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  • 1990-1994  (3)
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Year
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 580 (1990), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Alzheimer's disease (AD) is characterized by the presence of extracellular amyloid plaques, which contain a protein referred to as the amyloid or βA4 protein. The βA4 protein is derived from a larger precursor protein (APP). Studies of autosomal-dominant forms of AD have established the central role of APP in the pathogenesis of the disease. Despite considerable research, the function of APP is unknown. APP can be processed by at least two separate routes. The first route involves a protease known as “APP secretase,” which cleaves within the amyloid sequence, thereby mitigating amyloid formation. The second route may result in the production of potentially amyloidogenic fragments. Our studies suggest that following release from the cell membrane, APP interacts with components of the extracellular matrix (ECM) such as the heparan sulfate proteoglycans (HSPG's). The interaction of APP with HSPG's may be important for the function of APP. Substratum-bound APP was found to dramatically increase neurite outgrowth and survival of chick sympathetic neurons in vitro. This effect was dependent upon the presence of substratum-bound HSPG. The results suggest that normally, when bound to the ECM, APP functions to promote neurite outgrowth and/or cell survival. Loss of this normal trophic function might occur in AD, when APP is proteolytically processed via the amyloidogenic pathway.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Competition between neurons for limited amounts of trophic factors is believed to be the basis for large-scale neuronal death during the normal development of the vertebrate nervous system. In this study, an unbiased stereological counting method, an optical disector/Cavalieri combination, was used to estimate the total number of motor neurons in the lateral motor column of the developing chick and to assess the effects of four growth factors on neuronal numbers. The total number of neurons in lateral motor columns at embryonic day 6 (E6), E8, E10 and E12 were 18,747 ± 1,369 (mean ± SD), 15,037 ± 1,816, 10,245 ± 940, and 8,802 ± 797, respectively. Daily exposure from E6 to E9 to three of the growth factors (basic fibroblast growth factor, bFGF; leukemia inhibitory factor, LIF; nerve growth factor, NGF) had no effect on total neuron number at E10. However, exposure to ciliary neurotrophic factor (CNTF) from E6 to E9 significantly increased (P 〈 0.05) the number of neurons in the lateral motor column (13,610 ± 725, compared with 10,058 ± 204 in normal saline controls). These results are in agreement with previous reports of large scale neuronal death in the developing chick lumbar lateral motor column between E6 and E12 and confirm that exposure to growth factors such as CNTF can mitigate the course of normal ontogenetic cell death. The optical disector/Cavalieri combination is an efficient method for counting neurons: on average, following sectioning and staining, less than 30 min was required to estimate the total number of motor neurons in a lateral motor column with a coefficient of error of approximately 10%.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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