Dementia (Basel, Switzerland)最新文献

It is now known that immunologic mechanisms have a role in the initiation of atherosclerotic processes. No antibodies against vascular endothelial cell (VEC) specific antigenic systems have been demonstrated in the pathogenesis of small vessel (lacunar) infarcts, though autoantibodies have been detected in 80% of patients with multi-infarct dementia. We studied VEC-specific antibodies in 17 patients with a diagnosis of vascular dementia; in 17 nondemented patients with small vessel infarcts and in 16 healthy, nondemented control group patients by using the Terasaki microtoxicity method. All three groups were correlated according to known risk factors. VEC-specific antibodies were positive in 94% demented patients, whereas no antibodies were detected in patients with small vessel infarcts or in the control group. This result may suggest the existence of an immunologic mechanism in the etiopathogenesis of vascular dementia differing form small vessel infarcts.

Prosody is defined as the melodic line of language. In this study we included 25 patients with probable Alzheimer's disease and 14 with multi-infarct dementia for a comparative cross-sectional study of prosody. Neuropsychological analysis was based on Mini-Mental test, Blessed Scale and Clinical Dementia Rating. We used the criteria of Monrad-Krohn to evaluate prosodic categories. We found intrinsic aprosody in 8 patients with Alzheimer's disease and in none of the patients with multi-infarct dementia (prevalence ratio: 1.82, 95% CI: 1.32-2.51), and emotional aprosody in 17 patients with Alzheimer's disease in comparison to 4 with multi-infarct dementia (prevalence ratio: 1.8, 95% CI: 1.04-3.18). The differences in intellectual and inarticulate aprosody were not significant. We conclude that aprosody is more frequent and severe in Alzheimer's disease than in multi-infarct dementia.

The pharmacokinetics of the cholinesterase inhibitor tacrine was studied in 5 Alzheimer patients during 12-31 months of treatment. A mean average steady-state concentration in plasma ranging from 1.1 to 30 ng/ml was obtained with doses ranging from 40 to 160 mg of tacrine daily. During treatment with 80 mg daily a maximal plasma concentration of tacrine (8.7 +/- 0.6 ng/ml) was obtained 1.3 +/- 0.2 h after intake of the morning dose. The mean elimination half-life was estimated at 5-7 h and remained unchanged when the tacrine dose was increased. The plasma concentration of tacrine was stable during long-term treatment with tacrine and no tolerance was observed regarding its cholinesterase inhibitory effect. A maximal 40% inhibition of plasma cholinesterase (ChE) activity and 60% inhibition of acetylcholinesterase activity in red blood cells was measured following treatment with the highest dose of 160 mg tacrine daily. A significant correlation was obtained between the plasma concentration of tacrine and the inhibition of ChE activity (p < 0.001). The tacrine concentration in CSF was measured in each patient on 1-3 occasions during the treatment and the ratio CSF/plasma concentration was estimated to be 0.47 +/- 0.09 (n = 11).

It is unknown whether aging and Alzheimer's disease (AD) are on the same continuum, or whether they are qualitatively distinct. Tau protein has been identified as a major constituent of paired helical filaments (PHFs) and AD is characterised by a major redistribution of the normal tau protein pool into PHFs. Little is known about the changes in tau protein distribution that occur in the course of normal aging. We have examined PHF-bound and normal tau fractions in frontal, temporal, parietal and occipital neocortex, cerebellum, hippocampus and entorhinal cortex in 15 cognitively unimpaired individuals aged 19-88 years at death. Insoluble tau protein in the PHF fraction did not increase with aging in any brain region, despite the appearance of neurofibrillary pathology at low density in the more elderly cases. By contrast, normal tau protein decreased with aging (r = 0.32, p < 0.001), with an average loss of 14% of soluble tau per decade after the age of 20 years. This was unrelated either to neurofibrillary or beta-amyloid pathology. Frontal grey matter and hippocampus were most vulnerable to age-related tau loss, decreasing by as much as 90% in the older subgroup. These findings contrast with those we have previously reported in AD, where the redistribution of tau protein into the PHF-bound fraction was highly correlated with the extent of neurofibrillary pathology, and suggest that the mechanisms of tau loss in aging and AD are distinct. Age-related tau loss may underlie the neuropsychological impairments seen in the non-demented elderly.

