04 - 25 - 2017
How is our sense of smell built?
Our sense of smell is very complex. Some have calculated that our olfactory tissue could discriminate millions of olfactory substances, which, our brain is not able to do: the best noses recognize only a few thousand odours.
Researchers are curious to know whether the olfactory tissue takes into account its environment, have discovered thanks to genetically identical mice that olfactory stimuli of the environment significantly influence the construction of the olfactory tissue. This means that the olfactory tissue is an image not only of the genes but also of the history of each individual.
04 - 25 - 2017
Mice to understand ALS
Amyotrophic lateral sclerosis is a degeneration of the motor neurons which leads to the weakening and then hardening of the muscles. The most severe form is due to a mutation of the gene coding for a regulatory neuronal protein called FUS. The "Delocalization" of this protein from the nucleus to the cytoplasm could cause the death of motoneurons.
In order to reinforce this hypothesis, two mouse models have been developed which show either an absence or an accumulation of the FUS protein in the cytoplasm. When the protein is present in the cytoplasm, mice have motor neuron deficiency.
These results confirm that the accumulation of FUS in the cytoplasm leads to the death of motor neurons and paves the way for novel treatments against ALS that would inhibit FUS activity in the cytoplasm
04 - 24 - 2017
Multiple sclerosis: preventing neuronal death?
Multiple sclerosis (MS) is an autoimmune disease that targets the nervous system and causes severe disabilities. Current treatments are insufficient.
Many research teams around the world are trying to find new therapeutic solutions. One of these teams is trying to identify the mechanisms that causes the death of neurons. Using patient tissues’ and an animal model (mouse) they demonstrated the role of the Rab32 protein. It appears during the acute and chronic phases of MS and is capable of causing neuronal death.
Researchers will now investigate whether the inhibition of this protein can preserve in vivo the loss of neurons.
04 - 20 - 2017
News for the treatment of hepatic encephalopathy
Hepatic encephalopathy occurs when the liver fails to eliminate the ammonia produced by the intestinal bacteria. It is a complication of cirrhosis that causes neurological disorders such as confusion or even coma.
One study looking at twenty patients for five months ago, showed that fecal transplants improved the bacterial flora and corrected cognitive dysfunction. With these good results, the studies will continue.
The same team had verified two years ago in a mouse model, the importance of fecal microbiota transplants to treat hepatic encephalopathy.
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