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  • 1
    Online Resource
    Online Resource
    Molekulare Genetik und experimentelle Therapie von seltenen neurodegenerativen Erkrankungen (ALS, MSA, PSP) : Abschlußbericht (2007)
    Ulm
    Details Availability
    Keywords: Forschungsbericht
    Type of Medium: Online Resource
    Pages: Online-Ressource (10 S., 87,5 KB)
    URL: https://edocs.tib.eu/files/e01fb09/599985585.pdf
    URL: https://doi.org/10.2314/GBV:599985585
    URL: https://edocs.tib.eu/files/e01fb09/599985585l.pdf
    DOI: 10.2314/GBV:599985585
    Language: German
    Note: Förderkennzeichen BMBF 01GZ0313. - Engl. Berichtsblatt u.d.T.: Molecular genetics and experimental therapies of orphan neurodegenerative diseases (ALS, MSA, PSP) , Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden , Auch als gedr. Ausg. vorhanden , Systemvoraussetzungen: Acrobat reader.
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  • 2
    Electronic Resource
    Electronic Resource
    Protective Effects of Riluzole on Dopamine Neurons (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 75 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Riluzole is neuroprotective in patients with amyotrophiclateral sclerosis and may also protect dopamine (DA) neurons in Parkinson'sdisease. We examined the neuroprotective potential of riluzole on DA neuronsusing primary rat mesencephalic cultures and human dopaminergic neuroblastomaSH-SY5Y cells. Riluzole (up to 10 μM) alone affected neither thesurvival of DA neurons in primary cultures nor the growth of SH-SY5Y cellsafter up to 72 h. Riluzole (1-10 μM) dose-dependently reduced DAcell loss caused by exposure to MPP+ in both types of cultures.These protective effects were accompanied by a dose-dependent decrease ofintracellular ATP depletion caused by MPP+ (30-300 μM)in SH-SY5Y cells without affecting intracellular net NADH content, suggestinga reduction of cellular ATP consumption rather than normalization ofmitochondrial ATP production. Riluzole (1-10 μM) also attenuatedoxidative injury in both cell types induced by exposure to L-DOPA and6-hydroxydopamine, respectively. Consistent with its antioxidative effects,riluzole reduced lipid peroxidation induced by Fe3+ and L-DOPA inprimary mesencephalic cultures. Riluzole (10 μM) did not alterhigh-affinity uptake of either DA or MPP+. However, in the samecell systems, riluzole induced neuronal and glial cell death withconcentrations higher than those needed for maximal protective effects(≥100 μM). These data demonstrate that riluzole has protectiveeffects on DA neurons in vitro against neuronal injuries induced by (a)impairment of cellular energy metabolism and/or (b) oxidative stress. Theseresults provide further impetus to explore the neuroprotective potential ofriluzole in Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0752259.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Are Human Neurodegenerative Disorders Linked to Environmental Chemicals with Excitotoxic Properties? (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 648 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb24533.x
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  • 4
    Electronic Resource
    Electronic Resource
    Recessively inherited amyotrophic lateral sclerosis: a German family with the D90A CuZn-SOD mutation (2000)
    Springer
    Journal of neurology 247 (2000), S. 783-786 
    Details
    ISSN: 1432-1459
    Keywords: Key words Familiar amyotrophic lateral sclerosis ; Copper-zinc superoxide dismutase ; D90A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mutations of the SOD1 gene encoding the free radical scavenging enzyme copper-zinc superoxide dismutase (CuZn-SOD) occur in patients with familial amyotrophic lateral sclerosis (ALS). Recent reports have shown homozygosity for a CuZn-SOD mutation in exon 4, the D90A (Asp90Ala) mutation. Other mutations described to date show an autosomal dominant pattern of inheritance. This is the first description of autosomal recessively inherited ALS in an out-bred population in central Europe. This study confirms the earlier described characteristic phenotype reported in D90A homozygous ALS patients in Scandinavia and supports the theory of the existence of a strong modifying factor in some cases of ALS associated with mutations in the CuZn-SOD gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004150070093
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  • 5
    Electronic Resource
    Electronic Resource
    Psychiatric aspects of writer's cramp (1991)
    Springer
    European archives of psychiatry and clinical neuroscience 241 (1991), S. 170-176 
    Details
    ISSN: 1433-8491
    Keywords: Writer's cramp ; Neurotic disorder ; Focal dystonia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Although its aetiopathogenesis is still unknown, writer's cramp is meanwhile regarded essentially an organically induced disorder. However, as shown by this interdisciplinary study, psychodynamic factors should not be neglected. Special attention should be given to the patients' experience of the syndrome and secondary psychoreactive processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02219717
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  • 6
    Electronic Resource
    Electronic Resource
