Keywords:
Screening, Imaging sequences, MR, Neuroradiology brain, CNS, Segmentation, Dementia, Geriatrics
Authors:
E. Karavasilis1, T. Parthimos1, J. Papatriantafyllou1, F. Christidi1, S. Papageorgiou1, G. Kapsas2, A. Papanicolaou3, I. Seimenis2; 1ATHENS/GR, 2Alexandroupolis/GR, 3Memphis/US
DOI:
10.1594/ecr2018/C-1350
Aims and objectives
The diagnosis of depression in Alzheimer’s disease (AD) is often hampered by the concurrent dementia clinical symptoms,
considering that depressive symptoms are often similar to the symptoms and signs of dementia [1].
There is a growing body of evidence over an interrelation between depression and AD dementia,
which can be explained via multiple biological mechanisms [2]. Also,
there is growing evidence linking late-life depression (LLD) with the development of dementia [3],
even though a recent longitudinal study did not support such a link [4].
Thus,
the exact mechanism that may explain the interrelation between depression and AD dementia is still elusive.
Neuroimaging research of depression in AD has examined whether depression is related to volume loss and damage in specific brain structures (e.g,
gray matter (GM) regions).
Findings revealed,
decreased GM volume in left inferior temporal gyrus in AD patients with depression compared with AD patients without depression [5].
Correlation studies between GM volume and severity of depression yielded inconsistent findings [6-7].
Other studies including patients with mild cognitive impairment (MCI) observed GM atrophy in frontal,
temporal,
parietal and occipital regions,
as well as in subcortical structures (i.e.
amygdala,
hippocampus) [5,
8] and reduced cortical thickness in the entorhinal cortex [9].
Evidence from LLD neuroimaging studies suggest that depressive symptoms may constitute a prodromal symptom or early clinical expression of the AD-related neurodegenerative process in some cases rather than a very early risk factor for the AD pathological process [10].
Studies using region of interest (ROI)-based analysis that examine pre-defined GM structures based on previous findings in either AD or LLD groups present methodological caveats for the understanding of the neuroanatomical profile of depression in AD.
Therefore,
the simple approach of whole-brain analysis emerges as an attractive alternative that can address this issue appropriately.
We have recently employed this approach to compare AD patients with and without depression from a large multi-scanner dataset.
Using whole-brain GM analysis with the voxel-based morphometry (VBM) technique; a pattern of GM atrophy in specific GM structures which are part of the sensorimotor network was identified [11] .
The aim of this study is to further elucidate the gray matter volume (GMV) neuroanatomical profile of depression in Alzheimer’s disease (AD) by comparing depressive and non-depressive AD patients,
non-demented patients with LLD and healthy controls (HC).