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Query: UMLS:C0752347 (Dementia with Lewy bodies)
 1,653 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors recall the functional principles of thermoluminescent dosimeters: heating, apparatus for measuring the emitted light, circulation of nitrogen, reference source. They take this opportunity to stress the essential role played by the circulation of nitrogen over the dosimeters which equilibrates the temperature of the photo multiplier, reduces the emission of unwanted light, prevents the combustion of dust or other possible impurities and finally improves the reproductibility of the measurements even for high dosod for finding the optimum working conditions for the heating apparatus of the planchette in the most simple T.L.D. readers and in those where the heating apparatus of the planchette has a pre-heating phase. They then study the dosimetric properties of lithium borate incorporated in thin teflon discs (type DLB. 0.13 and 0.4). This shows itself to be very interesting for certain uses because it is a solid dosimeter which does not require annealing between two measurements. The reproductibility of the measurements obtained with this material, the stability of its response relative to the delay between radiation and reading (fading), its response relative to the absorbed dose plus the nature and the energy of the rays, are presented with the usual reservations made for this type of dosimetry. The authors conclude by citing a few applications where they have been able to achieve a satisfactory result with the aid of lithium borate.
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PMID:[Practical use of lithium borate in thermoluminescent dosimetry (author's transl)]. 99 91

To clarify axonal guidance mechanisms involved in pathway formation by spinal interneurons, the pattern of axonal outgrowth was examined following three kinds of perturbations: (1) rotation of three segments of the neural tube around the dorsal-ventral axis by 90 degrees or 180 degrees (D-V rotation), (2) rotation of three segments of the neural tube around the rostral-caudal axis (R-C rotation), and (3) transplantation of brainstem into thoracic spinal segments (BS transplantation). Following D-V rotation, it was observed that circumferential axons near the junction between rotated graft (RG) and host cord changed their course so as to project toward the ectopic floor plate. This supports the notion that the floor plate exerts a chemotropic-like effect on the directional projection of circumferential axons. The longitudinal fibers in the ventral funiculus (VF) were able to grow through the transplant junction when the VF was well apposed to the VF of the RG. However, in most cases, the longitudinal fibers in the VF that were not apposed to the VF of the RG made a medial turn at the junction. After turning, some of them made a U-turn into the contralateral VF, whereas others grew circumferentially around the junction zone, then exited the spinal cord; still others directly entered the RG. The majority of fibers that entered the RG were located in the VF, though a small number of such fibers were also located in both the lateral and dorsal funiculus (LF and DF, respectively). The fibers that entered the LF shifted ventrally, whereas the fibers in the DF remained within the DF. These results suggest that there may be some matching mechanism between specific fibers and the funiculus through which the fibers normally project. Moreover, there may be a barrier between the LF and the DF that prevents the fibers in the DF from shifting ventrally. In R-C rotation experiments, the projection of axons of dorsolateral border cells (DLB-cells), which are known to give rise almost exclusively to commissural ascending axons, was examined. Following the injection of HRP into the rostral junctional region, retrogradely labeled DLB-cells were observed in the rotated segments only on the side contralateral to the injection. Labeled DLB-cells were also observed in the segments caudal to the rotated segments. These results suggest that putative rostrocaudal directional cues that guide the axons of DLB-cells may arise from outside of the segments in which the decision to turn is made.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An experimental analysis of in vivo guidance cues used by axons of spinal interneurons in the chick embryo: evidence for chemotropism and related guidance mechanisms. 165 78

Canine pregnant sera were investigated for monocyte-specific cytotoxic antibodies against a cell panel from 50 unrelated dogs. Contaminating DLA and DLB reactivity was removed by absorption on a random pool of purified lymphocytes. Two monocyte-associated antigens were recognized by two independent clusters of antisera; the existence of further antigens is suggested. In preliminary segregation studies, the inheritance of these determinants in linkage with DLA could not be observed.
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PMID:Recognition of monocyte-associated antigens in the dog. 206 95