    Chemical preconditioning: A cytoprotective strategy (1997)
    Springer
    Molecular and cellular biochemistry 174 (1997), S. 249-254 
    Details
    ISSN: 1573-4919
    Keywords: preconditioning ; oxidative phosphorylation ; ischemic tolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Brief ischemic or hypoxic episodes may increase or decrease tolerance towards subsequent severe ischemia in heart and brain. A similar phenomenon is observed after mild chemical inhibition of oxidative phosphorylation – chemical preconditioning. We have shown that chemical preconditioning can be induced by chemical inhibition of mitochondrial complex I and mitochondrial complex II. With a time interval of three hours between chemical pretreatment and massive inhibition of oxidative phosphorylation, recovery of population spike amplitude in hippocampal region CA1 after stimulation of the Schaffer collaterals was 31 ± 9% in controls, 98 ± 14% after i.p. treatment with 1 mg/kg body weight haloperidol, an inhibitor of mitochondrial complex I and 90 ± 7% with pretreatment with 3-np, an inhibitor of mitochondrial complex II. Activation of ATP regulated potassium channels partakes in mediating the preconditioning effect. We conclude that chemical preconditioning is a practical prophylactic ph armacologic strategy to increase hypoxic tolerance. (Mol Cell Biochem 174: 249–254, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006820927262
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  • 7
    Electronic Resource
    Electronic Resource
    Benzodiazepine receptors and cerebral blood flow in partial epilepsy (1991)
    Springer
    European journal of nuclear medicine 18 (1991), S. 111-118 
    Details
    ISSN: 1619-7089
    Keywords: Partial epilepsy ; SPET ; Benzodiazepine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It was the aim of this study to compare benzodiazepine (Bz) receptor binding and cerebral perfusion in patients with partial epilepsy. Single photon emission tomography (SPET) studies with the flow-marker technetium 99m hexamethylpropylene amine oxine (99mTc-HMPAO) and with the 123I-labelled Bz-receptor ligand Ro 16-0154 (123I-Iomazenil) were performed in 12 patients with partial epilepsy, all with normal magnetic resonance imaging (MRI) and computed tomography (CT) scans. The SPET studies with 123I-Iomazenil were carried out 5 min and 2 h after injection. At 2 h the distribution of activity was very similar to the expected distribution of Bz-receptors in the human brain, known from positron emission tomography (PET) work and post-mortem studies. Early images showed a significantly higher tracer accumulation in the area of the basal ganglia, cerebellum, and naso-pharyngeal space. This finding is caused by non-specific binding and the contribution of the tracer in the blood pool in this phase. Also after 2 h p.i. of 123I-Iomazenil, 9 of the 12 patients showed a focal decrease of of Bz-receptor binding. Ten patients had focal flow abnormalities with 99mTc-HMPAO SPET. In 8 subjects impairment of flow was seen in sites of reduced 123I-Iomazenil uptake. 123I-Io-mazenil is suitable for Bz-receptor mapping. In this series of patients, Bz-receptor mapping with SPET seems to offer no advantage over 99mTc-HMPAO in the detection of epileptic foci.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175914
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  • 8
    Electronic Resource
    Electronic Resource
    Benzodiazepine receptors and cerebral blood flow in partial epilepsy (1991)
    Springer
    European journal of nuclear medicine 18 (1991), S. 111-118 
    Details
    ISSN: 1619-7089
    Keywords: Partial epilepsy ; SPET ; Benzodiazepine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It was the aim of this study to compare benzodiazepine (Bz) receptor binding and cerebral perfusion in patients with partial epilepsy. Single photon emission tomography (SPET) studies with the flow-marker technetium 99m hexamethylpropylene amine oxine (99mTc-HMPAO) and with the123I-labelled Bz-receptor ligand Ro 16-0154 (123I-Iomazenil) were performed in 12 patients with partial epilepsy, all with normal magnetic resonance imaging (MRI) and computed tomography (CT) scans. The SPET studies with123I-Iomazenil were carried out 5 min and 2 h after injection. At 2 h the distribution of activity was very similar to the expected distribution of Bz-receptors in the human brain, known from positron emission tomography (PET) work and post-mortem studies. Early images showed a significantly higher tracer accumulation in the area of the basal ganglia, cerebellum, and naso-pharyngeal space. This finding is caused by non-specific binding and the contribution of the tracer in the blood pool in this phase. Also after 2 h p.i. of123I-Iomazenil, 9 of the 12 patients showed a focal decrease of of Bz-receptor binding. Ten patients had focal flow abnormalities with99mTc-HMPAO SPET. In 8 subjects impairment of flow was seen in sites of reduced123I-Iomazenil uptake.123I-Io-mazenil is suitable for Bz-receptor mapping. In this series of patients, Bz-receptor mapping with SPET seems to offer no advantage over99mTc-HMPAO in the detection of epileptic foci.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00950756
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