Background/Aims: Subjective memory impairment (SMI) has been suggested as a manifestation of Alzheimer’s Disease (AD) preceding mild cognitive impairment (MCI). In this study, we determined the volumes of the hippocampus, the entorhinal cortex (EC) and the amygdala to provide biological evidence for AD in SMI. Methods: Regional volumetric measures were manually traced on 3-Tesla MRI scans. Results: Total brain volume did not differ between the groups. Individuals with SMI had reduced volumes of the hippocampus bilaterally (right p = 0.001; left p < 0.001), the bilateral EC (right p = 0.031, left p = 0.006) and the right amygdala (p = 0.01) compared to the control group. Conclusion: Volume reduction of bilateral hippocampus, bilateral EC and right amygdala supports the concept of SMI as a very early manifestation of AD prior to MCI. SMI may indicate awareness of a degenerative process that can still be functionally compensated.

Recently, an association of the Val66Met polymorphism of the brain-derived neurotrophic factor with hippocampal volume in patients with major depression has been reported. Here, we aimed at replicating this finding in an independent German sample. We included 79 patients with unipolar major depressive episodes and 84 healthy comparison participants. The brain-derived neurotrophic factor Val66Met polymorphism was determined in all participants. The volume of the hippocampus was manually traced on high-resolution magnetic resonance images. The hippocampal volumes of patients were significantly smaller than those of the comparison participants, confirming previous reports. There was, however, no Val66Met effect on hippocampal volume in either group. To conclude, we did not replicate the Val66Met effect on hippocampal volume in neither patients with major depression nor in healthy participants.

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The proline dehydrogenase locus must be considered as a positional and functional candidate in schizophrenia. It is located in the chromosomal region of the velocardiofacial syndrome on 22q11 that is suspected to contain genes relevant to schizophrenia, and is involved in the metabolism of neurotransmitters. Positive association between single-nucleotide polymorphisms at the proline dehydrogenase locus and schizophrenia further supported the role of proline dehydrogenase in the development of schizophrenia. In order to replicate these findings, we analyzed three single-nucleotide polymorphisms in a sample comprising 299 schizophrenic patients and 300 controls. In addition, we assessed whether proline dehydrogenase also contributes to bipolar affective disorder, because chromosome 22q11 is also implicated in bipolar affective disorder. We therefore included 300 patients with bipolar affective disorder. This is the first study on a potential involvement of the proline dehydrogenase locus in bipolar affective disorder. Neither single marker nor haplotype analysis revealed an association between variants at the proline dehydrogenase locus and schizophrenia or bipolar affective disorder.