There is a South Korean paper – ‘Frontal Dysfunction Underlies Depression in Mild Cognitive Impairment: A FDG-PET study’ by Lee and colleagues and freely available here. The researchers are interested in finding out if there is a relationship between cerebral glucose metabolism, depression and mild cognitive impairment. To investigate this they have used a small sample size of 52 patients. For an imaging study of this type it is a relatively large sample size but in terms of other clinical studies such as drug trials this would be considered small and although a number of the results reach statistical significance there are benefits to replication with a larger sample size.
The exclusion criteria are quite stringent and people with evidence of white matter hyperintensities are excluded. This means that the sample set is a very specific type of mild cognitive impairment – non-vascular MCI and the researchers use consensus criteria from 2004. The resulting MCI is not divided into amnestic or executive subtypes but remains undifferentiated. Nevertheless in the results section, the performance of the three groups MCI without depression, MCI with depression and a control group are quite impressive with the control group performing consistently better across the battery of cognitive tests than both of the other groups although not always significantly so.
The researchers detail the FDG-PET methods used and I note that in the voxel wise comparison they state that there is no control for multiple comparisons and instead they use quite a low cut-off point for the p value. While there are many results, those of particular interest relate to the glucose metabolism in Brocas area 6 in the MCI with depression group compared to the control group. Essentially there is reduced glucose metabolism in this area in the depressed group and the researchers note the connections of BA 6 with both primary motor cortex and superior prefrontal cortex.
The hypothesis that the authors draw from this is that reduced glucose metabolism in prodromal Alzheimer’s Disease (AD) in the superior prefrontal cortex is causally related to depression. Although this is a very clear hypothesis which can be investigated further there are some cautions. In order to draw conclusions about prodromal status in undifferentiated MCI it would be prudent to have some idea of well characterised biomarkers for conversion from MCI to AD including hippocampal volume as well as looking more closely at differentiating MCI into amnestic type and replicating the results above with a larger sample size. The researchers discuss their results and note previous research into glucose metabolism which supports their arguments. If this hypothesis holds however, it would facilitate research into new treatment paradigms in this area.
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