Prefer natural light to avoid age-related sleep disorders

© Adobe stock

One in three French adults is thought to have a sleep disorder. While the prevalence of these disorders increases with age, the biological mechanisms at play are relatively unknown, leaving scientists in doubt as to their origin. In a new study, Inserm researcher Claude Gronfier and his team at the Lyon Neuroscience Research Center (Inserm/CNRS/Université Claude-Bernard Lyon 1) hypothesised that their onset during ageing was linked to a desynchronisation of the biological clock caused by decreased light perception. In the course of their research, they identified a new adaptive mechanism of the retina during ageing that enables older individuals[1] to remain sensitive to light. These findings are also of clinical relevance in encouraging older people to have more exposure to daylight, rather than artificial light, to avoid developing sleep disorders. These results have been published in the Journal of Pineal Research.

Almost all biological functions are subject to the circadian rhythm, which is a 24-hour cycle. The secretion of the night hormone melatonin is typically circadian. Its production increases at the end of the day shortly before bedtime, helping us to fall asleep, and falls before we wake up.

Previous studies have shown that its secretion by the brain is blocked by light, to which it is very sensitive. This sensitivity to light can manifest as desynchronisation of the circadian clock, which can lead to sleep disorders. Other studies have also revealed the important role, in the control of melatonin production, of melanopsin – a photoreceptor present in certain cells of the retina which, being highly sensitive to light (mainly blue light), regulates pupillary reflex and circadian rhythm. Therefore, when exposed to light, melanopsin becomes a driver of melatonin suppression and biological clock synchronisation.

While sleep disorders are already common in adults, they increase with age: nearly one third of people over 65 chronically consume sleeping pills[2]. Yet there are no previous studies specifically focusing on the biological mechanism at work in age-related sleep disorders. Are we talking about the consequence of a problem of light perception? If so, at what level? And what is the role of melanopsin in this specific case?

A team at the Lyon Neuroscience Research Center tried to elucidate this mystery. The scientists observed the effects of light on melatonin secretion in a group of adults. The participants were all exposed to 9 different coloured lights (corresponding to 9 very precise wavelengths) to enable the scientists to identify the mechanisms involved via the photoreceptors concerned.

The participants were divided into two distinct groups, with mean ages of 25 and 59. This experiment was performed in the middle of the night, when the body normally releases the most melatonin.

The results show that, out of the lights tested, blue light (with a wavelength of approximately 480 nm) is very effective in suppressing melatonin production in the youngest individuals. More specifically, the scientists observed that in the young subjects exposed to blue light, melanopsin was the only photoreceptor driving melatonin suppression. Conversely, in the older participants, photoreceptors other than melanopsin appear to be involved, such as the S and M cones – photoreceptors that enable the world to be perceived in colour, and which are located in the outer retina.

These data suggest that while ageing is accompanied by decreased melanopsin involvement in visual perception, the retina is able to compensate for this loss through an increase in the sensitivity of other photoreceptors that were previously not known to be involved in melatonin suppression.

These observations enable the scientists to conclude that light perception – and light requirements – change with age.

While for young people, in whom only the melanopsin receptor is involved, exposure to blue light[3] is sufficient to synchronise their circadian clock over a 24-hour day, older people require exposure to light that is richer in wavelengths (colours) – a light whose characteristics are those of sunlight.

‘This is the discovery of a new adaptive mechanism of the retina during ageing – enabling older subjects to remain sensitive to light despite yellowing of the lens. These findings are also clinically relevant, encouraging older people to have more exposure to daylight, which is richer in wavelengths, rather than artificial light, in order to avoid developing sleep disturbances or mood or metabolism disorders, for example. Finally, they offer new possibilities for the optimal personalisation of phototherapies/light therapies for older people‘, explains Claude Gronfier, Inserm researcher and last author of the study.

Regarding this last aspect, the research team is now looking at the quantity and quality of light necessary for each individual, and the best time for light exposure during the day, to prevent the development of sleep disorders and health problems more generally.

