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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 724 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 673 (1992), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words     Alzheimer's disease ; Cell death ; DNA fragmentation ; β-Amyloid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract      Loss of nerve cells is a hallmark of the pathology of Alzheimer's disease (AD), yet the patterns of cell death are unknown. By analyzing DNA fragmentation in situ we found evidence for cell death not only of nerve cells but also of oligodendrocytes and microglia in AD brains. In average, 30 times more brain cells showed DNA fragmentation in AD as compared to age-matched controls. Nuclear alterations suggestive of apoptosis were rare in degenerating cells. Even though the majority of degenerating cells were not located within amyloid deposits and did not contain neurofibrillary tangles, neurons situated within areas of amyloid deposits or affected by neurofibrillary degeneration revealed a higher risk of DNA fragmentation and death than cells not exposed to these AD changes.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 83 (1992), S. 653-658 
    ISSN: 1432-0533
    Keywords: Tubuloreticular structures (TRS) ; Microglia ; Amyloid ; Alzheimer's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In two of six brain biopsies of patients with Alzheimer's disease (AD), tubuloreticular structures (TRS) were observed in the distended endoplasmic reticulum of microglial cells, endothelial cells of vessels, and pericytes. In the microglial cells that produce amyloid fibrils, TRS were found in the cytoplasmic channels, which were filled with newly formed amyloid fibrils. Co-localization of TRS and newly formed amyloid fibrils in the same cellular compartment strengthens the hypothesis that amyloid fibrils are formed in the endoplasmic reticulum of microglial cells. Formation of TRS in microglial cells, pericytes, and endothelial cells of vessels probably reflects local or systemic α-interferon production. In some cells, this pathological process coexists with the second type of pathological changes: formation of amyloid fibrils.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 54 (1994), S. 473-477 
    ISSN: 0730-2312
    Keywords: mitogenesis ; mitotic index ; recovery ; increased mitosis ; PHA ; reversible mitotic inhibition ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Aluminum, the third most common element in the earth's crust (second to oxygen and silicon) and recently suspected by some investigators to be implicated in Alzheimer disease etiology, has been studied in relation to its effect on mitogenesis, mitosis, and cell cycle. We have observed that 2-4 mM concentrations of AlCl3 have decreased the number of cells that undergo mitogenesis (PHA-induced blast transformation) and mitosis in human short term whole blood cultures. We have also shown that the rate of the cell cycle was slowed down, i.e., cell cycle time was increased in the presence of AlCl3. Also, we have demonstrated a reversible effect on aluminum-induced reduced mitotic index in long-term EBV-transformed lymphoblastoid cultures. Although safeguards such as limiting aluminum serum concentrations have been recommended to protect individuals undergoing dialysis, it should be realized that concentration accumulations of aluminum may increase over chronic exposures. Accordingly, if the number of cells stimulated by PHA is reduced in the presence of AlCl3, there may be a reduction of immune competence, since the degree of PHA stimulation has been used as an indicator of immune response. Similar reductions in mitotic index could affect every tissue involved with cell division. Although it may not be the same for higher concentrations, from our results, we have also shown that decreased mitotic rates were reversible in long-term EBV-transformed lymphoblastoid cultures.Increased numbers of mitoses were observed in human short-term whole blood cultures that were exposed to 2 μM concentrations of aluminum chloride. The concentration is close to those found in normal human serum and within the “safeguard” range recommended for dialysis patients. A similar trend for aluminum sulfate was also observed, while preliminary results for three other aluminum species, lactate, citrate, and maltol, were also reported. Although previous reports have indicated a positive effect of aluminum on mitosis in vitro or in vivo, this is the first such report involving human material.It is clear that higher concentrations of aluminum chloride at 2.0-4.0 mM reversibly inhibit mitosis while more dilute concentrations of 1-2 μM, closer to those found in normal serum, enhance mitosis. The present results, as well as those in the literature, suggest that aluminum may be an essential element in cellular processes for optimal growth, development, and health maintenance. Future research will further test this hypothesis.
    Additional Material: 6 Tab.
    Type of Medium: Electronic Resource
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