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  • 1
    Electronic Resource
    Electronic Resource
    Expression Pattern of Synucleins (Non-Aβ Component of Alzheimer's Disease Amyloid Precursor Protein/α-Synuclein) During Murine Brain Development (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 71 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The non-Aβ component of Alzheimer's disease amyloid precursor protein (NACP) is predominantly a neuron-specific presynaptic protein that may play a central role in neurodegeneration because NACP fragments are found in Alzheimer's disease amyloid and a mutation in the NACP gene is associated with familial Parkinson's disease. In addition, NACP may play an important role during synaptogenesis and CNS development. To understand better the patterns of NACP expression during development, we analyzed the levels of this protein as well as the levels of another synaptic protein (synaptophysin) by ribonuclease protection assay, western blotting, and immunocytochemistry in fetal, juvenile, and adult mouse brain. From embryonic day 12 to 15, there was a slight increase, which was then followed by a more dramatic increase at later time points. Immunocytochemical staining for NACP increases throughout these stages as well. Although NACP appeared early in CNS development, synaptophysin levels started to rise at a later stage. These findings support the contention that NACP might be important for CNS development. Furthermore, the cytosolic component of NACP precedes the particulate component in development, indicating that a redistribution of the protein to the membrane fraction may be important for events later in neuronal development and in synaptogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.71010338.x
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  • 2
    Electronic Resource
    Electronic Resource
    Vitamin E supplementation prevents spatial learning deficits and dendritic alterations in aged apolipoproteinE-deficient mice (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent studies have suggested that altered function of apolipoprotein E might lead to Alzheimer's disease via oxidative stress. In this context, the objective of this study was to determine if antioxidative treatment with vitamin E was neuroprotective in apolipoprotein E-deficient mice. For this purpose, 1-month-old control and apolipoprotein E-deficient mice received dietary vitamin E for 12 months. We showed that, compared to apolipoprotein E-deficient mice who received a regular diet, mice treated with vitamin E displayed a significantly improved behavioural performance in the Morris water maze. This improved performance was associated with preservation of the dendritic structure in vitamin E-treated apolipoprotein E-deficient mice. In addition, whilst untreated apolipoprotein E-deficient mice displayed increased levels of lipid peroxidation and glutathione, vitamin E-treated mice showed near normal levels of both lipid peroxidation and glutathione. These results support the contention that vitamin E prevents the age-related neurodegenerative alterations in apolipoprotein E-deficient mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2000.01308.x
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  • 3
    Electronic Resource
    Electronic Resource
    Amyloidogenic role of cytokine TGF-β1 in transgenic mice and in Alzheimer's disease (1997)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 389 (1997), S. 603-606 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Deposition of amyloid-β peptide in the central nervous system is a hallmark of Alzheimer's disease and a possible cause of neurodegeneration. The factors that initiate or promote deposition of amyloid-β peptide are not known. The transforming growth factor TGF-β1 plays a central ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/39321
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  • 4
    Electronic Resource
    Electronic Resource
    Topographical distribution of synaptic-associated proteins in the neuritic plaques of Alzheimer's disease hippocampus (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 135-142 
    Details
    ISSN: 1432-0533
    Keywords: Synaptophysin ; Synaptic vesicle proteins ; Hippocampus ; Neuritic plaque ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Studies of the molecular composition of the abnormal neuritic processes of the plaques in Alzheimer's disease (AD) have shown that these structures are immunoreactive with antibodies against growth-related molecules, synaptic/axonal proteins, and cytoskeletal proteins. These studies suggest that a subpopulation of abnormal neurites in the plaque are sprouting axons that eventually degenerate. To test this hypothesis further we studied the regional distribution of plaques in the hippocampus using a panel of monoclonal antibodies against synaptic proteins. With these antibodies we found a greater proportion of immunoreactive plaques compared to previous studies where a monoclonal antibody against synaptophysin was used. The most sensitive antobodies to detect neuritic plaques were SP11 and anti-p65, and the largest number of positive plaques was found in the entorhinal cortex and CA1 region. These results further support the theory that synaptic and axonal damage are involved in plaque formation in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296182
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  • 5
    Electronic Resource
    Electronic Resource
    Topographical distribution of synaptic-associated proteins in the neuritic plaques of Alzheimer's disease hippocampus (1994)
    Springer
    Acta neuropathologica 87 (1994), S. 135-142 
    Details
    ISSN: 1432-0533
