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  • 1
    Electronic Resource
    Electronic Resource
    Ca2+ and Reactive Oxygen Species in Staurosporine-Induced Neuronal Apoptosis (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Staurosporine (0.03–0.5 µM) induced a dose-dependent, apoptotic degeneration in cultured rat hippocampal neurons that was sensitive to 24-h pretreatments with the protein synthesis inhibitor cycloheximide (1 µM) or the cell cycle inhibitor mimosine (100 µM). To investigate the role of Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis, we overexpressed calbindin D28K, a Ca2+ binding protein, and Cu/Zn superoxide dismutase, an antioxidative enzyme, in the hippocampal neurons using adenovirus-mediated gene transfer. Infection of the cultures with the recombinant adenoviruses (100 multiplicity of infection) resulted in a stable expression of the respective proteins assessed 48 h later. Overexpression of both calbindin D28K and Cu/Zn superoxide dismutase significantly reduced staurosporine neurotoxicity compared with control cultures infected with a β-galactosidase overexpressing adenovirus. Staurosporine-induced neuronal apoptosis was also significantly reduced when the culture medium was supplemented with 10 or 30 mM K+, suggesting that Ca2+ influx via voltage-sensitive Ca2+ channels reduces this apoptotic cell death. In contrast, neither the glutamate receptor agonist NMDA (1–10 µM) nor the NMDA receptor antagonist dizocilpine (MK-801; 1 µM) was able to reduce staurosporine neurotoxicity. Cultures treated with the antioxidants U-74500A (1–10 µM) and N-acetylcysteine (100 µM) also demonstrated reduced staurosporine neurotoxicity. These results suggest a fundamental role for both Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68041679.x
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  • 2
    Electronic Resource
    Electronic Resource
    No correlation between aggregates of Cu/Zn superoxide dismutase and cell death in familial amyotrophic lateral sclerosis (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 82 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aggregates of Cu/Zn superoxide dismutase (SOD) have been demonstrated in familial amyotrophic lateral sclerosis (FALS) and other neurodegenerative diseases; however, their role in disease pathogenesis is unclear. In this study, we investigated the presence of SOD aggregates in nerve growth factor (NGF)-differentiated PC12 cells and cell viability following: (i) transduction with replication-deficient recombinant adenoviruses (AdVs) expressing wild-type SOD (SODWT) or mutant SOD (SODMT, V148G or A4V); (ii) transfection of yellow fluorescent protein-tagged SODWT (SODWT-YFP) or SODMT (SODA4V-YFP, SODV148G-YFP). SOD aggregates were more prominent in cells following transduction of AdSODMT than AdSODWT and following treatment with H2O2, suggesting that mutant SOD leads to oxidation of cellular components. In addition, cells expressing SODMT-YFP yielded SOD aggregates that were significantly larger and more frequent than SOD aggregates in cells expressing SODWT-YFP. Proteasome inhibitors, but not cathepsin B inhibitors, increased aggregate formation but did not increase cell death. In addition, treatments that increased cell viability did not significantly decrease SOD aggregates. Taken together, our data demonstrate that there is no association between SOD aggregates and cell death in FALS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.01056.x
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  • 3
    Electronic Resource
    Electronic Resource
    The clinimetrics of hypokinesia in Parkinson's disease: Subjective versus objective assessment (1994)
    Springer
    Journal of neural transmission 8 (1994), S. 117-121 
    Details
    ISSN: 1435-1463
    Keywords: Hypokinesia ; assessment ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In this study we evaluate the feasibility of measures that reflect different characteristics of motor activity and immobility in the objective quantification of hypokinesia. Because by definition hypokinesia can only be assessed over a period of time, continuous activity monitoring was used during 5 successive days in the home setting in 64 patients with Parkinson's disease (PD) and 104 healthy elderly subjects. In the patients we also evaluated the relation between the monitor measures and subjective measures of hypokinesia and age. Compared to the healthy elderly subjects, PD patients have a decreased activity level, increased proportion of time without movement, elevated mean duration of immobility, and decreased percentage of short-lasting immobility periods. Differences between both groups were most prominent for those measures that incorporate or reflect immobility. Moreover, in the PD patients the mean duration of immobility and percentage of short-lasting immobility periods show an apparent lack of relation with age and clinical ratings obtained from the UPDRS. In conclusion, our findings underscore the poor representation of hypokinesia in the UPDRS and value of objective quantification of this fundamental impairment of PD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02250922
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  • 4
    Electronic Resource
    Electronic Resource
    Sleep, excessive daytime sleepiness and fatigue in Parkinson's disease (1993)
    Springer
    Journal of neural transmission 5 (1993), S. 235-244 
    Details
    ISSN: 1435-1463
