Artificial neurons which could be implanted in the brain to repair the damage caused by Alzheimer’s disease or other neurodegenerative conditions, have been invented by scientists.

The electronic cells, developed by teams at the University of Bath and a team of international collaborators, sit on a silicon chip and mimic the responses of biological neurons when triggered by the nervous system.

Neurons are specialised cells which transmit nerve impulses, allowing parts of the body to communicate, and are the core components of the brain, spinal cord and nervous system. They are also present around the heart.

Artificial neurons on silicon chips that behave just like the real thing have been invented by scientists—a first-of-its-kind achievement with enormous scope for medical devices to cure chronic diseases, such as heart failure, Alzheimer’s, and other diseases of neuronal degeneration.

Critically the artificial neurons not only behave just like biological neurons but only need one billionth the power of a microprocessor, making them ideally suited for use in medical implants and other bio-electronic devices.

The research team, led by the University of Bath and including researchers from the Universities of Bristol, Zurich and Auckland, describe the artificial neurons in a study published in Nature Communications.

Researchers have long known that some genes can cause cancer when overactive, but exactly what happens inside the cell nucleus when the cancer grows has so far remained enigmatic. Now, researchers at Karolinska Institutet in Sweden have found a new mechanism that renders one canonical driver of cancer overactive. The findings, published in Nature Genetics, create conditions for brand new strategies to fight cancer.

One gene that is called MYC is central for normal cell growth. However, if the gene mutates and/or becomes overactive, it could lead to abnormal cell growth and cancer. It is previously known that so-called super-enhancers, large regions in the DNA that develop near cancer genes, could somehow make the MYC gene overactive.

The current study increases our understanding of how this process takes place by highlighting how environmental cues can conspire with the architecture of the cell nucleus to cause overexpression. With the help of new laboratory techniques and computer models, the researchers show how the activation of the pathway of the signal-molecule WNT charges the super-enhancer with proteins that lures the MYC gene to the cell nucleus pores. The pores are situated on the membrane of the cell nucleus and control the flow of information between the cell nucleus and the cytoplasm.