Can levels of CSF tau proteins and Aβ42 explain thinning of the cerebral cortex in MCI?
Our results indicate that especially tau-pathology is related to reductions in hippocampal volume in MCI. The findings of a reduced hippocampus in MCI are in accordance with previous reports,43,48 but the new finding was that this difference depended on the participants with pathologic CSF biomarkers. This fits with knowledge that tau-related pathologic features (neurofibrillary tangles) are initially limited to the hippocampus, the entorhinal cortex, and adjacent limbic structures,49 whereas amyloid deposition is more distributed.25,50,51 Our data are in accordance with recent results showing widespread cortical thinning in MCI.5 The current sample is small, but the similarity of findings indicates that the results probably are valid. The thinning was quite symmetric across hemispheres and was located mainly in the temporal (lateral and medial) and inferior parietal cortices, in addition to parts of the superior frontal cortex and some more scattered medial parietal and frontal effect
