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  • Key words Cell cycle  (2)
  • A69024  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Expression of cell division markers in the hippocampus in Alzheimer’s disease and other neurodegenerative conditions (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 294-300 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cell cycle ; Ki-67 ; Apoptosis ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies, showing that cell cycle-related nuclear proteins p105 and Ki-67 are associated with Alzheimer’s disease (AD)-related cytoskeletal pathology, suggested that these proteins, in addition to their functions in regulating the cell cycle, may have more specialised functions in the adult nervous system. In order to test this hypothesis we studied the expression of the cell cycle-related proteins Ki-67, pCNA and p53 in the hippocampi of 33 subjects, including some with AD or other neurodegenerative disorders and some with no neurological disease. By immunohistochemistry we found nuclear expression of Ki-67 in all subregions of the hippocampus, with the highest levels in the dentate gyrus. Both neurons and glial cells expressed this protein. The proportion of cells positive for Ki-67 and the distribution pattern varied considerably depending on the pathological diagnosis. Neuronal nuclear expression of Ki-67 was increased in AD but was also elevated in young Down’s syndrome subjects and in those with Pick’s disease. Expression of this protein was therefore not AD-specific. We did not find nuclear pCNA or p53 expressed in our patient groups. Contrary to previous studies AD-type neurofibrillary tangles were not labelled with any of the cell cycle markers used. The presence of nuclear Ki-67 expression indicates that some hippocampal neurons are not in the quiescent G0 phase but have re-entered the cell cycle. The absence of nuclear pCNA or p53 suggests that the cycle is arrested in G1. The significance of our findings and their relationship to the production of neurodegenerative cell death via an apoptotic mechanism are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050617
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  • 2
    Electronic Resource
    Electronic Resource
    Cell cycle markers in the hippocampus in Alzheimer’s disease (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 6-15 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cell cycle ; Alzheimer’s disease ; Down’s syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using immunohistochemistry we have analysed the nuclear expression of cyclins A, B, D, and E in neurones in the hippocampi of control subjects and patients suffering from various neurodegenerative disorders including Alzheimer’s disease (AD). Cyclins A and D could not be detected but varying degrees of cyclin E expression were found in all patient groups including control subjects. Cyclin B expression was not detected in control subjects but it was expressed in the subiculum, dentate gyrus and CA1 region in patients with AD-type pathology and in the CA2 region and the dentate gyrus of cases of Pick’s disease. These reults suggest that some neurones may have re-entered the cell cycle. The expression of cyclin E without cyclin A expression may indicate an arrest in G1 with the possibility of re-differentiation and exit from G1 to G0. The expression pattern of cyclin E indicates that re-entry into the cell cycle is possible even in control patients, but it is accentuated in patients with AD-related pathology. However, cyclin B was only expressed in AD patients and occurred in areas that were severely affected by pathology. Neurones with cyclin B-reactive nuclei in AD were AT8 positive but did not contain fully developed tangles. In neurones, where cyclin B is expressed, it would appear that the G1/S checkpoint has been bypassed and that the cell cycle is arrested in G2. It is proposed that these neurones do not have the opportunity for subsequent re-differentiation. Since factors known to be present in G2 seem to be responsible for microtubule destabilisation and hyperphosphorylation of tau we hypothesise that cell cycle disturbances may be important in the pathogenesis of AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050665
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Differential effects of dopamine receptor subtype blockade on performance of rats in a reaction-time paradigm (2000)
    Springer
    Psychopharmacology 148 (2000), S. 355-360 
    Details
    ISSN: 1432-2072
    Keywords: Key words Reaction time ; Motor impairment ; Eticlopride ; Nafadotride ; A69024 ; D1 receptor ; D2 receptor ; D3 receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Rationale: Pharmacological manipulation of the dopaminergic system with antipsychotic agents disrupts motor behavior. Although most antipsychotic drugs have high affinity for D2 receptors, they also interact with other dopamine receptor subtypes. Therefore, the role of each of these receptor subtypes on motor performance is unclear. Objective: The present study sought to investigate the relative importance of D1, D2, and D3 receptors on performance in a conditioned reaction-time task known to be extremely sensitive to dysfunction of the dopaminergic nigrostriatal pathway. Methods: Rats were trained to release a lever in response to a visual cue within a reaction-time limit to receive a reinforcer (45-mg food pellet). After the behavior of the rats had stabilized, the effects of a D1 (A69024), D2 (eticlopride), and D3 (nafadotride) receptor antagonists were assessed. Results: A-69024 had no effect on performance at any dose tested (0.3, 0.6, and 1.3 mg/kg s.c.). Nafadotride (0.1, 0.3, and 1 mg/kg s.c.) produced only a mild deficit in performance at the highest dose. This deficit was characterized by an increase in the number of delayed responses with a non-significant decrease in the number of premature responses indicative of non-specific sedative effects. In contrast, the D2 receptor antagonist eticlopride (0.005, 0.01, and 0.02 mg/kg s.c.) produced profound deficits in performance as evidenced by a dose-dependent decrease in the number of correct responses. This decrease was accompanied by an increase in the number of delayed responses and a lengthening of the reaction time at the highest doses. Conclusions: These results provide further evidence that the execution of the reaction-time task is dependent preferentially upon the activation of D2 receptors, but not D1 or D3 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050063
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    Paper (German National Licenses)
    Fulltext
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