    Keywords: Sleep ; daytime sleepiness ; fatigue ; Parkinson's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The objective of this questionnaire-based survey was to evaluate the prevalence and causes of sleep disturbances in 90 nondepressive patients with Parkinson's disease (PD) and 71 age-matched healthy subjects. We also assessed the prevalence and characteristics of excessive daytime sleepiness (both groups) and excessive fatigue (PD patients). A high prevalence of sleep disturbances in PD patients was found; this is to a large extent probably the result of aging. As compared with controls, patients had a more severely disturbed sleep maintenance because of nycturia, pain, stiffness, and problems with turning in bed. The prevalence of excessive dreaming is similar in both groups, but altered dream experiences almost exclusively occurred in PD. Patients rated themselves more often to be morning-types than controls. This finding may account for the reported adaptation effects in experimental settings and the reduced REM latency in PD patients. The prevalence of daytime sleepiness was similar in both groups. Excessive daytime sleepiness showed a clear diurnal pattern with a peak in the early afternoon. As for excessive fatigue, the majority of the patients did not report a preferential time for this symptom. Our findings further argue against an association of fatigue with any circadian factor, and instead suggest a relationship with the motor deficits of PD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02257678
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  • 5
    Electronic Resource
    Electronic Resource
    Gastrostomy and gastric colonization (1986)
    Springer
    Pediatric surgery international 1 (1986), S. 125-129 
    Details
    ISSN: 1437-9813
    Keywords: Gastrostomy ; Septicemia ; Gastric colonization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Quantitative bacterial counts were carried out on 161 gastric aspirates from 65 neonates with gastrostomies. Enterobacteriaceae, enterococci, Pseudomonas, and Candida were found far more frequently (P 〈00.01) than in 101 control cultures from premature infants without gastrostomies. Colonization of the sstomach was influenced by the duration of gastrostomy and the pH of gastric juice but not by systemic antibiotic therapy or type of food. Six newborns with gastrostomies developed septicemia caused by the same organisms present in elevated numbers in their gastric aspirates. The influence of non-absorbable antibiotics was studied prospectively in 72 gastric aspirates and 48 stool specimens. There was no significant difference between infants who had been treated with these antibiotics and those who had not.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166874
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  • 6
    Electronic Resource
    Electronic Resource
    Neuropathy accompanying IgMλ monoclonal gammopathy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 255-261 
    Details
    ISSN: 1432-0533
    Keywords: IgM monoclonal gammopathy ; Neuropathy ; Myelin-associated glycoprotein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A set of observations made on a patient with IgMλ monoclonal gammopathy and neuropathy implicate humoral immunity in the pathogenesis of the neuropathy. A sural nerve biopsy from the patient showed a characteristic increase in the width of the intraperiod lines. Deposits of μ-heavy chains and λ-light chains were found in myelin sheaths of the nerve biopsy. Immunohistochemically, it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin sheaths of normal peripheral nerves and to a lesser extent to myelin sheaths in the central nervous system (CNS). By immunoblots it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin associated glycoprotein but to no other antigens from the peripheral and central nervous systems. γ and α heavy chains and ϰ light chains from the patient's serum were also shown to bind to myelin-associated glycoprotein but not as distinctly as the μ and λ chains. It is postulated that the monoclonal gammopathy may have arisen on the background of polyclonal autoimmune attack directed against myelin-assoiated glycoprotein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691490
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  • 7
    Electronic Resource
    Electronic Resource
    Morphology of cerebral plaque-like lesions in hereditary cerebral hemorrhage with amyloidosis (Dutch) (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 674-679 
    Details
    ISSN: 1432-0533
    Keywords: Hereditary cerebral hemorrhage with amyloidosis ; Dutch type ; Amyloid β/A4 protein ; Diffuse plaques ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the presence and morphology of plaque-like lesions in the frontal cortex of six patients, aged 40 to 76 years, with hereditary cerebral hemorrhage with amyloidosis — Dutch type (HCHWA-D), using β/A4 immuno-, silver, Congo red and thioflavin S staining. Two types of β/A4 immunoreactive and Congo red-negative plaques were detected. The first type was composed of argyrophilic fibrous material in periodic acid-methenamine silver (PAM) and modified Bielschowsky staining and lacked silver-stained degenerating neurites. Therefore, this type of plaque has the same staining properties as the diffuse plaque described in Alzheimer's disease, Down's syndrome and nondemented elderly. The second type of plaque, occurring only in the three oldest patients and numerically increasing with age, consisted of a spherical non-argyrophilic area of granular texture with a rim of PAM-positive material. The PAM-positive fibrous material of both types of plaques was mingled with coarser and compact, irregular-shaped argyrophilic structures in the oldest patient. The described plaques did not show bright fluorescence with thioflavin S staining. These results indicate, that the morphology of plaques, encountered in HCHWA-D, is diverse and changes with age.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227745
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  • 8
    Electronic Resource
    Electronic Resource
