Visual‐motor and executive functions in children born preterm: The Bender Visual Motor Gestalt Test revisited

Böhm, B., Lundequist, A. & Smedler, A.‐C. (2010). Visual‐motor and executive functions in children born preterm: The Bender Visual Motor Gestalt Test revisited. Scandinavian Journal of Psychology, 51, 376–384. Visual‐motor development and executive functions were investigated with the Bender Test at age 5½ years in 175 children born preterm and 125 full‐term controls, within the longitudinal Stockholm Neonatal Project. Assessment also included WPPSI‐R and NEPSY neuropsychological battery for ages 4–7 ( Korkman, 1990 ). Bender protocols were scored according to Brannigan & Decker (2003) , Koppitz (1963) and a complementary neuropsychological scoring system (ABC), aimed at executive functions and developed for this study. Bender results by all three scoring systems were strongly related to overall cognitive level (Performance IQ), in both groups. The preterm group displayed inferior visual‐motor skills compared to controls also when controlling for IQ. The largest group differences were found on the ABC scoring, which shared unique variance with NEPSY tests of executive function. Multiple regression analyses showed that hyperactive behavior and inattention increased the risk for visual‐motor deficits in children born preterm, whereas no added risk was seen among hyperactive term children. Gender differences favoring girls were strongest within the preterm group, presumably reflecting the specific vulnerability of preterm boys. The results indicate that preterm children develop a different neurobehavioral organization from children born at term, and that the Bender test with a neuropsychological scoring is a useful tool in developmental screening around school start.     

Intrahippocampal administration of A beta(1-40) impairs spatial learning and memory in hyperglycemic mice

Age-related neurodegenerative dementia, particularly Alzheimer's disease (AD), may be exacerbated by several interacting risk factors including genetic predisposition, beta amyloid (A beta) protein accumulation, environmental toxins, head trauma, and abnormal glycolytic metabolism. We examined the spatial learning and memory effects of A beta(1-40) administration on hyperglycemic mice by their performance in the Morris water maze. Chronic hyperglycemia was induced in male C57BL/6J mice to mimic diabetes mellitus by intraperitoneal injection of streptozotocin (STZ), which specifically destroys pancreatic beta-islet cells. Ten days after STZ treatment, intrahippocampal infusion of vehicle, monomer, or oligomer A beta(1-40) was given to these hyperglycemic mice. Our results demonstrate that in comparison with vehicle or monomer A beta(1-40), oligomer A beta(1-40) induced significant deficits of spatial learning and memory in hyperglycemic mice. Apoptotic signals were identified in the CA1 and dentate gyrus of hippocampus in hyperglycemic mice. A beta accumulation, oxidative stress, and apoptosis in the CA1 region were more intensive in hyperglycemic mice than that in normoglycemic mice after acute treatment with oligomer A beta(1-40) peptide treatment. These results indicate that CA1 apoptosis was enhanced by oxidative stress resulting from accumulation of A beta. Considered together, these findings suggest that hyperglycemic mice are more vulnerable to the A beta-induced-oxidative stress than normal subjects. We therefore propose that A beta accumulation would be enhanced by hyperglycemia, and the oxidative stress caused by A beta accumulation would in turn enhance the AD symptoms.