Background
Neuropsychiatric Symptoms (NPS) are related to increased risk of age‐related cognitive decline. Three clusters are commonly highlighted in cognitive decline: a mood/affective cluster, a psychotic cluster and an hyperactivity/behavioral cluster. The mood cluster is formed by at least depression and anxiety and seems to increase the risk of dementia. Their implications to brain changes are not well‐known.
Method
217 cognitively healthy participants (CH), 362 patients with mild cognitive impairment (MCI) and 174 patients with Alzheimer’s disease (AD) were extracted from the Alzheimer’s Disease Neuroimaging Initiative database. Each subject was assessed with a NeuroPsychiatric Inventory and a comprehensive neuropsychological assessment and realized a 3T MRI. Statistical analysis was based‐on the General Linear Model (FreeSurfer 7.1.1 mri_glmfit) in which linear regression between affective NPS severity (depression and anxiety) and cortical area/thickness was analysed in each group and between groups two‐by‐two.
Result
In the CH group, severity of depression was positively correlated to the left anterior cingulate area and negatively to the left posterior cingulate thickness. In the AD group, severity of depression was positively correlated to right anterior cingulate thickness whereas severity of anxiety was positively correlated to rostral middle frontal thickness. There were no significant results in the MCI group. In two‐by‐two comparisons : (1) more severe was depression and anxiety, thinner was left middle, inferior temporal, entorhinal, inferior parietal, lateral occipital, precuneus, cingulate isthmus and superior, middle frontal cortices in MCI compared to CH; (2) more severe was depression and anxiety, thinner was left temporopolar, middle temporal, entorhinal, supramarginal, anterior cingulate, cingulate isthmus and superior, middle, inferior frontal cortices in AD compared to MCI; and (3) few cortices was no thinner in AD compared to CH : it concerned precentral, postcentral, occipitopolar, cuneus and lingual cortices.
Conclusion
Our data suggest that affective NPS induce size modifications of cortical areas during cognitive decline but also in CN subjects. Thus, this confirms data already present in the literature showing that the comorbidity of NPS with cognitive impairment could be a factor in accelerating decline and neurodegenerative processes. This underlines the importance of understanding the emergence of NPS in CH elderly subjects.
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