In recent years dementia histologically characterised by the presence of cortical Lewy bodies has been increasingly recognised. There is now need for a scheme for an internationally acceptable scheme for pathological diagnosis and classification so that clinical, pathological and molecular features of disease can be correlated. Recent observations made by different groups in large patient series have used slightly different pathological criteria resulting in at least seven different diagnostic terms. In some patients the only cortical pathology is the presence of Lewy bodies, while in the majority of patients there are coexisting pathological changes which either overlap with those seen in Alzheimer's disease (AD). Cortical Lewy bodies can also be present in patients who do not have any obvious cognitive abnormality. A problem with equating studies from different groups is that different criteria have been used to define AD, so that establishing the relevance of cortical Lewy bodies themselves to cognitive decline and separating this from the contribution which may be related to the AD pathology is problematic. The lesions which appear to be of most relevance to potential cognitive decline in DLB are cortical Lewy bodies, Lewy-related neurites, senile plaques, neurofibrillary tangles, neuronal and synaptic loss, spongiform change, and cortical cholinergic deficits. It is possible to operationally classify patients with cognitive decline and cortical Lewy bodies into three main groups, Cortical Lewy body disease, Cortical Lewy body disease with plaques, and Cortical Lewy body disease with plaques and tangles. There are frequent cases which overlap these groups making operational classification difficult in practice. A descriptive classification, in which the severity of different pathological changes is rated, is easy to use in practice. As new molecular risk factors for AD or DLB are revealed they will need to be related to morphological and clinical features. A descriptive diagnostic assessment for DLB will facilitate such studies and makes no judgements as to what these relationships will be.
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PMID:Pathological diagnostic criteria for dementia associated with cortical Lewy bodies: review and proposal for a descriptive approach. 947 Jan 32

A mutation in exon 4 of the alpha-synuclein (NACP) gene has been reported to explain the chromosome 4 linkage to autosomal dominant Parkinson's disease. We developed primers and methods for exonic sequencing of this gene and sequenced the entire coding region of the gene in 6 families with autosomal dominant disease and in 2 cases of lytico and bodig from Guam. In addition, we have sequenced exon 4 of this gene in 5 cases of familial disease and have screened for the specific mutation (A53T) in a 40 cases of idiopathic Parkinson's disease, 3 cases of multisystem atrophy, and 15 cases of Lewy body dementia. We have found no genetic variation in the gene. We discuss these findings with respect to both the epidemiology of Parkinson's disease and the possibility that NACP is not the chromosome 4 locus for disease.
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PMID:Low frequency of alpha-synuclein mutations in familial Parkinson's disease. 950 59

Current accepted clinical criteria for the diagnosis of Parkinson's disease (PD) provide high sensitivity for detecting parkinsonism but generally show poor specificity for identifying brainstem Lewy body disease. Biochemical markers that can be used to reliably diagnose clinical and preclinical PD have thus far been sought unsuccessfully. It is now known that some PD kindreds have a mutation of the alpha-synuclein gene, but this cannot be used as a genetic marker for most familial and sporadic cases. Functional imaging provides a means of discriminating typical from atypical PD, revealing characteristic patterns of loss of dopaminergic function. In addition, PET and SPECT show preserved levels of striatal metabolism and dopamine receptor binding in PD, whereas levels are reduced in the atypical variants. [18F]Dopa PET can also detect preclinical PD. In one series there was a reported 40% prevalence of preclinical dopaminergic dysfunction in asymptomatic adult relatives of familial PD patients. Finally, PET and SPECT can both be used to follow PD progression objectively. Such studies suggest an annual 4 to 12% loss of dopamine terminal function in early PD and a preclinical disease window of only a few years. In the future, functional imaging is likely to play an increasingly important role in assessing the efficacy of putative neuroprotective agents.
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PMID:The early diagnosis of Parkinson's disease. 974 69

The precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP) (also known as alpha-synuclein) is a presynaptic terminal molecule that abnormally accumulates in the plaques of Alzheimer's disease (AD) and in the Lewy bodies (LBs) of Lewy body variant of AD, diffuse Lewy body disease, and Parkinson's disease. To better understand the distribution of NACP/alpha-synuclein and its fragments in the LB-bearing neurons and neurites, as well as to clarify the patterns of NACP/alpha-synuclein compartmentalization, we studied NACP/alpha-synuclein immunoreactivity using antibodies against the C-terminal, N-terminal, and NAC regions after Proteinase K and formic acid treatment in the cortex of patients with LBs. Furthermore, studies of the subcellular localization of NACP/alpha-synuclein within LB-bearing neurons were performed by immunogold electron microscopy. These studies showed that the N-terminal antibody immunolabeled the LBs and dystrophic neurites with great intensity and, to a lesser extent, the synapses. In contrast, the C-terminal antibody strongly labeled the synapses and, to a lesser extent, the LBs and dystrophic neurites. Whereas Proteinase K treatment enhanced NACP/alpha-synuclein immunoreactivity with the C-terminal antibody, it diminished the N-terminal NACP/alpha-synuclein immunoreactivity. Furthermore, formic acid enhanced LB and dystrophic neurite labeling with both the C- and N-terminal antibodies. In addition, whereas without pretreatment only slight anti-NAC immunoreactivity was found in the LBs, formic acid pretreatment revealed an extensive anti-NAC immunostaining of LBs, plaques, and glial cells. Ultrastructural analysis revealed that NACP/alpha-synuclein immunoreactivity was diffusely distributed within the amorphous electrodense material in the LBs and as small clusters in the filaments of LBs and neurites. These results support the view that aggregated NACP/alpha-synuclein might play an important role in the pathogenesis of disorders associated with LBs.
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PMID:Abnormal distribution of the non-Abeta component of Alzheimer's disease amyloid precursor/alpha-synuclein in Lewy body disease as revealed by proteinase K and formic acid pretreatment. 975 60

Orthostatic hypotension and carotid sinus hypersensitivity were assessed in patients meeting clinical criteria for dementia with Lewy bodies (DLB; n=30) and AD (n=35). Cardioinhibitory carotid sinus hypersensitivity (CI) was the most common sign (AD patients, 28%; DLB patients, 41%). Preliminary data from a secondary analysis excluding patients with hypertension or EKG evidence of ischemia suggested that CI may be significantly more common in DLB. Larger studies are needed to evaluate the implications for treatment and to explore the underlying mechanisms.
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PMID:High prevalence of neurovascular instability in neurodegenerative dementias. 1053 86

We investigated the hippocampal pathology in diffuse Lewy body disease (DLBD) using alpha-synuclein immunohistochemistry. Ubiquitin-positive intrahippocampal structures caused by the degeneration of terminal axons of the perforant pathway were observed to be alpha-synuclein immunoreactive. These alpha-synuclein-positive degenerative terminals contained granulo-filamentous or vesiculo-tubular components similar to those of Lewy bodies (LB) immunoelectron microscopically, suggesting that alpha-synuclein may abnormally aggregate into filamentous or membranous cytoskeletal components including neurofilaments and synaptic vesicles in DLBD. A 'dying back' degenerating process due to a blockage of axonal transport may explain why the degenerative terminals and LB share similar alpha-synuclein-positive components, but the origin cells of the perforant pathway contain only a few LB.
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PMID:Degenerative terminals of the perforant pathway are human alpha-synuclein-immunoreactive in the hippocampus of patients with diffuse Lewy body disease. 987 32

Argyrophilic glial inclusions occur in the midbrain of patients with Parkinson's disease (PD) and diffuse Lewy body disease (DLBD). These inclusions are immunohistochemically positive for NACP/alpha-synuclein but negative for tau protein. The results of the present study suggest that a primary degenerative process involves NACP/alpha-synuclein in PD and DLBD and that the process takes place not only in neurons but also in glial cells. Argyrophilic cytoplasmic inclusions, both glial and neuronal, in a variety of degenerative diseases may be grouped into two major categories; one related to aggregates of abnormally phosphorylated tau protein and the other to unusual accumulations of NACP/alpha-synuclein.
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PMID:Argyrophilic glial inclusions in the midbrain of patients with Parkinson's disease and diffuse Lewy body disease are immunopositive for NACP/alpha-synuclein. 1002 63


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