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Neuropathological Study (neuropathological + study)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Delineation of Early Changes in Cases with Progressive Supranuclear Palsy-Like Pathology.

BRAIN PATHOLOGY, Issue 2 2009
Astrocytes in Striatum are Primary Targets of Tau Phosphorylation, GFAP Oxidation
Abstract Progressive supranuclear palsy (PSP) is a complex tauopathy usually confirmed at post-mortem in advanced stages of the disease. Early PSP-like changes that may outline the course of the disease are not known. Since PSP is not rarely associated with argyrophilic grain disease (AGD) of varible intensity, the present study was focused on AGD cases with associated PSP-like changes in an attempt to delineate early PSP-like pathology in this category of cases. Three were typical clinical and pathological PSP. Another case presented with cognitive impairment, abnormal behavior and two falls in the last three months. One case suffered from mild cognitive impairment, and two had no evidence of neurological abnormality. Neuropathological study revealed, in addition to AGD, increased intensity and extent of lesion in three groups of regions, striatum, pallidus/subthalamus and selected nuclei of the brain stem, correlating with neurological impairment. Biochemical studies disclosed oxidative damage in the striatum and amygdala. Together the present observations suggest (i) early PSP-like lesions in the striatum, followed by the globus pallidus/subthalamus and selected nuclei of the brain stem; (ii) early involvement of neurons and astrocytes, but late appearance of tufted astrocytres; and (iii) oxidative damage of glial acidic protein in the striatum. [source]

Early-onset Alzheimer's disease with presenilin-1 M139V mutation: clinical, neuropsychological and neuropathological study

EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2003
A. J. Larner
The clinical, neuropsychological and neuropathological features of a patient with early-onset Alzheimer's disease as a result of the M139V presenilin-1 (PSEN-1) mutation are presented, and compared with previous reports of patients with the same mutation. Similarities, such as the age at onset and the relative preservation of naming skills, and differences, such as the significant basal ganglia, thalamic and cerebellar pathology, are noted. This clinical and pathological heterogeneity in patients with the same PSEN-1 mutation suggests phenotype modulation by genetic and/or epigenetic factors. [source]

Decreasing myelin density reflected increasing white matter pathology in Alzheimer's disease,a neuropathological study

INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 10 2005
Martin Sjöbeck
Abstract Background White matter disease (WMD) is frequently seen in Alzheimer's disease (AD) at neuropathological examination. It is defined as a subtotal tissue loss with a reduction of myelin, axons and oligodendrocytes as well as astrocytosis. Studies quantitatively defining the myelin loss in AD are scarce. The aim was to develop a method that could provide numerical values of myelin density in AD. The purpose was to compare the myelin contents in increasing grades of pathology of WMD, with age and cortical AD pathology as well as in different regions of the brain in AD. Material and methods Sixteen cases with AD and concomitant WMD were investigated with an in-house developed image analysis technique to determine the myelin attenuation with optical density (OD) in frontoparietal, parietal, temporal and occipital white matter on whole brain coronal sections stained for myelin with Luxol Fast Blue (LFB). The OD values in LFB were compared grouped according to Haematoxylin/Eosin (HE) evaluated mild, moderate and severe WMD or normal tissue. The OD values were also correlated with age and cortical AD pathology and compared between the different studied white matter regions. Results Increasing severity of WMD was associated with a statistically significant OD reduction. No correlation was seen between age and OD or overall cortical AD pathology. The OD values were significantly lower in frontoparietal-compared to occipital white matter. Conclusions Myelin loss in AD with WMD is a marked morphologic component of the disease and it is possible to determine the reduction objectively in neuropathological specimens with quantitative measures. This may be of use for clinical diagnostics including brain imaging. Copyright © 2005 John Wiley & Sons, Ltd. [source]

Pathogenesis of equine herpesvirus-1 infection in the mouse model

APMIS, Issue 1 2009
GEORG GOSZTONYI
Equine herpesvirus-1 (EHV-1) is a major equine pathogen causing respiratory diseases, abortions and severe neurological disorders. The basis of neurological disturbances is, as in other organs, infection of endothelial cells, followed by vasculitis, thrombosis and ischaemic damage of the parenchyma. Here, a murine model was used to explore the mechanism of entry to, and spread within the brain, the cell affinity of the agent and the modulating role of the immune defence, which are all factors governing the pathogenesis of the neurological disease. Because controversial views exist about these mechanisms, we undertook a neuropathological study with intranasally infected adult mice. EHV-1 entered the brain through the olfactory neuroepithelium and along the olfactory nerves, and spread transsynaptically in rostro-caudal direction, using olfactory and limbic neuronal networks. Exclusively neurons were infected. The cellular immune reaction exerted a restraining effect on virus dissemination. Following nasal infection, the olfactory route was the major pathway for virus entry and dissemination, involvement of the trigeminal nerve in virus spread seems much less probable. In the adult mouse brain EHV-1 behaves as a typical neurotropic agent, using, similarly to other herpesviruses, the neuronal networks for dissemination. Vasculitis, the predominant type of lesion in natural infection, and endothelial cell positivity for EHV-1 were detectable only in the lung. Thus, this agent exhibits in the mouse a dual affinity: it is neurotropic in the brain, and endotheliotropic in visceral organs. Consideration of pathogenetic aspects of equine and experimental murine EHV-1 infections also helps a better understanding of human herpetic brain disease. [source]

Nonparametric One-way Analysis of Variance of Replicated Bivariate Spatial Point Patterns

BIOMETRICAL JOURNAL, Issue 1 2004
Sabine Landau
Abstract A common problem in neuropathological studies is to assess the spatial patterning of cells on tissue sections and to compare spatial patterning between disorder groups. For a single cell type, the cell positions constitute a univariate point process and interest focuses on the degree of spatial aggregation. For two different cell types, the cell positions constitute a bivariate point process and the degree of spatial interaction between the cell types is of interest. We discuss the problem of analysing univariate and bivariate spatial point patterns in the one-way design where cell patterns have been obtained for groups of subjects. A bootstrapping procedure to perform a nonparametric one-way analysis of variance of the spatial aggregation of a univariate point process has been suggested by Diggle, Lange and Bene, (1991). We extend their replication-based approach to allow the comparison of the spatial interaction of two cell types between groups, to include planned comparisons (contrasts) and to assess whole groups against complete spatial randomness and spatial independence. We also accommodate several replicate tissue sections per subject. An advantage of our approach is that it can be applied when processes are not stationary, a common problem in brain tissue sections since neurons are arranged in cortical layers. We illustrate our methods by applying them to a neuropathological study to investigate abnormalities in the functional relationship between neurons and astrocytes in HIV associated dementia. (© 2004 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source]