«Soutien aux personnes en situation de handicapLa dépense nette en faveur des personnes en situation de handicap a atteint 9,29 milliards d'euros l'an dernier. L'hébergement et l'accueil de jour ont représenté 62 % du total, la prestation de compensation du handicap (PCH) 32 % et les autres dépenses 6 %. Cette dépense a, elle aussi, à nouveau augmenté de manière importante, indique l'ODAS : 580 millions d'euros, soit + 6,7 % en dépense nette, et 47 millions d'euros en charge nette, soit + 5,9 % après compensation par la Caisse nationale de solidarité pour l'autonomie (CNSA). L'essentiel de la progression des dépenses tient à la PCH qui a progressé de 10,5 % (280 millions d'euros), après déjà une hausse de 11,8 % en 2022. Le relèvement de 13,8 % du concours de la CNSA conduit à une augmentation un peu plus faible de la charge nette : 9,1 %. Si la moitié de l'augmentation de la dépense nette s'explique par l'évolution du cout de la prestation, l'autre moitié provient de l'évolution du nombre de ses bénéficiaires, en progression continue depuis sa création en 2006, complètent les auteurs de l'enquête.»...

«Circadian dysfunction is prevalent in neurodevelopmental disorders, particularly in autism spectrum disorder (ASD). A plethora of empirical studies demonstrate a strong correlation between ASD and circadian disruption, suggesting that modulation of circadian rhythms and the clocks could yield satisfactory advancements. Research indicates that circadian dysfunction associated with abnormal neurodevelopmental phenotypes in ASD individuals, potentially contribute to synapse plasticity disruption. Therefore, targeting circadian rhythms may emerge as a key therapeutic approach. In this study, we did a brief review of the mammalian circadian clock, and the correlation between the circadian mechanism and the pathology of ASD at multiple levels. In addition, we highlight that circadian is the target or modulator to participate in the therapeutic approaches in the management of ASD, such as phototherapy, melatonin, modulating circadian components, natural compounds, and chronotherapies. A deep understanding of the circadian clock's regulatory role in the neurodevelopmental phenotypes in ASD may inspire novel strategies for improving ASD treatment.»...

«C'est dix euros par heure de cours non dispensée, a calculé le journal Le Parisien, qui révèle que l'Etat a été condamné cette semaine à verser 1360 euros à une famille parisienne, pour des professeurs absents et non remplacés pendant l'année scolaire 2021-2022. En tout, la fille de Kate, qui se trouvait alors inscrite en 4e au collège Marie-Curie de Paris (XVIIe) a perdu 136 heures de cours sur l'année. Assez donc pour une condamnation de l'Etat français, les magistrats du tribunal administratif de Paris ont jugé que ce jugement «résulte « résulte du volume élevé d'heures de cours non dispensés que Kate a nécessairement accusé un retard dans ses enseignements ». C'est presque 15% du volume d'heures totale de cours sur l'année.»...

«Le tribunal judiciaire de Paris a condamné le laboratoire à verser à cette mère et à ses deux enfants près de 285 000 euros d'indemnités pour «défaut d'information » sur les risques de malformation et neurodéveloppementaux causés par le produit « défectueux » commercialisé par le laboratoire.»...

«Circadian dysfunction is prevalent in neurodevelopmental disorders, particularly in autism spectrum disorder (ASD). A plethora of empirical studies demonstrate a strong correlation between ASD and circadian disruption, suggesting that modulation of circadian rhythms and the clocks could yield satisfactory advancements. Research indicates that circadian dysfunction associated with abnormal neurodevelopmental phenotypes in ASD individuals, potentially contribute to synapse plasticity disruption. Therefore, targeting circadian rhythms may emerge as a key therapeutic approach. In this study, we did a brief review of the mammalian circadian clock, and the correlation between the circadian mechanism and the pathology of ASD at multiple levels. In addition, we highlight that circadian is the target or modulator to participate in the therapeutic approaches in the management of ASD, such as phototherapy, melatonin, modulating circadian components, natural compounds, and chronotherapies. A deep understanding of the circadian clock's regulatory role in the neurodevelopmental phenotypes in ASD may inspire novel strategies for improving ASD treatment.»...

