Research & University News

The European Commission is to allocate more than €2 billion for the final two years of an experimental programme intended to nurture entrepreneurs and start-up companies across Europe.

A study of circadian rhythms in human fat have shown that fat cells have their own internal clocks which affect critical metabolic functions. This goes some way towards explaining how a misalignment of these rhythms with each other and the environment can contribute to obesity and poor health, according to a research group from the University of Surrey, UK.

Cellular senescence, or the process by which normal cells stop dividing in response to stress or damage to their DNA, can be both beneficial and harmful. It can be beneficial in assisting wound-healing and preventing the excessive growth seen in cancers. On the other hand, it can drive ageing and age-related diseases by changing the tissue environment. This happens when the senescent cells trigger a cascade of chemical signals that cause inflammation and damage to local cells and tissue. This cascade is known as the senescence-associated secretory phenotype (SASP).

The Innovative Medicines Initiative (IMI) has launched a call for proposals from the scientific community to help it create a large chemogenomics library for drug discovery, access to which would be unrestricted.

The project is one of three announced on 22 January which will have a budget of more than €80 million. The other two projects are on obesity and the environmental impacts of medicines. The library project is directed at the wider academic community, many of whom do not have access to proprietary tool compounds collected by industry.

A team of scientists at the VIB research institute and KU Leuven in Belgium has discovered that an amyloid-beta precursor protein, APP, modulates neuronal signal transmission by binding to a specific receptor called GABA_BR1a. This has implications for treating Alzheimer’s disease and probably other disorders.

Alzheimer’s-affected brains are clogged with amyloid-beta plaques. These fragments are produced from a precursor protein whose normal function has remained unclear for decades. 

Scientists at the University of Cambridge have identified mechanisms by which mutations in the ATM gene can lead to cancer drug resistance and how this can be counteracted by changes in other genes. The findings, reported on 8 January 2019 in Nature Communications, show how cells respond to DNA damage as well as highlight potential therapeutic targets for the genetic disease, ataxia-telangiectasia (A-T).

A Chinese scientist’s reported use of the Crispr gene editing tool to alter a gene in two  embryos which were implanted into a mother’s womb has created an uproar in the scientific community. The edit was performed when the embryos were just a day old and involved alterations to the CCR5 gene in order to prevent the offspring from contracting HIV. They were reported on YouTube videos, rather in a scientific journal, after twin girls bearing the DNA changes were born.

Two scientists who identified proteins which act as a break on the immune system have been awarded the 2018 Nobel Prize in Physiology or Medicine for their discovery, which is the scientific basis for the ‘immune checkpoint’ class of medicines. James P. Allison, who discovered CTLA-4, and Tasuku Honjo, who discovered PD-1, were cited by the Nobel Assembly at Karolinska Institutet for their landmark work in the global fight against cancer. Both proteins can prevent the immune system from recognising cancer cells.

Scientists from University College London have identified a second source of endothelial cells that line the interior of blood vessels, potentially opening up a path for exploring the use of stem cells to grow new blood vessels and repair damaged ones.

A study published in the journal Science on 7 September 2018 gives new insights into how exercise can improve memory and possibly help prevent or treat Alzheimer’s disease. The corollary is that pharmaceutical treatments might be designed to mimic this effect.