The research is being conducted in healthy subjects (children and adults), day and night workers, and patients (with sleep and biological rhythm disorders, genetic diseases, mood disorders and neurodegeneration)[4].


[1]In this study, the average age of the participants in the ‘older’ group was 59 years.


[3] The LED lights used are rich in blue light.


Defeating leukaemia cells by depriving them of energy

Cellules leucémiques

Selective activation of the AMPK enzyme would lead to the death of leukaemia cells (in purple in this image). © Jérôme Tamburini / UNIGE High resolution pictures

A Swiss-French team that includes UNIGE scientists has discovered how to trigger apoptosis in leukaemia cells by disrupting their energy maintenance mechanism.

Acute myeloid leukaemia, which affects blood and bone marrow cells, is a particularly dangerous form of cancer. More than half of patients under the age of 60 die. This proportion rises to 85% for patients over 60. A team from the University of Geneva (UNIGE), Switzerland, and from Inserm 1, in France, have identified a previously unknown mechanism that could lead to the development of new therapies. The selective activation of AMPK, a key enzyme in the energy balance of tumour cells, would indeed lead to their death by triggering the cells stress response. Moreover, the scientists have successfully exploited this energy gap in an animal model of the disease: a combination of two drugs — one of which is already on the market — has indeed shown promise. However, their effectiveness has yet to be confirmed on leukaemia stem cells, which have the ability to escape many treatments to restart tumour growth. These results can be found in the journal Cell Reports.

Jérôme Tamburini, an associate professor in the Department of Medicine and in the Translational Research Centre in Onco- Haematology (CRTOH) of UNIGE Faculty of Medicine and at the Swiss Cancer Center Léman (SCCL) and a professor at Université de Paris, is working on the energetic mechanisms of tumour cells in acute myeloid leukaemia. A cell signalling pathway called AMPK is of particular interest to him. “AMPK is the main detector of the cells energy level”, explains Jérôme Tamburini. “This pathway is activated when energy is lacking and initiates the degradation of certain nutrients to produce the necessary energy – a process called catabolism. As without energy, no cell can survive, could it be possible to selectively manipulate this mechanism in tumour cells to cause their destruction, while preserving healthy cells?” In 2015, Jérôme Tamburini and his colleagues at Inserm in Paris participated in the development with the GlaxoSmithKline (GSK) laboratory of a pharmacological component — GSK621 — which proved to be an excellent activator of AMPK in vitro. “After this initial proof of principle, we had to decipher the biochemical mechanisms at work in order to understand them in detail, and in particular which cellular pathways did GSK621 activate in leukaemia cells, the first step in hoping to exploit this phenomenon for therapeutic purposes,” explains Jérôme Tamburini.

An effective combination of two drugs

The first step was to perform a gene expression analysis of human tumour cells, which identified an enzyme, PERK, particularly activated in response to the presence of GSK621.This is a key element in the stress response of the endoplasmic reticulum, an intracellular structure specialised in the metabolism of proteins and lipids. “The activation of AMPK thus triggers the activation of PERK, followed by a chain of reactions leading to apoptosis, the programmed death of the cell,explains Jérôme Tamburini. “In addition, the activation of AMPK by GSK621 sensitises the cells to the effects of another pharmacological drug, the venetoclax, which is now widely used to treat acute myeloid leukaemia, although with limited effectiveness when used alone.”

The scientists then combined the two drugs in mice carrying human tumour cells, and found that this combination controlled tumour development much more effectively than in monotherapy. While GSK621 was not designed to be a drug, other products are currently in clinical trials to combat metabolic diseases, which activate the AMPK pathway. “Understanding the mechanism involved has brought to light potential therapeutic targets that were previously unknown,explains Jérôme Tamburini. “We will now be able to review all the drugs known to have an effect on these pathways and determine which combinations would be the most effective.

What about leukaemic stem cells?

Leukaemic stem cells consists in a small population of cells within the tumour that can only be detected by their ability to spread again the tumour after an initially successful treatment. The main cause of relapse, these cells are sensitive to very few of the therapies usually used in leukaemia. Furthermore, evidence is still lacking to determine the effect that massive activation of AMPK would have on them. “Before testing drug combinations targeting this AMPK/PERK mechanism in human beings, we need to determine their effeleukaemic stem cells,” the authors conclude.


