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Kurt A Jellinger

Publications and source records attributed to Kurt A Jellinger.

47 records · Page 3Linked to original sources
PubMed2003

The impact of cerebrovascular lesions in Alzheimer disease--a comparative autopsy study.

BACKGROUND: Recent epidemiological and clinico-pathological data suggest overlaps and some synergistic effects between Alzheimer disease (AD) and cerebrovascular pathology, but the results of studies of the relationship between the two types of lesion have been controversial. OBJECTIVE: Comparison of the frequency of cerebral infarcts, hemorrhages and minor cerebrovascular lesions in AD and age-matched control brains. SUBJECTS AND METHODS: 730 consecutive cases of autopsy-proven AD and 535 age-matched controls were compared using current routine and immunohistochemical methods. Results The total prevalence of cerebrovascular pathology in AD was significantly higher than in controls (48.0 vs 32.8%, p<0.01). Minor to moderate cerebrovascular lesions (lacunes, amyloid angiopathy with and without minor vascular lesions) were more frequent in AD than in controls (31.6 vs 23.4 %), the frequency of severe vascular pathology (old and recent infarcts and hemorrhages) in AD was significantly higher than in controls (16.7 % and 7.4 % vs 2.1% and 3.2%, respectively, p<0.01). There was no correlation between the severity of cerebral amyloid angiopathy with minor to severe subcortical lacunes and Ammon's horn sclerosis or to acute and old ischemic infarcts. On the other hand, acute and old cerebral hemorrhages were significantly correlated with severe amyloid angiopathy. The brain weight and severity of cognitive decline did not correspond to the degree of vascular pathology, but higher neuritic Braak scores and reduced brain weight contributed to the production of cognitive impairment. CONCLUSION: In accordance with previous findings in AD and in Parkinson disease, our data indicate a higher incidence of cerebrovascular lesions and greater susceptibility to death from stroke in AD in the population studied, but further prospective clinicopathological studies are warranted.

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PubMed2002

The pathology of ischemic-vascular dementia: an update.

In Western memory clinic-based series, ischemic-vascular dementia (IVD) is seen in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series ranges from 0.03% to 58% with reasonable values of 4-10%, while in Japan, IVD is seen in 22-35% and mixed-type dementia (MTD) (Alzheimer disease/AD+IVD) in 6-11%. In a large Viennese autopsy series, "pure" IVD was observed in 9.4% of demented elderly and in 2.9% of those clinically diagnosed as possible/probable AD MTD was observed in 3.1% and 1.3% respectively. The major morphological types of IVD are multi-infarct encephalopathy (MIE), small vessel infarct type-strategic infarct dementia (SID), subcortical arteriosclerotic leukoencephalopathy (Binswanger), multilacunar state, mixed cortico-subcortical type, granular cortical atrophy, and post-ischemic encephalopathy. In contrast to previous suggestions that IVD is mainly the result of large hemispheral infarcts or losses of over 100 ml of brain tissue, recent data indicate that cognitive decline is commonly associated with widespread small ischemic or vascular lesions (microinfarcts, lacunes) throughout the brain with predominant involvement of the basal ganglia, white matter, and hippocampus. The lesion pattern of "pure" IVD, which is related to arteriolosclerosis and hypertensive microangiopathy, differs from that in mixed-type dementia, more often showing large infarcts. Although recent studies suggest that concomitant small cerebral infarcts do not significantly influence the overall rate of cognitive decline in AD patients or may be important for mental decline in early AD, both mild AD pathology and microvascular cerebral lesions appear to be common and may interact in "unmasking" or promoting dementia.

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PubMed2002

Reduction of chromogranin B-like immunoreactivity in distinct subregions of the hippocampus from individuals with schizophrenia.

Synaptic disturbances may play a key role in the pathophysiology of schizophrenia. This study was designed to further investigate possible synaptic alterations in the brains of chronic schizophrenic patients. Chromogranin B was applied as a marker for large dense core vesicles and synapsin I as a protein associated with the synaptic vesicle membrane. The distribution and density of chromogranin B-and synapsin I-like immunoreactivity in subregions of the hippocampus was compared between controls (n = 16) and patients with schizophrenia (n = 17). The overall distribution of hippocampal chromogranin B- and synapsin I-like immunoreactivity was similar in controls and in schizophrenic patients with the highest densities in the terminal field of mossy fibers and in the inner molecular layer of the dentate gyrus. In schizophrenic hippocampi, a significant reduction in the density of chromogranin B-like immunoreactivity was found in the CA4 and CA3 but not in the CA1 area of the dentate gyrus based on computerized image analysis. The loss of immunoreactivity was localized to mossy fibers and terminals surrounding hilar interneurons. Double-labelling immunohistochemistry revealed that synapsin I was co-expressed with chromogranin B in these neuronal structures and was also significantly reduced in schizophrenic hippocampi. The present study demonstrates an area-specific reduction of chromogranin B which is paralleled by a decrease of synapsin I. The loss of presynaptic proteins involved in distinct steps of exocytosis may cause complex synaptic disturbances in specific hippocampal subregions resulting in an imbalanced neurotransmitter availability in schizophrenic patients.

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PubMed2002

Incidence of cerebrovascular lesions in Alzheimer's disease: a postmortem study.

Recent epidemiological and clinico-pathological data suggest overlaps between Alzheimer's disease (AD) and cerebrovascular lesions (CVL) that may show some synergistic effects, but the results of studies of the relationship between AD and stroke have been controversial. The objective of this study was to compare the frequency of cerebral infarcts, hemorrhages and minor cerebrovascular lesions in autopsy-confirmed AD and age-matched control brains. Using current routine and immunohistochemical methods 173 consecutive cases of autopsy-confirmed AD and 130 age-matched controls were compared. The total incidence of vascular pathology (56.5%) in AD was significantly less than in a previously reported smaller AD autopsy cohort (82.3%) (P<0.01), and was higher than in controls (42.4%). The incidence of severe CVL (old and recent infarcts, hemorrhages) in our cohort was slightly higher (12.7%) than in controls (8.5%), that of minor to moderate CVL (lacunes, cerebral amyloid angiopathy with or without minor vascular lesions) was more frequent in AD (43.8%) than in controls (33.9%), but the results were not statistically significant (P<0.03). The brain weight and severity of cognitive decline did not correspond to the degree of vascular pathology, but higher neuritic Braak scores and reduced brain weight contributed to the production of cognitive impairment. Like previous findings in Parkinson's disease, our data do not indicate a protective effect from stroke or a significantly greater susceptibility to death from stroke in AD in the population studied, but further prospective clinico-pathological studies are necessary.

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