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Brain alterations in depression

Published online by Cambridge University Press:  18 September 2015

Witte J.G. Hoogendijk*
Affiliation:
Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam, The Netherlands Research Institute Neurosciences, Free University, Faculty of Medicine, Dept. of Psychiatry, Valerius Hospital Graduate School Neurosciences Amsterdam, The Netherlands
Gerben Meynen
Affiliation:
Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam, The Netherlands Research Institute Neurosciences, Free University, Faculty of Medicine, Dept. of Psychiatry, Valerius Hospital Graduate School Neurosciences Amsterdam, The Netherlands
Piet Eikelenboom
Affiliation:
Research Institute Neurosciences, Free University, Faculty of Medicine, Dept. of Psychiatry, Valerius Hospital Graduate School Neurosciences Amsterdam, The Netherlands
Dick F. Swaab
Affiliation:
Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam, The Netherlands
*
Valeriuskliniek Valeriusplein 9 1075 BG Amsterdam, The Netherlandswitteh@pca-znw.nl

Summary

This article describes a number of studies by our research group to find brain structures that may be involved in the symptoms of idiopathic depression, depression in Alzheimer's disease and depression in Parkinson's disease. Until recently, idiopathic depression has generally been related to deficiencies of aminergic systems. In Alzheimer patients we found a strong decrease in the number of neurons in the locus coeruleus and brain noradrenaline concentrations, but in depressed Alzheimer patients we did not find an extra de crease. This is in agreement with the finding that there is no cell loss in the locus coeruleus in idiopathic depression. We did find, however, that the number of corticotropin-releasing hormone-, vasopressin- and oxytocin expressing neurons, the number of corticotropin-releasing hormone neurons co-expressing vasopressin and the amount of corticotropin-releasing hormone -mRNA in idiopathic depression were strongly increased in the paraventricular nucleus of the hypothalamus. This result supports the hypothesis on the pathogenetic involvement of the hypothalamo-pituitary-adrenal axis in depression and is of clinical relevance, since it may provide a theoretical rationale for antidepressive therapy with CRH antagonists.

Type
Articles
Copyright
Copyright © Scandinavian College of Neuropsychopharmacology 2000

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