1. Several laboratories were involved, including Institut Cochin (Inserm/CNRS/University of Paris), the Cancer Research Center of Lyon (Inserm/CNRS/Claude Bernard Lyon 1 University/ Léon Bérard Centre) and the Toulouse Cancer Research Center (Inserm/CNRS/Toulouse III –Paul Sabatier University)

Identification d’une nouvelle cible thérapeutique du myélome multiple

Multiple Myeloma cells © KGH, CC BY-SA 3.0, via Wikimedia Commons

Multiple myeloma is a cancer of the bone marrow, with a life expectancy of less than 5 years post-diagnosis. Proteasome inhibitors, the therapeutic backbone of current treatments, are very effective in treating newly diagnosed cancers but resistance or intolerance to these molecules inevitably develop, leading to relapses. While studying a neglected tropical disease[1], Buruli ulcer, researchers from the Institut Pasteur and Inserm discovered a novel therapeutic target for multiple myeloma that could allow to bypass this resistance. The results of this study were published in EMBO Molecular Medicine on January 11th, 2022.

Multiple myeloma is a cancer caused by the abnormal proliferation of plasma cells, white blood cells producing antibodies, in the bone marrow. Scientists from the Institut Pasteur and Inserm, in collaboration with the University of Paris and the Saint Louis Hospital (AP-HP) describe a new mechanism to selectively kill these cancer cells.

Researchers in the Immunobiology of Infection Unit at the Institut Pasteur made this discovery while working on a completely different disease: Buruli ulcer. This neglected tropical disease, caused by infection with a bacterium (Mycobacterium ulcerans), can provoke severe and irreversible skin necrosis. Lesions are due to bacterial production of a toxin called “mycolactone” in infected skin. In 2016, this team discovered how mycolactone causes the clinical manifestations of Buruli ulcer: by targeting the translocon (Sec61).

The translocon is a channel anchored in the wall of a cell compartment called the endoplasmic reticulum that plays a crucial role in the synthesis of a subset of proteins: those that are destined to be secreted in the extracellular medium. The translocon controls the import of these proteins into the endoplasmic reticulum, and it is the main gateway to the secretory pathway. By blocking Sec61, mycolactone retains these proteins inside the cell and provokes their degradation by the proteasome, a stressful process that can evolve towards programmed cell death.

Using murine models and tumors from patient biopsies, researchers demonstrated that mycolactone is highly toxic to multiple myeloma cells, including those that have become resistant to proteasome inhibitors, at doses that are non-toxic to normal cells. In addition, they showed that mycolactone and proteasome inhibitors work in synergy, mutually potentiating their anti-cancer effects.

This study provides the proof of concept that the translocon is a new therapeutic target in multiple myeloma. The next step will be to identify drug-like molecules inhibiting Sec61, which could constitute a new treatment for this cancer. In addition, we aim to study whether this target could be common to other cancers.” explains Caroline Demangel, head of the Immunobiology of Infection Unit at the Institut Pasteur.


[1] WHO definition: Neglected tropical diseases (NTDs) are a diverse group of 20 diseases with one thing in common: their impact on impoverished communities. Together, NTDs affect over a billion people with devastating consequences on public health and economy.

The first French cell therapy trial in a form of retinitis pigmentosa on the horizon


A team of scientists led by Christelle Monville (professor at University of Evry) at I-Stem, the laboratory created by AFM-Téléthon, University of Evry and Inserm, in partnership with the team led by Olivier Goureau, Inserm Research Director within the Institute of Vision, has managed to improve vision in rats with retinitis pigmentosa, by transplanting a cell bandage obtained from human embryonic stem cells. The results published today in Science Translational Medicine, notably achieved thanks to Téléthon donations, pave the way for cell therapy retinitis pigmentosa, but also for very common retinal degenerative diseases, such as certain forms of age-related macular degeneration (AMD).

