This week in animal research 02/12/16

2 December 2016

Posted by: UAR news team

Category: Research & medical benefits

This week in animal research 2 Dec 2016

Parkinson's disease 'may start in gut'

The big story of the week - scientists in California say they have transformed understanding of Parkinson's disease.

Their animal experiments, published in the journal Cell, suggest the brain disorder may be caused by bacteria living in the gut.

The findings could eventually lead to new ways of treating the disease, such as drugs to kill gut bugs or probiotics.

Researchers used mice genetically programmed to develop Parkinson's as they produced very high levels of the protein alpha-synuclein, which is associated with damage in the brains of Parkinson's patients.

But only those animals with bacteria in their stomachs developed symptoms. Sterile mice remained healthy.

Further tests showed transplanting bacteria from Parkinson's patients to mice led to more symptoms than bacteria taken from healthy people.

http://www.cell.com/cell/fulltext/S0092-8674%2816%2931590-2

http://www.bbc.co.uk/news/health-38173287

https://www.newscientist.com/article/mg23231024-100-parkinsons-disease-may-start-in-the-gut-and-travel-to-the-brain/

CRISPR used to treat haemophilia in mice

CRISPR/Cas9, a powerful genome editing tool, is showing promise for efficient correction of disease-causing mutations. For the first time, researchers from the Perelman School of Medicine at the University of Pennsylvania have developed a dual gene therapy approach to deliver key components of a CRISPR/Cas9-mediated gene targeting system to mice to treat haemophilia B.

https://www.alnmag.com/news/2016/12/scientists-use-crispr-first-time-correct-clotting-newborn-and-adult-mice

New life, new epigenetics
 
“Using fertilized mouse eggs, we showed that the egg cell actively triggers demethylation of the paternal DNA – in other words, it initiates epigenetic reprogramming by stripping any previous epigenetic memory passed on from the father. This allows the zygote to start afresh and create its own epigenetic memory and life history. This process is not without risks: demethylation can cause lesions in the DNA that can be fatal for the new organism. It is known that these lesions can lead to chromosome fragmentation, embryo loss or infertility.”

“A surveillance mechanism ensures repair of DNA lesions during zygotic reprogramming”, Ladstätter, Tachibana-Konwalski, Cell: http://dx.doi.org/10.1016/j.cell.2016.11.009

Tweaking muscle regeneration in old age

The development of the embryo during pregnancy is one of the most complex processes in life. Genes are strongly activated, and developmental pathways must do their job in a highly accurate and precisely timed manner. So-called Hox-genes play an important regulatory role in this process.

Although remaining detectable in stem cells of adult tissues throughout life, after birth they are only rarely active. Now, however, researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany have shown that, in old age, one of these Hox-genes (Hoxa9) is strongly re-activated in murine muscle stem cells after injury; leading to a decline in the regenerative capacity of skeletal muscle.

Interestingly, when this faulty gene re-activation was inhibited by chemical compounds, muscle regeneration was improved in aging mice, thus suggesting novel therapeutic approaches aimed at improving muscle regeneration in old age.

Epigenetic stress responses induce muscle stem cell aging by Hoxa9 developmental signals. Nature 2016 (in press). Doi: 10.1038/nature20603.

New diabetes treatment from platypus?

Scientists have found the same hormone produced in the gut of the platypus and the echidna to regulate blood glucose is also surprisingly produced in their venom. The same hormone may pave the way for the treatment of diabetes in humans, they believe.

http://www.telegraph.co.uk/news/2016/12/01/platypus-echidna-venom-may-hold-key-new-diabetes-medication/

http://www.nature.com/articles/srep37744