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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 88 (1994), S. 565-570 
    ISSN: 1432-0533
    Keywords: Dementia ; Alzheimer's disease ; Neurofibrillary tangles ; Limbic Alzheimer pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In a consecutive autopsy series of 580 demented elderly subject, 256 with the clinical diagnosis of probable/possible Alzheimer's disease (AD), there were 10 cases aged between 80 and 99 years with moderate to severe dementia or confusional state in which neuropathological studies revealed abundant neurofibrillary tangles with predominant involvement of the allocortex (entorhinal region, subiculum, CA 1 sector of hippocampus, amygdala) but no or only very few senile plaques. Small numbers of diffuse deposits of βA4 amyloid protein were present in the entorhinal cortex of 3 and in the isocortex of 5 brains, while neuritic plaques were totally absent. Only a few cases of this “senile dementia with tangles only” or, more correctly, “neurofibrillary predominant type of AD” corresponding to the limbic stage of neuritic AD pathology have been described in the literature. This rare subtype occurring in very old (over 80 years of age) subjects that does not fall within the currently used neuropathological criteria for diagnosis of AD warrants further clinico-pathological documentation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 84 (1992), S. 478-483 
    ISSN: 1432-0533
    Keywords: Progressive supranuclear palsy ; Steele Richardson ; Olszewski syndrome ; Neurofibrillary changes ; Entorhinal region ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Silver techniques for intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy (three were mentally unimpaired and three showed moderate degrees of dementia). Deposits of A4-amyloid protein occurred in small numbers or were absent. Neurofibrillary tangles and neuropil threads were present in all cases and were largely confined to the allocortex. A characteristic pattern of changes was found in the entorhinal cortex. The three mentally unimpaired individuals had mild cortical changes virtually confined to the transentorhinal region while all of the demented patients showed severe destruction of the superficial cellular layer in both the transentorhinal and entorhinal region. This pattern of allocortical destruction closely resembles that seen in clinically incipient Alzheimer's disease or in mentally impaired cases of Parkinson's disease. The entorhinal region receives dense input from isocortical association areas and projects via the perforant path to the hippocampal formation. The cells of origin of major portions of the perforant path are located within the superficial entorhinal cellular layer. Destruction of this layer partially or totally disconnects the hippocampus from the isocortex. The specific pattern of entorhinal destruction is considered to contribute to cognitive impairment and personality changes, frequently seen in patients with progressive supranuclear palsy.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 239 (1989), S. 177-179 
    ISSN: 1433-8491
    Keywords: Quinolinic acid ; Senile dementia of Alzheimer type ; Huntington's disease ; Neurotoxin ; Dementia ; Postmortem brain ; Gas chromatography/mass spectrometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Quinolinic acid (QA) content was measured in postmortem frontal and temporal cortex, putamen and cerebellum obtained from patients with senile dementia of Alzheimer type (SDAT), Huntington's disease (HD) and controls, using a gas chromatography/mass spectrometry method. There were no significant group differences in QA content of any of the regions examined. The data do not support the hypothesis that an accumulation of QA plays a role in neuronal degeneration occurring in the frontal and temporal cortex, putamen and cerebellum of patients with SDAT.
    Type of Medium: Electronic Resource
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