In France, nearly 30,000 individuals are affected by retinitis pigmentosa – a group of rare diseases affecting vision – and more than 1.5 million by age-related macular degeneration (AMD). These incurable diseases are characterized by gradual degeneration of the retinal cells, ultimately leading to blindness.

In order to replace deficient cells in patients, the initial studies, conducted in humans by American teams from 2012 onwards, involved injecting the eye with retinal pigment epithelial cells placed in suspension – i.e., separated from each other – obtained from human embryonic stem cells. However, this technique was not optimized in terms of the assimilation and survival of the delivered cells. In the study by French scientists, published today, these problems were circumvented owing to an innovative approach: after the human embryonic stem cells had differentiated into epithelial cells, they were inoculated on a segment of human amniotic membrane to create a “cell patch”. This patch was then transplanted into the most peripheral layer of the retina in rats spontaneously presenting genetic retinitis pigmentosa. At the same time, other rodents were administered an injection of suspended cells with a view to comparing both techniques.

Watch the video (DR I-

After 13 weeks of observation, the scientists noted that the rats having been transplanted with a patch showed the best visual performance, and over a longer time-frame, relative to the animals having received the suspended cells.

On the strength of these results, in the coming weeks, the scientists will be submitting an authorization application for a phase I/II clinical trial in approximately twelve patients with retinitis pigmentosa, which is thus expected to start in about a year’s time, at Hôpital des Quinze-Vingts, under the supervision of Professor José-Alain Sahel. This will be the first cell therapy trial in the field of vision disorders, in France.

 Ultimately, this new approach could be applied to all disorders in which damage to the retinal pigment epithelium is observed, notably in dry (or atrophic) forms of AMD.

According to Christelle Monville, research professor at University of Evry and at I-Stem “We have been working with the whole team for the past 6 years to develop this innovative technique. This is, in fact, the first time that a “cell patch” has been created with embryonic stem cells and a human amniotic membrane. We have shown that this technique, being more effective, opens up new therapeutic prospects for retinal diseases, whether rare genetic diseases or common age-related diseases. Now we are about to begin trials in patients, this is a very exciting time indeed.”

Marc Peschanski, I-Stem Director, confirms this: “This new proof of concept shows the extent to which research in the field of cell therapy – driven by the team at -Stem – is making progress, together with the therapeutic prospects that it offers. We have now spent over 10 years working on developing this new medicine, and I am proud that my teams are on the verge of initiating the first French cell therapy trial for rare vision diseases.”

According to Olivier Goureau, Inserm Research Director at the Institute of Vision, “The realization of this collaborative project, and the forthcoming transfer to patients are driving us even more to continue developing these cell therapy strategies related to the use of pluripotent stem cells to help patients.

“Humanized” Mouse Model Developed to Study Hepatitis B Infection


The ANRS consortium “Humanized Mouse Models for Viral Hepatitis”1, made up of 6 teams of researchers, has developed a mouse model for studying the interaction between the immune system and the liver following infection by the hepatitis B virus. This research, coordinated by Dr. Hélène Strick-Marchand (Inserm joint unit 1223, “Physiopathology of the Immune System”, Institut Pasteur), responds to a real lack of animal models for studying this disease and thus opens up the possibilities for evaluating new therapeutic strategies. These results have been published in the journal Gastroenterology.

Over 250 million people around the world are chronic carriers of the hepatitis B virus (HBV), and this figure is growing despite the existence of a highly effective preventive vaccine. Once it has developed, chronic hepatitis can progress to liver fibrosis, cirrhosis, and hepatocellular carcinoma (liver cancer). There are treatments to prevent the disease from progressing by keeping the virus under control, but they must be taken for life as they do not eliminate it completely. In order to better understand the consequences of HBV infection, interactions between the infected hepatocytes (liver cells) and the immune system response, and to be able to test new therapeutic strategies, researchers required an animal model with a physiology similar to that of humans. For a number of years, the ANRS consortium “Humanized Mouse Models for Viral Hepatitis”1, which is made up of 6 teams of researchers and coordinated by Dr. Hélène Strick-Marchand (Inserm joint unit 1223, “Physiopathology of the Immune System”, Institut Pasteur), has therefore been working to develop so-called “humanized” mice. This research has led to development of the HIS-HUHEP model, for which promising results have been published in the journal Gastroenterology.

