Toggle light / dark theme

A study by the University of the Basque Country (UPV/EHU) demonstrates that the drug WIN55,212–2 protects the brain and reverses early cognitive damage caused by dementia, while also explaining its mechanism of action.

Over two decades of research conducted by the Neurochemistry and Neurodegeneration group at UPV/EHU, led by Dr. Rafael Rodríguez-Puertas, has uncovered a promising pathway for developing therapies aimed at improving memory in cases of cognitive impairment caused by neurodegenerative diseases like Alzheimer’s.

Alzheimer’s disease is a progressive neurological disorder that primarily affects older adults, leading to memory loss, cognitive decline, and behavioral changes. It is the most common cause of dementia. The disease is characterized by the buildup of amyloid plaques and tau tangles in the brain, which disrupt cell function and communication. There is currently no cure, and treatments focus on managing symptoms and improving quality of life.

A research team at KAIST has identified the core gene expression networks regulated by key proteins that fundamentally drive phenomena such as cancer development, metastasis, tissue differentiation from stem cells, and neural activation processes. This discovery lays the foundation for developing innovative therapeutic technologies.

A joint research team led by Professors Seyun Kim, Gwangrog Lee, and Won-Ki Cho from the Department of Biological Sciences has uncovered essential mechanisms controlling gene expression in animal cells.

The findings were published on January 7 in the journal Nucleic Acids Research in a paper titled “Single-molecule analysis reveals that IPMK enhances the DNA-binding activity of the transcription factor SRF.”

In the first study of its kind at the Large Hadron Collider (LHC), the CMS collaboration has tested whether top quarks adhere to Einstein’s special theory of relativity. The research is published in the journal Physics Letters B.

Along with , Einstein’s special theory of relativity serves as the basis of the Standard Model of particle physics. At its heart is a concept called Lorentz symmetry: experimental results are independent of the orientation or the speed of the experiment with which they are taken.

Special relativity has stood the test of time. However, some theories, including particular models of string theory, predict that, at very high energies, special relativity will no longer work and experimental observations will depend on the orientation of the experiment in space-time.

Cancer cells need to acquire a different metabolic state than that of non-tumor cells in order to proliferate, invade, and metastasize. During cancer progression, cancer cells encounter various kinds of metabolic stress. First, tumor microenvironments are generally hypoxic and acidic and have a distinct nutrient composition compared to non-tumor tissues from the primary site, which forces cancer cells to adapt in order to grow and invade in these environments. Second, to enter and survive in vessels, cancer cells must reprogram their metabolic state, allowing for anchorage-independent growth that induces extensive oxidative stress in cancer cells. Finally, once cancer cells colonize other organs, they must adapt to quite distinct metabolic environments than those present in primary sites [1]. Overall, because cancer cells need to reprogram their metabolic state during each step of cancer progression, metabolic reprogramming has been recognized as one of the hallmarks of cancer [2].

Elucidating the mechanisms underlying metabolic reprogramming during cancer progression can reveal the metabolic vulnerabilities of cancer cells. This may ultimately result in the identification of new therapeutic targets for cancer and improvement of patients’ prognosis. In this review, we describe each step of the metabolic reprogramming that occurs in cancer cells during cancer progression, including during growth and invasion in primary sites, survival in vessels, and colonization of other organs. Finally, we also describe emerging therapeutic strategies that target cancer-specific metabolism.

Researchers outline a bold strategy to scale neuromorphic computing, aiming to match human brain functionality with minimal energy use.

This involves developing advanced neuromorphic chips and fostering strong industry-academic partnerships, potentially transforming AI and healthcare through improved efficiency and capability.

Scaling Up Neuromorphic Computing

In today’s AI news, Mark Zuckerberg announced a huge leap in Meta Platforms’s capital spending this year to between $60 billion to $65 billion, an increase driven by artificial intelligence and a massive new data center.

Zuckerberg plans to increase the company’s capital expenditures by as much as roughly 70% over 2024.

In other advancements, Hugging Face has achieved a remarkable breakthrough in AI, introducing vision-language models that run on devices as small as smartphones while outperforming their predecessors that require massive data centers. The company’s new SmolVLM-256M model, requiring less than one gigabyte of GPU memory, surpasses the performance of its Idefics 80B model from just 17 months ago — a system 300 times larger.

And, Anthropic has launched a new feature for its “Claude” family of AI models, one that enables the models to cite and link back to sources when answering questions about uploaded documents. The new feature, appropriately dubbed “Citations,” is now available for developers through Anthropic’s API.

Meanwhile, can AI agents reliably click on all images showing motorcycles or traffic lights for us? It might be too early to tell, considering that a robot will essentially have to tell a website that it is not a robot. However, it looks like at least one of OpenAI’s Operator users was able to have the AI agent beat CAPTCHAs for him.

Whether we are ready or not, neuro-tech is about to cause a radical social shift that will change our understanding of the mind and our very conception of reality. Telepathy, or even a super humanity based on a symbiotic relationship with artificial intelligence, will no longer be a dream.

This documentary revisits the history of neuroscience and explores the frontiers of this groundbreaking field. It introduces technological advancements that come with catastrophic risks, which is why experts are advocating for the Neuro-Rights — regulations that ensure the privacy of our conscious AND subconscious.
——

Chapters.
▷ 00:00 – Intro.
▷ 03:02 – The enigma of human brain.
▷ 07:36 – Why neuroscience.
▷ 10:27 – Merging with the digital.
▷ 12:53 – Neuro-Revolutions: the 90s to today.
▷ 15:50 – From lab to real world (\.

Can a file be stored on DNA? What would be the advantages of such storage? And what developments can we expect in the future? All these answers in 12 minutes!

0:00 — Introduction.
2:00 — Inspiration from life, DNA
3:24 — Storing files.
7:35 — A technology under development.
10:51 — Conclusion.

Video produced for EchoSciences Sud Provence-Alpes-Côte d’Azur https://www.echosciences-paca.fr with CNRS research director Marc Antonini (I3S — CNRS/UCA). Based on an original idea by Play Azur Prod. Video coordinated by Gulliver https://www.gulliver-sciences.fr and Play Azur Prod: https://playazur-prod.fr/

Calculations and sources of the figures :

The core components of CRISPR-based genome-editing therapies are bacterial proteins called nucleases that can stimulate unwanted immune responses in people, increasing the chances of side effects and making these therapies potentially less effective.

Researchers at the Broad Institute of MIT and Harvard and Cyrus Biotechnology have now engineered two CRISPR nucleases, Cas9 and Cas12, to mask them from the immune system. The team identified protein sequences on each nuclease that trigger the immune system and used computational modeling to design new versions that evade immune recognition. The engineered enzymes had similar gene-editing efficiency and reduced immune responses compared to standard nucleases in mice.

Appearing today in Nature Communications, the findings could help pave the way for safer, more efficient gene therapies. The study was led by Feng Zhang, a core institute member at the Broad and an Investigator at the McGovern Institute for Brain Research at MIT.