Working memory training in autism: Near and far transfer.

INTRODUCTION: The autistic population is expanding. It is generally recognized that executive function deficits (EFs) are at the core of this disorder. Working memory (WM) is considered a critical element in executive functioning. WM training is regarded as a promising new therapy that can improve EFs and reduce symptoms of autism by targeting WM through repetitive exercises. AIM: To investigate the impact of WM training on WM, cognitive flexibility, planning, and clinical symptoms. Also, to examine whether age influences the remediation effects. METHODS: Only one group of 20 verbal autistic participants aged 6 to 21 years was included. They received 40 training sessions. The program used is called "Cogmed". Neuropsychological measures were administered before and after the intervention to assess the three EFs. The Social Communication Questionnaire (SCQ) was exploited to evaluate its effects on clinical symptoms. RESULTS: Only 17 participants have completed the training. They showed significant and large improvements in WM subtests (p<0.01, η^2>0.06), cognitive flexibility (p<0.05, η^2>0.06), planning (p<0.01, η^2 >0.06), and symptoms (p<0.01, η^2 >0.06). Also, the ANOVA test revealed that the age and the intervention effects are not correlated in our sample (p >0.05). CONCLUSION: WM training influences EFs positively in autism and reduces the severity of its clinical characteristics. Thus, it's an effective therapy that can be added to the management of this disorder.

Acute mitochondrial actions of glitazones on the liver: a crucial parameter for their antidiabetic properties.

BACKGROUND/AIMS: Glitazones are synthetic insulin-sensitizing drugs which act as agonists of peroxisome proliferator-activated receptor gamma (PPARγ). However, TZDs action does not exclude independent PPARγ-activation effects. Remarkably, direct mitochondrial action of these agents has not been fully studied yet. METHODS: Oxygen consumption rates (JO(2)) were measured using a Clark-type oxygen electrode in intact hepatocytes and isolated liver mitochondria. Mitochondrial reactive oxygen species (ROS) production was quantified by fluorescence assay. Moreover, activities of mitochondrial respiratory chain complex I, II and III were spectrometrically determined. RESULTS: Pioglitazone and rosiglitazone inhibited JO(2) in liver cells and mitochondria. This inhibition affected the state 3 of respiration (in the presence of ADP) and the uncoupled state (after addition of dinitrophenol). Moreover, these agents dramatically reduced mitochondrial ROS production in all situations tested. We also demonstrated that both glitazones specifically inhibited the activities of complex I and complex III, by 50% and 35% respectively. Additionally, they do not modify neither the oxidative phosphorylation yield nor the permeability transition pore opening. CONCLUSIONS: Pioglitazone and rosiglitazone reduce both respiration intensity and ROS production, acutely and by a probable PPARγ-independent way, through inhibition of complex I and III activities. This new finding could positively contribute to their anti-diabetic properties.