With the aim of modeling interactions between human hepatocytes (the target of HBV infection) and the human immune system, the HIS-HUHEP model is doubly engrafted with a humanized immune system, and human hepatocytes in its liver. Researchers analyzed the physiological responses of these mice to HBV infection, which proved to be comparable to those observed in humans. In addition, giving the infected HIS-HUHEP mice entecavir (an antiviral used to treat HBV infection) reduced their viral load and liver inflammation.

The doubly “humanized” HIS-HUHEP mice represent an important animal model for studying the interactions that take place between the immune system and the liver in liver disease. This new model fills a real gap. It opens the way to better understanding of the immune response developed to HBV, and to testing new therapeutic strategies with the final goal of eliminating the virus completely from the bodies of infected individuals.


1 For further information on the Humanized Mouse Models for Viral Hepatitis consortium, see:

Usher syndrome: gene therapy restores hearing and balance

The cochlear sensory epithelium (organ of Corti), and the vestibular sensory epithelia, ampullar cristas (inset) of the inner ear ijntected with the AAV8 virus producing GFP and the SANS protein. The cochlear and vestibular sensory cells were immunostained for GFP and myosin VI and analyzed with a confocal microscope. The green and orange cells produce the protein of the therapeutic gene.
© Institut Pasteur

Scientists from the Institut Pasteur, Inserm, the CNRS, Collège de France, University Pierre et Marie Curie, and University Clermont Auvergne*, have recently restored hearing and balance in a mouse model of Usher syndrome type 1G (USH1G) characterized by profound congenital deafness and vestibular disorders caused by severe dysmorphogenesis of the mechanoelectrical transduction apparatus of the inner ear’s sensory cells. By locally injecting the USH1G gene, critical for the formation and maintenance of the hair bundle, the mechanosensory antenna of these cells, the scientists successfully restored the function and the structure of this apparatus, resulting in the first recovery of hearing and balance by gene therapy for this mouse model. These findings, published in the journal PNAS, open up new possibilities for the development of gene therapy treatments for hereditary forms of deafness.

Hearing loss, sometimes associated with other disorders such as balance defects, is the most common sensory deficit, affecting more than 280 million people worldwide, according to WHO. In France, one child in 700 is born with severe or profound hearing loss, and one in every 1,000 will lose their sense of hearing before adulthood.

Over the past 20 years, scientists have made remarkable progress in deciphering the genetic origins of congenital hereditary hearing loss, which is usually caused by inner ear dysfunction. The inner ear comprises the hearing organ or cochlea, together with the five balance organs (the saccule, utricle and three semicircular canals), which contain the sensory cells, or hair cells, that detect mechanical vibrations and convert them into electrical signals. To date, mutations in more than 100 genes have been associated with inner ear defects, and it is estimated that mutations in more than 100 genes can cause genetic forms of deafness.

The various hereditary forms of hearing loss include Usher syndrome type 1 (USH1), a particularly severe clinical form of deaf-blindness, and specifically the USH1G genetic form. USH1G patients are profoundly deaf and have no balance function at birth, and they subsequently suffer from prepubertal-onset sight loss leading to blindness. USH1G syndrome is due to mutations in the gene encoding the scaffold protein sans, which is essential for the cohesion of the hair bundle of the inner ear hair cells.

Patients with hearing loss and balance dysfunction are currently fitted with auditory prostheses and may be given balance rehabilitation therapy, but the outcomes are variable. One possible alternative for treating such hereditary inner ear defects is gene therapy. This approach entails transferring a healthy (non-mutant) copy of the defective gene to restore the expression of the missing protein. So far, gene therapy attempts have only resulted in partial improvements of hearing in mouse models of specific human deafness forms that did not include severe anomalies in hair cell structure.

