José Javier Miguel-Hidalgo
Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, Mississippi, USA
Comorbidity of Depression and Alcohol Use Disorders. Hauppauge, New York: Nova Science Publishers, 2009, 198 pages.
Major depression and alcoholism are often comorbid, suggesting that common pathological mechanisms may be responsible for the increased comorbidity. In fact, neuropathological studies have demonstrated reductions in the density of neurons and glial cells in specific areas of the prefrontal cerebral cortex both in alcoholism and depression. However, some of these studies also show that a refinement of morphological and immunohistochemical analysis reveals significant differences in the prefrontal neuropathological profile of depression and alcoholism, with alcoholism showing a more widespread reduction of glial densities across cortical layers as compared to depression, and a marked negative correlation between duration of alcoholism and reduction of neuronal density. Among alcoholics, those with comorbid depressive symptoms show lower glial densities than those without comorbid depression. Also in comorbid alcoholism and depression the expression of glutamate transporters and glutamine synthetase, essential components of the glutamate recycling machinery in astrocytes, appears to be reduced as compared to alcoholics without depression or to normal controls, resembling the also lower expression of those components in major depressive subjects without comorbid alcoholism. The available data, particularly in the orbitofrontal cortex, support the hypothesis that in alcoholics with comorbid depression neuropathological changes eventually develop a pattern consistent with depression. Whether these changes observed in comorbid subjects are effects of alcohol abuse that target specific circuits or there are preexisting alterations that are related to both alcoholism and depression remains to be elucidated.