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Tuesday, October 10, 2017, is National “Dys” Day (dyslexia, dysphasia, dysorthographia, etc.)

©Inserm

The 11th edition of National “Dys” Day will be held on Tuesday, October 10, 2017. Created by the Fédération Française des DYS, it mobilizes parents who are members of associations together with professionals from across France. The various learning disabilities that begin with “dys”, and which are now better understood by the general public, affect around 6 million people in France [1](METTRE CHIFFRE). An event is held in Paris each year, attended by around 10,000 people. This year, it will take place on Saturday, October 14, 2017, from 9 a.m. to 6 p.m., at Université Paris 8.

There are five main learning disabilities: dyslexia, dyspraxia, dyscalculia, dysphasia, and the attention disorders. Dyslexia, dyspraxia and dysphasia are the most common. In cases in which these difficulties persist, solutions can be envisaged to improve and/or compensate the impaired functions.

* Dyslexia

Dyslexia is the poor association between graphemes (written characters) and phonemes (sounds). It also involves the inability to quickly grasp a word in its entirety, meaning that the person deconstructs the words slowly and makes mistakes. That is why dyslexia is very often confused with dysorthographia.

In 2015, Inserm showcased a solution proposed by an Inserm team, which involves correcting dyslexia with the help of music. Since music and language are processed in the same part of the brain, a relationship has been established.

To learn more, consult our article : “Corriger la dyslexie en rythme” [Correcting dyslexia in rhythm (in French)]

One cause of dyslexia could be a visual attention disorder. A team of Inserm researchers is studying this hypothesis, which has been partially confirmed.

To learn more, consult our article : “La dyslexie pourrait être liée à un problème d’attention” [Dyslexia could also be related to an attention disorder (in French)]

Read our press release : “Une seule anomalie à l’origine des trois manifestations principales de la dyslexie” [Just one abnormality responsible for the three main signs of dyslexia (in French)]

* Dyspraxia

Dyspraxia is the difficulty to program, plan and coordinate complex movements, which prevent sufferers from automatizing a large number of voluntary movements, such as writing, and thus leading to dysgraphia.

Caroline Huron, researcher at Inserm Unit 992 Cognitive Neuroimaging, is also president of the association Cartable Fantastique, founded in 2010. This association combines the expertise of researchers in cognitive sciences with that of teachers to facilitate the schooling of children with dyspraxia. As part of a partnership with the French Ministry of National Education, a bank of language study exercises, Les Fantastiques Exercices, intended for elementary school pupils, has been made available to everyone. These exercises have been created in a digital format to meet the specific needs of dyspraxic pupils and then adapted on paper for the other members of the class, so that everyone can do the same exercise at the same time.

* Dysphasia

Dysphasia represents a verbal language development disorder, i.e. difficulty with verbal expression (indistinct words, syntax disorders, poorly constructed words…). Dyslexia very often appears in the wake of this disorder.

For more information, consult our report : “Troubles des apprentissages : les troubles “dys”” [Learning disabilities: the various “dys’s” (in French)]

 

[1]Source: www.ffdys.com

Colon cancer: APC protein affects immunity by preventing pre-cancerous inflammation

Immune system attack on a tumor. Left-hand image: in mice, when certain immune system killer cells (T lymphocytes, in red) are injected in the bloodstream they enter the tumor (in yellow). Right-hand image: after a few days the killer cells have destroyed the cancer cells, as observed in this model.
© Institut Pasteur

Adenomatous polyposis coli (APC) is a gene whose mutations are associated with a rare, hereditary form of colorectal cancer known as familial adenomatous polyposis. Research led by scientists at the Institut Pasteur and Inserm have recently demonstrated that mutations to this gene do not only lead to the emergence of colon polyps; they also harm the immune system, leaving it unable to tackle inflammation of the colonic mucosa. This dual impact supports the development of cancer. The finding, published in the journal Cell Reports on October 3rd, 2017, advances scientific knowledge on the development mechanisms of colorectal cancer.

Familial adenomatous polyposis is an inherited condition characterized, from puberty, by the formation of a very large number of polyps, small growths on the inner surface of the colon and the rectum which can develop into tumors. If left untreated, these polyps may result in colorectal cancer before the age of 40.

Colon cancer is one of the most deadly forms of cancer, and familial adenomatous polyposis currently represents 1% of all cases of colorectal cancer. Those affected by this hereditary disease therefore need close medical supervision.