In this context, scientists from the Institut Pasteur, Inserm, the CNRS, Collège de France, University Pierre et Marie Curie, and University Clermont Auvergne*, have now succeeded in restoring hearing and balance in a mouse model of USH1G syndrome using gene therapy. With a single local injection of the USH1G gene just after birth, the scientists observed a restoration of the structure and mechanosensory function of the inner ear hair bundles – profoundly damaged before birth –, resulting in a long-term partial recovery of hearing, and complete recovery of vestibular function in these mice. These results unexpectedly establish that inner ear defects due to major morphogenetic abnormalities of the hair bundle can be reversed even after birth, with durable efficacy, by gene therapy.

Hair bundles of vestibular sensory cells analyzed using scanning electron microscopy. The image shows a normal hair bundle with its characteristic “staircase” pattern (in yellow), a defective Usher type 1G hair bundle (in pink) and a treated Usher type 1G hair bundle (in green), whose normal/characteristic form was restored with gene therapy.
© Institut Pasteur

The scientists injected the USH1G gene into the inner ear using the innocuous AAV8 virus, which enabled them to specifically target the hair cells. The expression of the therapeutic gene was detected 48 hours after injection. The team demonstrated that a single injection to restore the production and localization of the missing protein in hair cells successfully improved hearing and balance functions in the young mice. These findings suggest that the therapeutic protein was able to interact normally with its binding partners among the USH1 molecular complex (the proteins cadherin 23, protocadherin 15, myosin VIIA and harmonin), as required for the mechanoelectrical transduction apparatus of the hair bundle to function correctly.

As Saaïd Safieddine, CNRS Director of Research at the Institut Pasteur and co-senior author of the study with Prof. Christine Petit, explains, “we have just shown that it is possible to partially correct a specific form of hereditary hearing loss accompanied by balance problems using local gene therapy performed after the embryogenesis of the ear, which is primarily affected by the mutation responsible for the disorder. This suggests that the time window for effectively treating USH1 syndrome using gene therapy may be larger than initially thought.

This study represents a significant step towards the development of clinical trials in gene therapy for the curative treatment of hereditary deafness and balance loss in humans.

*From the Genetics & Physiology of Hearing Laboratory (Institut Pasteur/Inserm/UPMC), the Genes, Synapses and Cognition Laboratory (CNRS/Institut Pasteur, the Center for Neurophysics, Physiology and Pathology (CNRS/Paris-Descartes University), and the Sensory Biophysics Laboratory (University Clermont Auvergne).

Regulating or Stimulating Our Antibodies Based on Our Immunological Needs Will Soon Be Possible



Clinician-researchers from the Université Pierre et Marie Curie (UPMC) and Inserm, in collaboration with the Biological Therapy Department of the Pitié-Salpêtrière Hospital (AP-HP), have revealed a new mechanism for regulating antibody production. The results of this study were published in Science Immunology on Friday, September 8, 2017.


The immune system protects the body from pathogenic agents, in particular infectious ones, that cause damage or disease in humans. Two types of defense work in parallel: cell-mediated immunity, which destroys the infected cells, and humoral immunity, which produces antibodies. These antibodies neutralize the pathogens in a targeted manner.

“As with all immune responses, the humoral immune response must be controlled. Too weak a response would be ineffective, but too strong a response against our own tissues could lead to autoimmune disease,” explains Professor David Klatzmann, clinician-researcher at UPMC and the Pierre et Marie Curie Faculty of Medicine, director of the Immunology – Immunopathology – Immunotherapy laboratory (UPMC/Inserm) and head of the Biological Therapy Unit at the Pitié-Salpêtrière Hospital (AP-HP).


Professor Klatzmann’s team is interested in cells that control the intensity of the humoral response: follicular helper T cells (Tfh), which stimulate the production of antibodies, and follicular regulatory T cells (Tfr), which reduce it. Tfr cells were discovered in 2011. Their numbers are limited, and little is currently known about their mechanisms of action.

The research group first redefined the characteristics for identifying Tfr cells. From this basis, the researchers were able to identify a new mechanism for regulating antibody production

by showing the key role of interleukin-1 (IL-1), a soluble mediator, in triggering these responses. Tfh cells receive IL-1, which activates them and enables an increased antibody response; conversely, Tfr cells reduce the antibody response by neutralizing IL-1 and depriving the Tfh cells of this stimulation.