    Age-related plaque morphology and C-terminal heterogeneity of amyloid β in Dutch-type hereditary cerebral hemorrhage with amyloidosis (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 409-419 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyloid β ; Cerebral amyloid angiopathy ; Hereditary cerebral hemorrhage with amyloidosis-Dutch type ; Senile plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The evolvement of amyloid β (Aβ) deposition in the frontal cerebral cortex of 24 patients of increasing age with Dutch-type hereditary cerebral hemorrhage with amyloidosis (HCHWA-D) was studied using end-specific monoclonal antibodies to Aβx-42 (Aβ42) or Aβx-40 (Aβ40) and markers for degenerating neurites. Aβ42 immunostaining revealed parenchymal Aβ deposits with a heterogeneous morphology and distribution, i.e., clouds, fine/dense diffuse, coarse, and homogeneous plaques. Clouds and diffuse plaques were associated with glial Aβ granules. Aβ40 labeling was absent in clouds/fine diffuse plaques, inconsistent and variably intense in dense diffuse/¶coarse plaques and consistent in homogeneous plaques. In a subset of Aβ40-positive plaques, degenerating neurites – without tauopathy – and/or amyloid cores were observed. Electron microscopy revealed no apparent amyloid fibrils in fine diffuse plaques, small bundles of fibrils in dense diffuse/homogeneous plaques, and amyloid masses in coarse plaques. The parenchymal Aβ pathology was age-related: the ratio of fine to dense diffuse plaques decreased with age, clouds were limited to younger patients; coarse plaques to the oldest old. Homogeneous/cored plaques were present most consistently in older patients. Plaque density did not increase with age. Vascular Aβ deposits stained for both Aβ species, but exclusively Aβ42-positive, presumably recent deposits were also observed. This study suggests that HCHWA-D is a model of plaque evolution in which clouds leave fine diffuse plaques, which may become dense diffuse and ultimately coarse or homogeneous plaques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051143
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  • 9
    Electronic Resource
    Electronic Resource
    Hereditary cerebral hemorrhage with amyloidosis (Dutch): a model for congophilic plaque formation without neurofibrillary pathology (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 371-378 
    Details
    ISSN: 1432-0533
    Keywords: Key words Amyloid angiopathy ; Enzymehistochemistry ; Hereditary cerebral hemorrhage with amyloidosis (Dutch) ; Immunohistochemistry ; Senile plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plaque-like lesions and amyloid angiopathy were investigated in the frontal cerebral cortex of four patients with hereditary cerebral hemorrhage with amyloidosis (Dutch) (HCHWA-D), using immunohistochemical [antibodies to β amyloid protein (Aβ), β protein precursor (βPP), synaptophysin, ubiquitin (UBQ), cathepsin D, paired helical filaments (PHF) and glial fibrillary acidic protein (GFAP)], enzymehistochemical (acid phosphatase) and silver [methenamine silver (MS) and Palmgren] staining methods. Whereas Aβ- and MS-positive diffuse plaques were found in all patients, only the three older patients showed neuritic or congophilic plaques, which were acid phosphatase and cathepsin D positive and contained βPP-, synaptophysin- and UBQ-positive, but PHF-negative neurites. These plaques were surrounded by reactive astrocytes. Similar immuno- and enzymereactivity was found around congophilic blood vessels. Thus, apart from neuronal degeneration in a subset of plaque-like lesions and around blood vessels, this study shows an age-related morphology of the plaques in HCHWA-D, corresponding to that in Down's syndrome (DS), with the difference that neurofibrillary (NF) pathology is absent in HCHWA-D in contrast to DS. HCHWA-D may be considered as a model for congophilic plaque formation not associated with NF pathology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310382
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  • 10
    Electronic Resource
    Electronic Resource
    Hereditary cerebral hemorrhage with amyloidosis (Dutch): a model for congophilic plaque formation without neurofibrillary pathology (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 371-378 
    Details
    ISSN: 1432-0533
    Keywords: Amyloid angiopathy ; Enzymehistochemistry ; Hereditary cerebral hemorrhage with amyloidosis (Dutch) ; Immunohistochemistry ; Senile plaques
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plaque-like lesions and amyloid angiopathy were investigated in the frontal cerebral cortex of four patients with hereditary cerebral hemorrhage with amyloidosis (Dutch) (HCHWA-D), using immunohistochemical [antibodies to β amyloid protein (Aβ), β protein precursor (βPP), synaptophysin, ubiquitin (UBQ), cathepsin D, paired helical filaments (PHF) and glial fibrillary acidic protein (GFAP)], enzymehistochemical (acid phosphatase) and silver [methenamine silver (MS) and Palmgren] staining methods. Whereas Aβ-and MS-positive diffuse plaques were found in all patients, only the three older patients showed neuritic or congophilic plaques, which were acid phosphatase and cathepsin D positive and contained βPP-, synaptophysin-and UBQ-positive, but PHF-negative neurites. These plaques were surrounded by reactive astrocytes. Similar immuno-and enzymereactivity was found around congophilic blood vessels. Thus, apart from neuronal degeneration in a subset of plaque-like lesions and around blood vessels, this study shows an age-related morphology of the plaques in HCHWA-D, corresponding to that in Down's syndrome (DS), with the difference that neurofibrillary (NF) pathology is absent in HCHWA-D in contrast to DS. HCHWA-D may be considered as a model for congophilic plaque formation not associated with NF pathology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310382
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