Research led by scientists from the Institut Pasteur and Inserm recently demonstrated that mutations in the adenomatous polyposis coli (APC) gene, known to be involved in familial adenomatous polyposis, do not only lead to the emergence of colon polyps; they also harm the immune system, leaving it unable to tackle inflammation of the colonic mucosa. This dual impact may favor the development of cancer.

As Andrés Alcover, Head of the Lymphocyte Cell Biology Unit at the Institut Pasteur and last author of the paper, explains, “the APC protein, associated with the microtubule cytoskeleton, has a major effect on the structure and differentiation of intestinal epithelial cells. By disrupting these functions in intestinal cells, APC mutations can lead to the development of tumors.” 

Scientists already knew that APC mutations could influence the immune system, but they had not yet identified the molecular mechanisms involved and the link with colorectal cancer development. The teams of scientists elucidated how the APC protein activates a particular type of immune cell known as T lymphocytes. “The protein activates T lymphocytes using a factor known as NFAT[1],” continues Andrés Alcover. “Polyposis patients have a mutant version of the gene, which leads to a deficiency in APC protein and could reduce the presence of NFAT in cell nuclei” – thereby preventing lymphocyte activation.

Human T lymphocytes expressing or lacking APC. Lack of APC impairs microtubule cytoskeleton organization (green filaments). © Institut Pasteur

One family of T lymphocytes, known as regulatory T cells, is particularly sensitive to APC mutations. The scientists observed a dysfunction in these regulatory T cells – which are present in large numbers in the intestine – in mice with these mutations that are predisposed to develop polyposis like the patients. This dysfunction leads to a deregulation of the immune system in the intestine and a failure to control local inflammation. “This is the first time that we have characterized at molecular level how mutations in the APC protein affect the immune system, creating favorable conditions for cancer development,” emphasizes Andrés Alcover.

These findings suggest that mutations in the APC gene play a dual role in the development of colorectal cancer. Not only do they trigger the development of polyps; they also reduce the action of the immune system, preventing it from controlling gut inflammation. This vicious circle supports the development of cancer.

It remains to be seen whether defects in the APC protein in patients with familial adenomatous polyposis have consequences for the other cells in the immune system, especially those that directly eliminate cancer cells. If so, this research might pave the way for the development of new therapies to improve the efficacy of treatment for patients with familial adenomatous polyposis or other forms of intestinal cancer.


 [1] NFAT: nuclear factor of activated T cells.

This project was funded by the ARC Foundation for Cancer Research, the Institut Pasteur, Inserm, the ANR, NIDDK-USA and the People Programme (Marie Skłodowska-Curie Actions) of the European Union’s Seventh Framework Programme FP7/2007-2013/ under REA grant agreement no. 317057 HOMIN-ITN.

2017 Nobel Prize in Medicine

On Monday, October 2, three Americans, Jeffrey C. HallMichael Rosbash and Michael W. Young, were awarded the 2017 Nobel Prize in Physiology or Medicine for their research on the control of circadian rhythms.

A field which is also being studied by researchers from Inserm:

Claude Gronfier, Inserm researcher and chronobiologist, Stem-cell and Brain Research Institute, Lyon

Howard Cooper, Research Director, Stem-cell and Brain Research Institute, Lyon

Joëlle Adrien, Inserm Research Director, Brain & Spine Institute, Paris

Franck Delaunay, Inserm Researcher, Institute of Biology Valrose

Press releases:

Dimly lit working environments: correcting your body clock is possible!

Men and women have different clocks…

 

Further reading:

  • Health and Research From A-Z:Chronobiologie, les 24 heures chrono de l’organisme” [Chronobiology, the body’s 24-hour clock (in French)]
  • Watch the POM Bio à croquer video (in French) on Light and rhythms: Researchers are beginning to discover how the blue light emitted by LEDs, computer screens and smartphones impacts our health. This light affects a specific region of the brain responsible for regulating our biological rhythms, explains Claude Gronfier, chronobiologist at Laboratory U846 “Stem-cell and Brain Research Institute”.
  • Watch the POM Bio à croquer video (in French) on Sleep and metabolism: Sleep is not just for rest. It is essential for the proper functioning of the immune, hormone and cardiovascular systems, among others. Adolescents often present a large sleep debt. What are the effects on their health? Explanations with Claude Gronfier, chronobiologist at Laboratory U846 “Stem-cell and Brain Research Institute”.
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