IL-1 therefore appears to play a major role in the stimulation of humoral immunity via the Tfh cells, and this axis appears to be regulated by the Tfr cells. “We aim to stimulate the antibody response with vaccinations, and reduce it in autoimmune disease,” explains Professor Klatzmann. “This discovery therefore means that we have a new method for regulating antibody immune response.” 


The full results can be found in Science Immunology, published on Friday, September 8.

Forensic odorology scientifically validated

Odorology is a technique that uses specially-trained dogs to identify human scent. It is used in police investigations to establish that an individual has been at the scene of a crime. However, there is no international norm on how these dogs are trained. At the Centre de recherche en neurosciences de Lyon (CNRS/Université Claude Bernard Lyon 1/Inserm), researchers specializing in scents and their memorization have analyzed data, provided since 2003 by the Division of the Technical and Scientific Police (DTSP, Ecully) on dog performances in scent identification tasks. Their results show that, at the end of a 24-month training program, the dogs are able to recognize the smell of an individual in 80-90% of cases and never mistake it for that of another. These findings validate the procedures that are currently in use and should convince the international community of the reliability of this method. This work was published on 10 February 2016 in the journal PLOS ONE.

PhotoCP odorologie

Cisko, one of the police dogs, during a scent detection test (c) DGPN – SICOP

Odorology, or the science of smells, is a method of identifying human scents. It has been used in France since 2003 in police investigations to establish that an individual has been present at a crime scene. The method is based on the fact that each person has their own scent and relies on the powerful canine sense of smell (which can be 200 to 10,000 times more sensitive than that of a human being[1]). It involves a long period of dog training.

This technique consists in using a specially-trained dog to compare a human scent collected from an object found at a crime scene with scents from several people, including that of a suspect or victim. As the results of these tests are of critical importance for investigators, they need to be obtained through viable and reproducible methods. However, there are no internationally recognized norms for the training of these dogs or for their inclusion in investigations—hence the occasional reluctance to treat their evidence as proof. By analyzing results collected since 2003 at the Division of the Technical and Scientific Police (DTSP, Ecully), researchers from the Centre de recherche en neurosciences de Lyon have succeeded in demonstrating the viability of the technique used.

During basic training, the German and Belgian shepherd police dogs must learn to make the link between two scents from the same individual through the completion of increasingly complex tasks. By the end of this training, the dogs are able to carry out identification exercises during which they sniff a reference human scent and then compare it with five different human odors, one of which is the reference scent. When a dog matches the scent in the jar to the reference one (which it shows by lying down in front of the correct jar) it is rewarded with a treat or a game. The human odors may consist of traces collected from an object that someone has touched or of a scent collected directly from a person.

The analysis of the data obtained with the 13 DTSP dogs since 2003 shows that after they have learned the task’s principles, 24 months of regular training is necessary for stable and optimal performances. At the end of the first twelve months, the dogs no longer made any recognition errors, i.e., they did not confuse the scent of one person with that of another. Furthermore, their olfactory sensitivity increased significantly over the training period: on average, after two years, the dogs managed to recognize two scents from the same person in 85% of cases. The remaining 15% of cases in which no match was obtained, were mostly the result of poor scent sampling rather than poor recognition.

The researchers also found that German shepherds were better than Belgian shepherds, undoubtedly because they are more disciplined and attentive.

At the end of their basic training, the dogs are able to participate in criminal cases and receive continuing training throughout their lives. In practice, each identification test is carried out by at least two dogs. Additionally, each dog performs at least two tests with the same panel of scents: the collected scent is presented either as a sample to be sniffed at the start of the task, or in one of the jars that the dog sniffs successively. Between 2003 and 2016, odorology was used in 522 cases at the SDPTS and helped to resolve 162 cases.

In these criminal cases, the sampled scents were only a few hours or days old. The researchers now want to study how the dogs perform on older scents. Scent samples can in fact be stored in scent libraries over several years.

