FEATURE ARTICLE
Depression and the Birth and Death of Brain Cells
The turnover of neurons in the hippocampus might help to explain the onset of and recovery from clinical depression
Henriette van Praag, Barry Jacobs, Fred Gage
Depression and the Hippocampus
Several pieces of evidence link clinical depression to changes in the hippocampus. Nevertheless, we do not suggest that this is the only change in the brain associated with depression, nor do we suggest that alterations in the hippocampus underlie all of the phenomenological aspects of depression.
Utilizing the brain imaging technique of MRI, Yvette Sheline and her colleagues at Washington University in St. Louis reported smaller hippocampal volumes in a group of older women with recurrent major depression. Although the subjects were in remission, they had smaller left and right hippocampal volumes—but comparable total cerebral volumes—in comparison with carefully selected controls. Sheline's group also found a significant negative correlation between total days of depression and the volume of the left hippocampal gray matter. The investigators speculate that this hippocampal loss might result from glucocorticoid-induced neurotoxicity associated with recurrent episodes of depression. In a more recent study, this same group confirmed their original report and also showed that the decrease in hippocampal volume correlated with total lifetime duration of depression and not with age. Other studies confirm the relationship between depression and hippocampal volume. For example, Premal Shah and his colleagues at the Royal Edinburgh Hospital also reported smaller hippocampal volumes in chronically depressed patients but found no decrease in hippocampal volume in recovered patients.
Temporal-lobe epilepsy also points to a connection between hippocampal damage and depression. First of all, temporal-lobe epilepsy involves a massive loss of cells in various structures in and around the hippocampus. Second, depression is the most common psychiatric complication in patients with epilepsy. Moreover, patients with temporal-lobe epilepsy experience depression more than patients with other forms of epilepsy or than patients with comparably debilitating diseases. If there is a causal relation between temporal-lobe epilepsy and depression, some evidence indicates that it might be bidirectional. Because the neuropathology in temporal-lobe epilepsy encompasses most of the temporal lobe, however, no definitive conclusion can be drawn regarding the site of specific damage that might underlie the psychopathology.
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