Cortical Thickness and Hippocampal Volume in Vascular and Non-vascular Depressed Patients.

Dakota A Egglefield,Joel R Sneed,Bret R Rutherford,Jeffrey N Motter,Sophie Schiff,Alice Grinberg

doi:10.3389/fpsyt.2021.697489

Abstract

Background: Reduced cortical thickness and hippocampal volume are prevalent markers of late life depression as well as mild cognitive impairment (MCI) but are conspicuously absent in the vascular depression (VD) literature. The present study aimed to determine differences in cortical thickness and hippocampal volume between VD and non-VD patients.Methods: Participants were enrolled in an 8-week open treatment antidepressant trial. Forty-one depressed individuals aged 50 and older underwent brain magnetic resonance imaging at baseline and were classified as VD or non-VD. Cortical thickness values for the left and right entorhinal, parahippocampal, and precuneal cortices, as well as left and right hippocampal volume, were linearly regressed on VD status to determine mean differences between VD and non-VD. Covariates included site, age, sex, and mean thickness or intracranial volume.Results: No statistical differences were found between VD and non-VD patients in cortical thickness of the bilateral precuneal, entorhinal, or parahippocampal cortices, or hippocampal volume (p > 0.001).Conclusions: The absence of statistical differences in gray matter between VD and non-VD patients raises several diagnostic, etiological, and developmental possibilities, namely that VD may not be connected with other late-life psychiatric illnesses such as MCI or dementia and that vascular disease may not be a common etiological risk factor for depression and dementia. Larger datasets, prospective longitudinal studies, and cognitively intact controls are needed to further address these types of questions.

Highlights

Depression in late life is often associated with cognitive impairment and has been shown to increase risk for developing dementia [1], but the heterogeneity of late life depression (LLD) complicates a complete understanding of this relationship [2]
Patients were excluded from participating in the study if they had other Axis I diagnoses such as bipolar disorder, obsessive compulsive disorder, psychotic disorder, or current substance abuse or dependence within the past year; were actively suicidal or had a past suicide attempt within the last 6 months; or had a Mini Mental Status Exam (MMSE) score lower than 24
One possible reason for the lack of statistical differences observed is that Vascular depression (VD) is a valid subtype of LLD, etiologically distinct from other late-life psychiatric disorders

Summary

Introduction

Depression in late life is often associated with cognitive impairment and has been shown to increase risk for developing dementia [1], but the heterogeneity of late life depression (LLD) complicates a complete understanding of this relationship [2]. One strong possibility is that depression is a causal risk factor or else moderator of neurodegenerative processes leading to Mild Cognitive Impairment (MCI) and dementia. Consistent with this possibility is that while some depressed patients remain. The VD hypothesis proposes that vascular risk factors lead to DWMHs which disconnect prefrontal cortical regions from subcortical regions, resulting in the onset of depressive symptoms, executive dysfunction, and poor response to antidepressant treatment [6, 10]. Reduced cortical thickness and hippocampal volume are prevalent markers of late life depression as well as mild cognitive impairment (MCI) but are conspicuously absent in the vascular depression (VD) literature. The present study aimed to determine differences in cortical thickness and hippocampal volume between VD and non-VD patients

Objectives

Methods

Results

Conclusion