## 4 Discussion
MCI represents a preclinical transitional stage between healthy aging and dementia. Hypoperfusion and hypometabolism in the temporoperial cortex and mesial temporal lobe atrophy, particularly in the rhinal cortex, have been described [24; 25]. This explains our findings of atrophy in the right hippocampus and parahippocampal gyrus. Additionally, we found significant atrophy in the MTG and STG. Maybe due to the connection of the anterior cingulate with the hippocampus, there is significant adjacent white matter atrophy (subcallosalWM-ACC, rostralWM-ACC) [26]. Since there is no verified atrophy in other associated cortical structures to these white matter fibers, this could support the theory that hippocampal atrophy is a precursor leading to white matter degeneration of the corresponding axons. There are studies stating that anterior cingulate cortex disruptions can be found in AD and MCI patients [27; 28]. High-level functions for the ACC such as focused problem solving and error recognition have been described [26], which might be unrecognized in the diagnosis of MCI. Our finding of atrophy in the left IFO seems complex. The inferior fronto-occipital fasciculus contains fibers that connect the frontal lobe with the posterior part of the parietal and temporal lobes. In the temporal lobe, the inferior occipitofrontal fasciculus is associated with the inferior longitudinal fasciculus, which interconnects the occipital cortex (lingula, cuneus, and lateral surface) with the cortex of the superior, middle and inferior temporal (and possibly the hippocampal) gyri. This complex pathway of connections may account for a degeneration of associated fibers to the hippocampus and temporal gyri in the IFO. Defects in the IFO can cause visual hallucinations and global aphasia, and there is also evidence that trauma to the IFO can cause amnesia and cognitive impairment [29; 30]. Additionally, we found atrophy of the left mammillary body, which in turn can be present in AD [31]--MCI being a prodomal state of AD. Previous studies have found the mammillary bodies to be structurally connected to memory function, partially linked to the hippocampus via pathways, which explains cognitive deficits in patients with Wernicke-Korsakoff syndrome [32]. Numerous studies have convincingly documented hippocampal atrophy as well as atrophy of temporal brain regions (STG, MTWM) for patients diagnosed with AD in comparison to aging controls [33], which we can reproduce. Volume reduction in the cingulum (CGH) could be a consequence or precursor, as it is connected to the hippocampal formation (e.g., subiculum) via projection fibers [34]. Our findings of adjacent white matter atrophy in our MCI cohort insinuate that atrophy in the cingulum could be consequential; however, we cannot reproduce significant atrophy in subcallosal WM-ACC or rostral WM-ACC for AD patients, which makes this a rather questionable conclusion. As expected, and in contrast to FTD patients, we could not find significant proof of striatal atrophy [35], except for the left caudate tail. The caudate tail is not well examined, although a prior study has suggested that there is especially relevant atrophy in the left caudate head and body for AD patients compared to CO, yet seems to be more present in the FTD spectrum [36]. This in turn suggests striatal degeneration to be a good diagnostic biomarker for FTD [36; 37]. Atrophy of SOG is rarely described and might be present in patients suffering from atypical AD. As these patients do not primarily present with memory impairment but atypical symptoms, e.g., in the fields of language or vision [38], posterior cortical atrophy seems to play an important role. However, we did not observe significant atrophy of parietal lobe structures such as the precuneus, which has been described for (a)typical and early-onset AD patients [39].