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Abstract
<p class="first" id="d434583e179">Low cerebral levels of brain-derived neurotrophic
factor (BDNF), which plays a critical
role in many brain functions, have been implicated in neurodegenerative, neurological
and psychiatric diseases. Thus, increasing BDNF levels in the brain is considered
an attractive possibility for the prevention/treatment of various brain diseases.
To date, BDNF-based therapies have largely focused on neurons. However, given the
cross-talk between endothelial cells and neurons and recent evidence that BDNF expressed
by the cerebral endothelium largely accounts for BDNF levels present in the brain,
it is likely that BDNF-based therapies would be most effective if they also targeted
the cerebral endothelium. In this review, we summarize the available knowledge about
the biology and actions of BDNF derived from endothelial cells of the cerebral microvasculature
and we emphasize the remaining gaps and shortcomings.
</p>
Recent findings with animal models have suggested a possible role for brain-derived neurotrophic factor (BDNF) in depression. We have therefore hypothesized that depression could be characterized by low levels of serum BDNF. Major depressed patients (15F + 15M) diagnosed according to DSM-IV criteria and healthy controls (15F + 15M) participated in the study. Serum BDNF was assayed with the ELISA method and the severity of depression was evaluated with Montgomery-Asberg-Depression Rating Scale (MADRS). BDNF levels were significantly lower in patients than in controls: 22.6 +/- 3 and 26.5 +/- 7 ng/ml (t-test = 2.7; d.f. = 58; P < 0.01). They were negatively correlated to the MADRS scores (r = -0.55; P < 0.02). Female patients were more depressed and released less BDNF than men. Analysis of covariance (MADRS and gender as independent variable vs. BDNF as dependent variable) indicated that depression severity mainly accounted for the negative correlation. These results suggest that major depression is characterized by low serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.