We evaluated pattern visual evoked potentials (PVEPs) in patients with Alzheimer's disease (AD) and correlated the neurophysiological results with visuospatial performances in order to understand better the underlying causes of visual disturbances. Latencies and topographical distribution of PVEP components were evaluated in 20 AD patients who underwent an extensive battery of neuropsychological tests. Mean latencies of N70 and P100 were normal in AD patients, while mean latencies of N140 and P200 were significantly increased in comparison with age-matched healthy controls. The topographical distribution of PVEP components did not show any significant difference between the two groups. Visuospatial impairment was detected in 8 patients (40%). Statistically significant positive correlations were observed between P200 amplitude (posterior right hemisphere mean z score) and performance in visuospatial tests. Our data are consistent with a sparing of foveal retinocortical pathways and with the selective dysfunction of either corticocortical connections between the striate cortex and the visual associative structures or of right temporo-parieto-occipital visual analyzers.

Patient EDS presented with an amnesic disorder of insidious onset (4 years) that remained stable and restricted to memory functions over a 10-year course. Repeated neuropsychological evaluations over 6 years showed a moderate-to-severe, stable impairment of long-term memory and of memory for public events, and a milder, stable impairment of autobiographic memory and of short-term memory. Language, perception, praxis and 'frontal' functions were fully preserved. MRI showed atrophy of the right hippocampus, of the right mammillary body and of the sylvian fissure (bilaterally, but more marked on the left). On PET scan, metabolic activity in the mesial temporal structures was significantly reduced on the right and was at lower normal levels on the left. The disorder observed in EDS is similar to that recently reported in other patients. Possible etiologies of the selective amnesia observed in EDS are considered and their implications discussed.

To compare subcortical involvement of Parkinson's disease (PD) with that of Binswanger's disease (BD), we examined visual evoked potentials (VEPs) and somatosensory evoked potentials (SEPs) in 29 patients with PD and 7 patients with BD and 11 control subjects. The patients with PD were divided into two groups: PD without dementia (nD-PD: n = 18) and PD with dementia (D-PD: n = 11). The D-PD patients showed significantly longer P100 latencies in VEPs compared with the nD-PD patients or controls. The P100 latencies were negatively correlated with Mini-Mental State Examination (MMSE) score in the PD patients. The BD patients showed significantly longer central conduction time (CCT) in SEPs (interpeak latency between N13 and N20 responses) compared with the nD-PD patients or controls. There was no correlation between CCT and MMSE score in the BD patients. These results suggest that PD has a predilection for sensory system involvement distinct from that of BD. In D-PD, the visual system seems more vulnerable than the somatosensory system, but almost the reverse is true of BD.

The aim of the study was to assess the specificity of temporal amygdala (TA) atrophy with magnetic resonance imaging (MRI) by comparing a group of early impaired patients with Alzheimer's disease (AD) with 'other types of dementia' and controls. In this prospective case-control study, 41 patients were selected: 12 with probable AD according to NINCDS-ADRDA and CERAD inclusion and exclusion criteria, 14 with other types of dementia and 15 age-matched control subjects. Two radiologists blindly measured the TA volumes on coronal oblique contiguous slices with a 1.5-tesla MRI scanner. TA volume measurements obtained by the 2 observers and right-left TA values were not significantly different. A significant TA atrophy was found in the AD group as compared to the other groups, with 39.7% (p < 0.001) difference in TA volumes between AD and other types of dementia groups and 41.4% (p < 0.0005) difference between AD and control groups. There was no significant difference between other types of dementia and control groups. There was an overlap between the three groups for 4 patients. TA atrophy assessed with MRI could be of diagnostic value in AD, especially in the early stage of the disease.