol, or obesity have a higher likelihood of developing Alzheimer’s disease.

The conditions can all affect the , damaging blood vessels and leading to strokes. But the connection between vascular disease in the brain and Alzheimer’s has remained unexplained despite the intense efforts of researchers.