Journal ArticleDOI
GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons
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TLDR
In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake and did not increase total neuron or astrocyte numbers or transmitter uptake.Abstract:
A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.read more
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TGF-beta signal transduction.
TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
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The TGF-beta superfamily: new members, new receptors, and new genetic tests of function in different organisms.
TL;DR: Four areas have seen major progress in the TGF-p superfamily in the last 3 years: structural characterization of the signal ing molecule, isolation of new family members, cloning of receptor molecules, and new genetic tests of the func tions of these factors in different organisms.
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Neuroinflammation in Parkinson's disease: a target for neuroprotection?
TL;DR: Overall, available data support the importance of non-cell-autonomous pathological mechanisms in Parkinson's disease, which are mostly mediated by activated glial and peripheral immune cells.
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ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions
Lucie Bruijn,Mark W. Becher,Michael K. Lee,K. L. Anderson,Nancy A. Jenkins,Neal G. Copeland,Sangram S. Sisodia,Jeffrey D. Rothstein,David R. Borchelt,Donald L. Price,Don W. Cleveland +10 more
TL;DR: It is reported here that even low levels of another mutant, G85R, cause motor neuron disease characterized by an extremely rapid clinical progression, without changes in SOD1 activity.
Journal ArticleDOI
Direct brain infusion of glial cell line–derived neurotrophic factor in Parkinson disease
Steven S. Gill,Nikunj K. Patel,Gary Hotton,Karen O’Sullivan,Renée McCarter,Martin Bunnage,David J. Brooks,Clive N. Svendsen,Peter Heywood +8 more
TL;DR: Positron emission tomography scans of [18F]dopamine uptake showed a significant 28% increase in putamen dopamine storage after 18 months, suggesting a direct effect of GDNF on dopamine function, and warrants careful examination ofGDNF as a treatment for Parkinson disease.
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