[1] Marshall and Moulton, Chem Senses,1981; Krestel et al., Neurosci Biobehav Rev, 1984.

binôme édition #6 at the Avignon Festival

The les sens des mots company, Inserm (French National Institute of Health and Medical Research) and ICM (Brain and Spinal Cord Institute) are pleased to invite you to a show presented during binôme édition #6 at the Avignon Festival:

Stimulation Cérébrale Profonde (Deep Brain Stimulation), by Camille Chamoux, author, following her meeting with Eric Burguière, a researcher in neurobiology with CNRS – INSERM – ICM.

Clotilde proudly introduces her new man, a researcher, to her entourage. But as Gérard, Clotilde’s father says, “a neurobiologist paid from our taxes to do experiments on mice—now that raises a good few questions.”

Monday 13 July 2015, 5:30-6:30 pm at Maison Jean Vilar (8 bis rue de Mons, 84000 Avignon)

In order to reach an increasingly wider audience, Inserm is creating new visions of science by uniting the world of research with that of arts and culture. It is in this context that Inserm has been a partner in binôme for the last 5 years.

binôme is a series of Theatre and Science shows based on scripts written by playwrights after interviewing researchers on film, inspired by an idea by Thibault Rossigneux, artistic director of the theatre company les sens des mots (the meaning of words).

Eric Burguière

The repetitive behaviours characteristic of a certain number of illnesses, particularly OCD (obsessive compulsive disorder), are central to Eric Burguière’s research. His Inserm team works to better understand the brain mechanisms that cause these behaviours, in order to better treat them.

Camille Chamoux

Camille Chamoux became known from her first one-woman-show, Camille Attaque, and her columns on Canal Plus television in l’Édition Spéciale or on Europe1 radio. She also co-wrote the film Les Gazelles (2013), directed by Mona Achache, and played the lead role in it. In 2014, she created her second show Née sous Giscard (Born under Giscard), which she published with Solitaires Intempestifs, at the Théâtre du Petit Saint-Martin, with stage direction by Marie Dompnier. She is currently writing a second feature-length film, acting in four films in 2015, and is preparing her next one-woman-show.

This show will be rerun three times in autumn:

– 25 September, at Théâtre de la Reine Blanche (Paris 18), programme in preparation

– 26 September, as part of the Curiositas festival in Gif sur Yvette, programme in preparation
– 7 October at 7 pm, at ICM (Paris 13) during Fête de la Science

Supported by SACD, CEA, CNRS, ICM, INERIS, INSERM, IRD, OSU Pythéas, PACA Region, DRRT and Culture Science PACA. In partnership with Maison Jean Vilar, Festival d’Avignon, Faïencerie–Théâtre de Creil, and proarti.

Inserm launches Labo des Métiers (Career Lab): 3D immersion to discover careers in research

Inserm is launching the virtual Career Lab, in partnership with Sisso. This interactive tool, which is highly innovative and fun to use, is aimed at making young people aged 14-25 years aware of all the pieces that make up the great mosaic of scientific research.


screenshot –

Accessible right now via, from computers, tablets and smart phones, this virtual space enables those young adults who are tempted by jobs in research, but discouraged by the long studies they presume are involved, to discover the range of careers offered by the sector.

What is daily life like for a researcher? What are the studies that lead to such a career? What is the role of an engineer in a scientific project or the role of an assistant manager in a laboratory? Such are the questions that we try to answer via the virtual Career Lab,” explains Claire Lissalde, Manager of the audiovisual unit at Inserm’s Department of Scientific Information and Communication.

Visitors to the website are immersed in the heart of a laboratory, and a voiceover helps them to meet professionals working in biomedical research. An opportunity to learn about their career paths and shed light on careers that are often little understood, or considered beyond reach.

Thus Marie, an assistant in biological techniques, and Stéphanie, a researcher and joint manager of an Inserm team, Boris, manager of a phenotyping platform, Joanna, a technician in animal experimentation, Pablo, a post-doctoral fellow, and even Lila, secretary/manager of a research unit, will share their passion about their jobs with you.