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Am J Psychiatry 2004;161:A48-A48. doi:10.1176/appi.ajp.161.10.A48

People with alcoholism actually have less response to alcohol than do healthy people. The genetic effects on alcoholism risk suggest that the difference is biological. One mechanism in alcoholic response may be dysfunction of the N-methyl-d-aspartate (NMDA) nerve receptor, which is among the highest-affinity targets of ethanol in the brain. To assess NMDA receptor functioning in people at genetic risk of alcoholism, Petrakis et al. (p. 1776) administered ketamine, an NMDA receptor antagonist, to subjects who had alcoholic relatives but were not alcoholic themselves. Ketamine produced less perceptual distortion and less anxiety or depression in these subjects than in people with no family history of alcoholism, confirming the role of NMDA receptors. This reduction in negative reactions is not a benefit if it deprives drinkers of important warning signs of alcohol’s ill effects.

Close relatives of patients with schizophrenia display attenuated versions of characteristics seen in patients, including emotional anomalies. Some of the brain regions that process emotions have been identified as structurally abnormal in both schizophrenia patients and their first-degree relatives. Habel et al. (p. 1806) examined the relationship of brain functioning and emotion in men with schizophrenia, their brothers, and unrelated healthy men. Brain activity was tracked as the men tried to feel happiness and sadness induced by emotional facial expressions as well as a nonemotional control task. There were no differences between groups in the brain responses to the happy faces or cognitive task. While reacting to the sad faces, the patients and their brothers reported feeling just as sad as the healthy men but had significantly less activation in the amygdala, a crucial node in emotional processing. The similarity between brothers demonstrates a genetic basis for the emotional deficit in schizophrenia, for which nonschizophrenic relatives apparently are able to compensate.

Comparisons of bipolar disorder in monozygotic and dizygotic twins indicate a genetic contribution to the illness, but the strength of the genetic influence varies widely among studies. Kieseppä et al. (p. 1814) improved on previous methods by using national population and hospitalization registries in Finland to identify all same-sex twins hospitalized for bipolar I disorder. The patients’ co-twins were then evaluated in face-to-face structured psychiatric diagnostic interviews. For 43% of the monozygotic twin pairs, bipolar disorder was diagnosed in the co-twin of the hospitalized patient, compared to 6% of the dizygotic pairs. Expanding the co-twins’ diagnoses to include a broad range of mood disorders increased the concordance rates to 75% for monozygotic pairs and 11% for dizygotic pairs. The total absence of schizophrenia among the co-twins argues against the proposition that schizophrenia and bipolar disorder fall along the same illness continuum.

Patients with schizophrenia have abnormalities in the structure and function of synapses, the connections between nerve cells, particularly in a brain region called the hippocampus. However, the evidence is primarily based on studies of the presynaptic terminal and is incomplete. Law et al. (p. 1848) measured the expression of two genes for proteins found in dendrites, the postsynaptic "receivers," and dendritic spines, the protuberances adjacent to most excitatory synapses. Expression of spinophilin (dendritic spine marker), but not microtubule-associated protein 2 (MAP2; dendrite marker), was lower in the postmortem hippocampus of patients with schizophrenia and patients with mood disorders than in normal subjects. The spinophilin reduction could be due to loss of dendritic spines and//or decreased activity or plasticity of the spines. As spines are the targets of most of the synapses involved in transmission of glutamate, this finding adds to the evidence that glutamatergic neurotransmission in the hippocampus is particularly affected in schizophrenia.

Depressed patients commonly have sleep problems, and they also note that the sleep they do get does not leave them feeling rested. Germain et al. (p. 1856) demonstrated that the brains of depressed patients do not get the same "relaxation" that healthy brains do, possibly because the frontal cortex already is underactive when the patients are awake. The combination of EEG sleep recording and positron emission tomography (PET) scanning showed that depressed patients had a smaller decrease in frontal metabolism than healthy subjects when they drifted from wakefulness into non-REM sleep. Smaller decreases were also seen in the dorsomedial thalamus and parietal and temporal lobe regions. The latter differences suggest that abnormalities in arousal-mediating areas of the brain may also contribute to sleep problems in depression.F1

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