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  • 1
    Electronic Resource
    Electronic Resource
    Association of apolipoprotein ɛ4 allele and neuropathologic findings in patients with dementia (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 239-243 
    Details
    ISSN: 1432-0533
    Keywords: Apolipoprotein E ; Dementia ; Diffuse Lewy body disease ; Alzheimer's disease ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apolipoprotein E (APOE) is a lipoprotein expressed in liver and brain as one of three isoforms (APOE 2, APOE 3 and APOE 4). Recent findings suggest that the presence of APOE 4 is associated with an increased risk for both familial Alzheimer's disease and late-onset Alzheimer's disease. We extended these observations by determining the frequency of APOE alleles in patients with pathologically confirmed Alzheimer's Disease (AD), Parkinson's disease (PD), diffuse Lewy Body disease (DLBD), AD with concomitant PD pathology, demented PD patients without or with concomitant AD pathology and in schizophrenics with a progressive dementia (SCHIZ+DEM). The APOE genotype was determined by restriction digestion of polymerase chain reaction-amplified DNA isolated from frozen brain samples. The frequency of the APOE ɛ4 allele was highest among sporadic AD and DLBD patients (0.30 and 0.38, respectively) and lowest in the SCHIZ+DEM and non-demented PD patients (0.06 and 0.1, respectively). Thus, the APOE ɛ4 allele is over-represented selectively in patients with dementias associated with plaques and tangles and/or cortical Lewy bodies, but not in demented schizophrenics or non-demented PD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296506
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 469-481 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyotrophy ; Axonopathy ; Neurofilaments ; Tau protein ; Transgenic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Coding region and intronic mutations in the tau gene cause frontotemporal dementia and parkinsonism linked to chromosome 17. Some of these mutations lead to an overproduction of tau isoforms with four microtubule-binding repeats. Here we have expressed the longest four-repeat human brain tau isoform in transgenic mice under the control of the murine Thy1 promoter. Transgenic mice aged 3 weeks to 25 months overexpressed human tau protein in nerve cells of brain and spinal cord. Numerous abnormal, tau-immunoreactive nerve cell bodies and dendrites were seen. In addition, large numbers of pathologically enlarged axons containing neurofilament- and tau-immunoreactive spheroids were present, especially in spinal cord. Signs of Wallerian degeneration and neurogenic muscle atrophy were observed. When motor function was tested, transgenic mice showed signs of muscle weakness. Taken together, these findings demonstrate that overexpression of human four-repeat tau leads to a central and peripheral axonopathy that results in nerve cell dysfunction and amyotrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051148
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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