2 de Setembro de 2024

 
 

EARA News Digest 2024 - Week 36


Welcome to your Monday morning update, from EARA, on the latest news in biomedical science, policy and openness on animal research. 

This week: New Alzheimer's drug & animal studiesWound healing using roundwormsHuntington's organoid study

New Alzheimer’s drug - the role of animal studies

A first-of-its-kind Alzheimer’s drug that slows cognitive decline in early-stage patients, that was developed using animal research, has now been licensed for use around the world, including China, Japan, USA and most recently in the UK.

Lecanemab is the first Alzheimer’s drug that directly targets aspects of the disease itself, rather than just the symptoms. It works by removing an abnormal build-up of beta-amyloid proteins in the brain, which have been implicated in Alzheimer's.

The drug, an antibody derived from mice, highlights the long-standing role of animal research in its development and approval.

Before being tested in humans, studies in mice showed that lecanemab could work by reaching the brain, specifically binding to beta-amyloid and successfully protecting neurons.

As a humanised mouse antibody – that is made to be more ‘human-like’ so it does not trigger an immune reaction in people – lecanemab can recognise and bind to the amyloid proteins in human patients.

One clinical trial showed that it reduced beta-amyloid levels and slowed cognitive decline by 27%.

It was also originally thanks to studying genetically modified mice, that researchers first understood the toxic effect that beta-amyloid can have in Alzheimer’s disease.

The UK Alzheimer’s Society said in a recent statement that the drug approval was 'a defining moment for people with early-stage Alzheimer’s disease in the UK and a significant step towards a more hopeful future'.

 

 

Healing wounds with roundworms

Proteins produced by parasitic roundworms could offer a better way to heal skin wounds without leaving scars, a new US study has found.

Research at Rutgers University, New Jersey, and also involving the University of Glasgow, UK, investigated the theory that molecules secreted externally by these worms may help with regenerating tissue, by controlling either the immune cells that promote healing, or those that promote scarring.

To test this, the team purified a protein produced by a specific roundworm (Heligmosomoides polygyrus) found in the intestines of mice.

When the protein was applied daily to skin wounds on mice - over 12 days - the animals showed a growth of collagen (a core component of skin) similar to normal, unwounded skin, compared to mice who were not given the treatment, where more scarring occurred.

William Gause, at Rutgers, said: “It provides a significant framework for the potential use of an easy-to-produce parasite protein as a therapy to promote cutaneous [skin] wound healing.”

 

 

New gene target for Huntington’s treatment?

Using 3D brain organoids, researchers have linked a gene with Huntington’s disease for the first time, which may provide a new target for treatment.

Huntington’s is an incurable neurodegenerative disorder that affects movement, thinking ability and mental health. It is caused by mutations in the HTT gene, which leads to the progressive death of nerve cells in the brain.

In the study, led by EARA member the Max Delbrück Center, Berlin, and Heinrich Heine University (HHU), Dusseldorf, both in Germany, researchers used CRISPR-Cas9 gene editing to make genetic changes to healthy human stem cells, resembling the HTT mutations seen in Huntington’s.

As stem cells are able to develop into any type of cell, the edited stem cells could then be grown into brain organoids that resemble aspects of the early-stage brain.

Analysing the organoids at different developmental stages showed there were lower levels of a particular gene (CHCHD2), which hampered how the nerve cells carried out vital chemical reactions in the brain.

Selene Lickfett, at HHU, discussed whether this effect could be reversed by restoring CHCHD2: “It suggests in principle that this gene could be a target for future therapies.

“The organoid model suggests that HTT mutations damage brain development even before clinical symptoms appear.”

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