Behavioral and psychological symptoms assessed with the BEHAVE-AD-FW are differentially associated with cognitive dysfunction in Alzheimer's disease.

To assess the possible neurological basis of behavioral and psychological symptoms of dementia (BPSD), the relationships between BPSD and cognitive function were evaluated in 40 patients with Alzheimer's disease (AD). BPSD was assessed using the Behavioral Pathology in Alzheimer's Disease Frequency Weighted Severity Scale (BEHAVE-AD-FW) for behavioral symptoms and psychological symptoms separately, and cognitive function was also assessed using the Cognitive Abilities Screening Instrument (CASI). We found that only behavioral symptoms were associated with cognitive function based on the CASI total score and the score for the CASI attention domain. Administration of risperidone, an atypical anti-psychotic drug, for one month, improved the behavioral symptoms and the scores for the CASI attention and orientation domains. Our data suggest that BPSD in AD may reflect two largely independent pathophysiological processes: one associated with behavioral symptoms partly overlapping with attention, and the other associated with psychological symptoms predominantly unrelated to cognitive function.

Assessment of mental deterioration with the Cognitive Abilities Screening Instrument (CASI) and glucose hypometabolism in Alzheimer's disease: the Osaki-Tajiri Project.

The Cognitive Abilities Screening Instrument (CASI) is a screening test for dementia consisting of 9 domains. We investigated the relationships between CASI domain scores and cerebral glucose metabolism (CMRglc) as shown by positron emission tomography. Fifteen patients with very mild Alzheimer's disease (AD) and 15 with mild AD were studied using the [(18)F]fluoro-deoxyglucose method. The 9 CASI domains were classified into four clusters (recent memory, frontal cortex cluster, posterior cortex cluster, and orientation). Using the region of interest method, the recent memory cluster was correlated with the bilateral hippocampal CMRglc, the frontal cortex cluster was correlated with the bilateral anterior and right inferior frontal CMRglc, the posterior cortex cluster was correlated with the bilateral temporo-parieto-occipital and occipital CMRglc, and the orientation cluster was correlated with the left anterior frontal CMRglc (Spearman's correlations). The use of statistical parametric mapping showed that most CASI domains were correlated with CMRglc of the left frontal lobe, the temporal lobe, and the angular gyrus. These findings show that the mental dysfunction assessed using CASI in AD patients has a neurobiological basis.

Non-obese-diabetic mice: immune mechanisms of pancreatic beta-cell destruction.

The sequence of events shortly before the initiation of diabetes in female non-obese diabetic mice was studied. Immunologically, anti-lymphocyte antibodies appeared most frequently at 3 weeks of age and decreased thereafter. Insulin concentrations dropped after the initiation of mononuclear cell infiltration into the islets. The majority of female mice lost approximately 85% of their insulin at aged 22 weeks. Islet cell surface antibodies appeared most frequently during this period (12-18 weeks). Morphological examination revealed that mononuclear cells start to infiltrate islets at 6 weeks of age and involve major areas of the islets in females aged 22 weeks. Among these mononuclear cells, IgM-positive cells were found to be a major constituent, forming follicular (nodular) cell aggregates. T-helper and/or T-cytotoxic cells (Lyt-1-, and/or Lyt-2-positive cells) were fewer and located mainly around the follicular structures. Asialo GM 1-positive lymphocytes (natural killer cells), though present, were far fewer. The process of destruction of pancreatic islets in non-obese diabetic mice is discussed with emphasis on the characteristic local immune response in the pancreas.