Glial Cell-Line Derived Neurotrophic Factor (GDNF) Concentrations in Cerebrospinal Fluid and Serum of Patients with Early Alzheimer's Disease and Normal Controls
As neurotrophic factors play an important role in development and maintenance of global central nervous system (CNS) function, we supposed that glial cell-line derived neurotrophic factor (GDNF), which has been extensively studied for its survival promoting effects especially concerning catecholamin...
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Published in | Journal of Alzheimer's disease Vol. 18; no. 2; pp. 331 - 337 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.01.2009
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Subjects | |
Online Access | Get full text |
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Summary: | As neurotrophic factors play an important role in development and maintenance of global central nervous system (CNS) function, we supposed that glial cell-line derived neurotrophic factor (GDNF), which has been extensively studied for its survival promoting effects especially concerning catecholaminergic neurons, also plays a significant role in neurodegenerative disease characterized mainly by damage of cholinergic CNS neurons like AD. Here we compared GDNF concentrations in serum and cerebrospinal fluid (CSF) of patients with probable Alzheimer's disease (AD) and normal controls (NC). While GDNF concentrations in CSF were significantly increased in patients with AD (291.7 ± 85.8 pg/ml) compared with NC subjects (218.7 ± 93.3 pg/ml, p = 0.012), GDNF concentration of AD patients (486.5 ± 72.3 pg/ml) in serum were significantly decreased compared with the NC group (711.5 ± 186.5 pg/ml, p < 0.001). Increased GDNF in CSF of AD might be due to an upregulated expression in CNS as an adaptive process of the impaired brain to enhance neurotrophic support at least in early stages of disease and/or impairment of CSF turnover. Decreased serum concentration of GDNF might be related to altered function of the blood brain barrier thus disturbing clearance or facilitating passover of potentially harmful metabolites. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Conference-1 ObjectType-Feature-3 content type line 23 SourceType-Conference Papers & Proceedings-2 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 1387-2877 1875-8908 1875-8908 |
DOI: | 10.3233/JAD-2009-1146 |