    Keywords: Key words: Synaptophysin – Synaptic vesicle proteins – Hippocampus – Neuritic plaque – Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Studies of the molecular composition of the abnormal neuritic processes of the plaques in Alzheimer's disease (AD) have shown that these structures are immunoreactive with antibodies against growth-related molecules, synaptic/axonal proteins, and cytoskeletal proteins. These studies suggest that a subpopulation of abnormal neurites in the plaque are sprouting axons that eventually degenerate. To test this hypothesis further we studied the regional distribution of plaques in the hippocampus using a panel of monoclonal antibodies against synaptic proteins. With these antibodies we found a greater proportion of immunoreactive plaques compared to previous studies where a monoclonal antibody against synaptophysin was used. The most sensitive antibodies to detect neuritic plaques were SP11 and anti-p65, and the largest number of positive plaques was found in the entorhinal cortex and CA1 region. These results further support the theory that synaptic and axonal damage are involved in plaque formation in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296182
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Neurofibrillary tangles in the dentate granule cells of patients with Alzheimer’s disease, Lewy body disease and progressive supranuclear palsy (1996)
    Springer
    Acta neuropathologica 93 (1996), S. 7-12 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neurofibrillary tangle ; Dentate granule cell ; Alzheimer’s disease ; Lewy body disease ; Progressive ; supranuclear palsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have shown that the dentate granular cells of the hippocampus are affected in patients with Alzheimer’s disease (AD). To gain a better understanding of the cytoskeletal alterations in these cells, we carried out immunocytochemical and immunoelectron microscopic analysis of the dentate gyrus of patients with primary degenerative dementias, using a monoclonal antibody against paired helical filaments (TG3). This antibody labeled a large number of spherical inclusions in the dentate granule cells of patients with AD and its Lewy body variant (LBV). These inclusions consisted of straight tubular structures (about 18–25 nm in diameter), similar to those found in progressive supranuclear palsy (PSP). These inclusions, although in a smaller number, were also found in demented patients with PSP, but not in those with diffuse Lewy body disease or age-matched controls. These findings indicate that the neurofibrillary alterations in the dentate granule cells of patients with AD, LBV and PSP share cytoskeletal similarities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050576
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  • 7
    Electronic Resource
    Electronic Resource
    In vitro synaptotrophic effects of Cerebrolysin in NT2N cells (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 437-446 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cerebrolysin ; Synaptotrophic effect ; Amyloid precursor protein ; NT2N cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have shown that Cerebrolysin can enhance synaptic function and ameliorate synapto-dendritic alterations in animal models of neurodegeneration, suggesting a synaptotrophic effect. We hypothesize that Cerebrolysin might exert this effect, in part, by regulating the expression of amyloid precursor protein (APP). We studied the patterns of expression of synaptic proteins during differentiation of human teratocarcinoma cell line NTera 2 (NT2) in the presence or absence of Cerebrolysin. This study showed that the terminally differentiated neurons (NT2N) expressed a wide variety of synaptic markers and that expression of these synaptic-associated proteins coincided with the shift in expression from APP770/751 to APP695. Furthermore, APP immunoreactivity was colocalized with synaptophysin-immunoreactive neuritic varicosities in NT2N neurites, and Cerebrolysin treatment of NT2N cells resulted in an augmented and earlier expression of synaptic-associated proteins. This increased synaptic protein expression coincided with an increase in APP695 over APP770/751. These results support the possibility that synaptotrophic effects of Cerebrolysin might be mediated via regulation of APP expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051012
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  • 8
    Electronic Resource
    Electronic Resource
    Alterations in glutamate receptor 2/3 subunits and amyloid precursor protein expression during the course of Alzheimer’s disease and Lewy body variant (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 539-548 
    Details
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Lewy body variant ; Glutamate receptor ; Amyloid precursor protein ; expression ; Vulnerability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations in the processing and patterns of trophic and/or toxic factors might lead to the increased neuronal vulnerability in the entorhinal cortex in Alzheimer’s disease (AD) and Lewy body variant (LBV). Therefore, patterns and levels of amyloid precursor protein (APP) and glutamate receptor (gluR) expression in the entorhinal cortex and hippocampus in relation to disease severity were investigated. Sections from the hippocampus and entorhinal cortex were single and double immunolabeled for APP, gluR2/3, and n-methyl-d-aspartate receptor (NMDA-R). Within the hippocampus and entorhinal cortex, image analysis revealed progressively decreased APP and gluR2/3 levels during the course of AD and LBV, whereas levels of NMDA-R were unaltered. Furthermore, the present study showed a positive correlation and close co-localization of APP and gluR2/3 immunoreactivity in neurons, suggesting a possible interaction between these two factors. In conclusion, these data imply that alterations in neuronal APP and gluR2/3 expression in the entorhinal cortex lead to increased susceptibility to neurodegeneration and might be markers of vulnerability.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050748
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