Our aim was to identify risk factors for falling and establish a method to assess risk for falls in adults with intellectual disabilities. In a cross-sectional survey of 144 Japanese adults, we found that age, presence of epilepsy, and presence of paretic conditions were independent risk factors. The Tinetti balance and gait instrument was successfully administered to this population and resulted in high diagnostic accuracy (sensitivity 88.9%, specificity 91.9%) for identifying individuals at risk when the cutoff score was set at 25. Participants whose balance and gait deteriorated showed a decrease in the Tinetti score of at least 2 points per year. Thus, the Tinetti instrument may be an effective tool to detect an increased risk of fall in this population.

No abstract

The SAMP10 mouse is a model of accelerated ageing in which senescence is characterized by age-related atrophy of the cerebral cortex and limbic structures, poor learning and memory task performance with depressive behaviour and cholinergic and dopaminergic alterations. Here we studied age-related changes in the dendritic arbors and spine density of pyramidal cells in the medial prefrontal cortex of SAMP10 mice using a quantitative Golgi method. Dendrites of prefrontal neurones gradually retracted with ageing towards the soma with the relative preservation of overall complexity. Apical dendrites were much more severely affected than basal dendrites. The combined length of the apical dendrites and spine density were decreased by 45% and 55%, respectively, in mice at 12 months, compared with mice at 3 months of age. Immunohistochemical and immunoblot analyses indicated that expression of microtubule-associated protein (MAP) 2, a marker of dendrites, decreased in an age-related manner not only in the anterior cortex but also in the posterior cortex and olfactory structures in SAMP10 mice. Decreased expression of MAP2 mRNA caused the decrease in MAP2 protein expression. These results suggest that retraction of apical, but not of basal dendrites, with a loss of spines in prefrontal neurones, appears to be responsible for poor learning and memory performance in aged SAMP10 mice. It is also suggested that age-related dendritic retraction occurs in a wide area including the entire cerebral cortex and olfactory structures.

SAMP10 mouse is a model of brain aging in which senescence is characterized by cerebral atrophy most prominent in the frontal cortex, deterioration in performance of learning and memory tasks, and alterations of the central dopaminergic system. The present study investigates age-related changes in the expression of synapse-related proteins to determine whether the number of synapses is decreased in SAMP10 mice. We quantified expression levels of synaptophysin, a presynaptic protein, and of PSD-95, a postsynaptic protein in various brain regions by immunoblotting. Both synapse-related proteins (52% of synaptophysin and 55% of PSD-95) were lost from the anterior cerebral cortex in SAMP10 mice at age 10-12 months compared with those in mice at age 3 months. Synaptophysin was lost by 30% from the posterior cerebral cortex of SAMP10 mice at age 15-16 months. The level of synaptophysin, but not of PSD-95 decreased by about 25% in the brain stem of SAMP10 mice aged 7 and 10-12 months. A loss of synapse-related proteins was not significant in other brain regions. Age-related loss of synaptophysin or PSD-95 was not evident in normal aging control SAMR1 mice that do not develop brain atrophy. In summary, synapses were lost with aging in SAMP10 mice and the synaptic loss was most prominent in the anterior cerebral neocortex. Since a loss of neocortical synapses is the primary correlate with the intellectual decline in human neurodegenerative diseases, SAMP10 mouse is a useful model with which to study the mechanisms underlying synaptic loss in human neurodegenerative dementias.

In this study, we applied a novel psycho-educational horseback riding (PEHR) program to the treatment of four Japanese children with pervasive developmental disorders (PDD) in order to facilitate the acquisition of verbal and nonverbal communication skills. The behavioral changes in each child were evaluated using a psychological and behavioral scale. The scale for evaluating the effect of Human-Equips-Interaction on Mental activity (HEIM scale) was designed to assess the behavioral improvement of children based on the following 10 items: Human relationships, Imitation, Emotional expression, Sudden physical movement, Fixative behavior, Adaptation to change, Visual response, Fear or nervousness, and Verbal and nonverbal communication. After taking part in the PEHR program for several months, all subjects showed remarkably improved HEIM scores and marked improvements were observed in eye contact with others (instructors, side walkers, and leaders) in the riding area. A statistical difference was found in items 1, 2, 3, 6, 7, 8, and 9. However, no statistical difference was found in items 4, 5, and 10. As the program progressed, the children showed enhanced verbal and nonverbal communication skills, and became more expressive in their emotional and empathetic interaction with their parents. These observations suggest that the normal functioning of pleasurable emotions and empathy may facilitate further improvements in joint attention, imitation and empathy, and may result in successful verbal expression by PDD children. Therefore, horseback riding can play a very important role in the psycho-educational support required for the communication ability of PDD children.

No abstract

SummaryHereditary erythroblastic anaemia was found in a homozygous mutant (hea/hea) of an inbred strain CFO, which originated from noninbred CF#1 mice from Carworth Inc. This newly-described anaemia is inherited as an autosomal recessive and is lethal at 15-25 days of age. Erythrocytes of anaemic mice show striking polychromasia, anisocytosis, and poikilocytosis. One of the most marked features of this anaemia is the presence of large numbers of nucleated cells, mainly orthochromatophilic erythroblasts and myeloid cells, in the circulation. They also include immature erythroid and myeloid cells. Many naked nuclei appear on smears from circulating blood of anaemic infants. Erythrocytes, haematocrit percentage, and haemoglobin content of older anaemic infants were only about 50% of those of the normal. Formation of erythroid, myeloid cells, and megakaryocytes in the bone marrow seems to be progressively affected by mutant alleles in the anaemic infants.

The genetic polydactyly/arhinencephaly mouse, Pdn/Pdn, exhibits severe polydactyly both in the fore‐and hindlimbs, agenesis of the olfactory bulbs, corpus callosum, anterior commissure, and hydrocephalus. A candidate gene for the Pdn mouse has been speculated to be Gli3, because Pdn has been considered to be an allele of Xt whose responsible gene has been clarified to be Gli3. Recently, it has been cleared that retro‐transposons are inserted into nitron 3, upstream of zinc finger domain, of the Gli3 gene in the Pdn mouse, resulting to the severe suppression of Gli3 gene expression in Pdn/Pdn embryos. Meanwhile, XtJ/XtJ mice exhibit more severe polydactyly than that of Pdn/Pdn. Arhinencephaly and microholoprosencephaly including agenesis of the olfactory bulbs, corpus callosum, anterior commissure, hippocampal commissure, habenular commissure, and posterior commissure, and moreover, the cerebral cortical plates and hippocampus are not formed in the XtJ/XtJ mice. The XtJ/XtJ mouse has a large deletion in Gli3 structural gene and shows null expression. From these corroborations, we speculated that the differences in the Gli3 gene expression levels resulted in the phenotypic differences between the Pdn/Pdn and XtJ/XtJ mice.