«Summary: Researchers have uncovered critical insights into how autism spectrum disorders (ASD) may develop at early stages of brain formation. Using mouse models, the team discovered that environmental factors causing autism-like symptoms are linked to early changes in neurotransmitter activity in the brain.Specifically, they observed that a temporary switch from the inhibitory neurotransmitter GABA to the excitatory neurotransmitter glutamate in neonatal mice could lead to the development of ASD-like behaviors, such as repetitive actions and reduced social interaction, later in life. By intervening during this early stage and reversing the neurotransmitter switch, the researchers were able to prevent the onset of these behaviors in adulthood.»...

«Summary: Researchers have uncovered critical insights into how autism spectrum disorders (ASD) may develop at early stages of brain formation. Using mouse models, the team discovered that environmental factors causing autism-like symptoms are linked to early changes in neurotransmitter activity in the brain.Specifically, they observed that a temporary switch from the inhibitory neurotransmitter GABA to the excitatory neurotransmitter glutamate in neonatal mice could lead to the development of ASD-like behaviors, such as repetitive actions and reduced social interaction, later in life. By intervening during this early stage and reversing the neurotransmitter switch, the researchers were able to prevent the onset of these behaviors in adulthood.»...

«Individuals diagnosed with autism spectrum disorder (ASD) frequently exhibit abnormalities in auditory perception, a phenomenon potentially attributed to alterations in the excitatory and inhibitory cells constituting cortical circuits. However, the exact genetic factors and cell types affected by ASD remain unclear. The present study investigated the balance of excitatory and inhibitory activity in the auditory cortex using BTBR T Itpr3/J (BTBR) mice, a well-established model for autism research. Our investigation unveiled a reduction in parvalbumin-positive (PV) neurons within the AC of BTBR mice. Remarkably, in vivo magnetic resonance spectroscopy studies disclosed an elevation in glutamate (Glu) levels alongside a decrement in γ-aminobutyric acid (GABA) levels in this cortical region. Additionally, transcriptomic analysis of the mouse model facilitated the classification of several ASD-associated genes based on their cellular function and pathways. By comparing autism risk genes with RNA transcriptome sequencing data from the ASD mouse model, we identified the recurrent target gene Scn1a and performed validation. Intriguingly, we uncovered the specific expression of Scn1a in cortical inhibitory neurons. These findings hold significant value for understanding the underlying neural mechanisms of abnormal sensory perception in animal models of ASD.»...

«Individuals diagnosed with autism spectrum disorder (ASD) frequently exhibit abnormalities in auditory perception, a phenomenon potentially attributed to alterations in the excitatory and inhibitory cells constituting cortical circuits. However, the exact genetic factors and cell types affected by ASD remain unclear. The present study investigated the balance of excitatory and inhibitory activity in the auditory cortex using BTBR T Itpr3/J (BTBR) mice, a well-established model for autism research. Our investigation unveiled a reduction in parvalbumin-positive (PV) neurons within the AC of BTBR mice. Remarkably, in vivo magnetic resonance spectroscopy studies disclosed an elevation in glutamate (Glu) levels alongside a decrement in γ-aminobutyric acid (GABA) levels in this cortical region. Additionally, transcriptomic analysis of the mouse model facilitated the classification of several ASD-associated genes based on their cellular function and pathways. By comparing autism risk genes with RNA transcriptome sequencing data from the ASD mouse model, we identified the recurrent target gene Scn1a and performed validation. Intriguingly, we uncovered the specific expression of Scn1a in cortical inhibitory neurons. These findings hold significant value for understanding the underlying neural mechanisms of abnormal sensory perception in animal models of ASD.»...