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

2021 ◽  
Vol 12 ◽  
Author(s):  
Dakota A. Egglefield ◽  
Sophie Schiff ◽  
Jeffrey N. Motter ◽  
Alice Grinberg ◽  
Bret R. Rutherford ◽  
...  
Keyword(s):  
Cortical Thickness ◽  
Brain Magnetic Resonance Imaging ◽  
Late Life ◽  
Hippocampal Volume ◽  
Intracranial Volume ◽  
Late Life Depression ◽  
Open Treatment ◽  
Left And Right ◽  
Mean Differences ◽  
Prospective Longitudinal

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.

scholarly journals Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

2013 ◽  
Vol 21 (8) ◽  
pp. 794-802 ◽  
Author(s):  
R. Scott Mackin ◽  
Duygu Tosun ◽  
Susanne G. Mueller ◽  
Jun-Young Lee ◽  
Philip Insel ◽  
...  
Keyword(s):  
Cortical Thickness ◽  
Late Life ◽  
Late Life Depression

scholarly journals Cortical Thickness of the Salience Network and Change in Apathy Following Antidepressant Treatment for Late-Life Depression

2020 ◽  
Author(s):  
Monique A. Pimontel ◽  
Nili Solomonov ◽  
Lauren Oberlin ◽  
Theodora Kanellopoulos ◽  
Jennifer N. Bress ◽  
...  
Keyword(s):  
Cortical Thickness ◽  
Antidepressant Treatment ◽  
Late Life ◽  
Salience Network ◽  
Late Life Depression

INCREASED CORTICAL THICKNESS IN LATE-LIFE DEPRESSION AFTER ANTI-DEPRESSANT TREATMENT WITH LEVOMILNACIPRAN

2019 ◽  
Vol 27 (3) ◽  
pp. S197-S198
Author(s):  
Michaela Milillo ◽  
Beatrix Krause ◽  
Lisa Kilpatrick ◽  
Prabha Siddarth ◽  
Linda Ercoli ◽  
...  
Keyword(s):  
Cortical Thickness ◽  
Late Life ◽  
Late Life Depression

scholarly journals No Association of Lower Hippocampal Volume With Alzheimer’s Disease Pathology in Late-Life Depression

2017 ◽  
Vol 174 (3) ◽  
pp. 237-245 ◽  
Author(s):  
François-Laurent De Winter ◽  
Louise Emsell ◽  
Filip Bouckaert ◽  
Lene Claes ◽  
Saurabh Jain ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Life ◽  
Hippocampal Volume ◽  
Late Life Depression

The influence of negative life events on hippocampal and amygdala volumes in old age: a life-course perspective

2014 ◽  
Vol 45 (6) ◽  
pp. 1219-1228 ◽  
Author(s):  
L. Gerritsen ◽  
G. Kalpouzos ◽  
E. Westman ◽  
A. Simmons ◽  
L.-O. Wahlund ◽  
...  
Keyword(s):  
Life Events ◽  
Early Life ◽  
Linear Models ◽  
Negative Life Events ◽  
Critical Time ◽  
Late Life ◽  
Hippocampal Volume ◽  
Life Course Perspective ◽  
Intracranial Volume ◽  
Early Life Events

Background.Psychosocial stress has been related to changes in the nervous system, with both adaptive and maladaptive consequences. The aim of this study was to examine the relationship of negative events experienced throughout the entire lifespan and hippocampal and amygdala volumes in older adults.Method.In 466 non-demented old adults (age range 60–96 years, 58% female), hippocampal and amygdala volumes were segmented using Freesurfer. Negative life events and the age at which these events occurred were assessed by means of a structured questionnaire. Using generalized linear models, hippocampal and amygdala volumes were estimated with life events as independent variables. The statistical analyses were adjusted for age, gender, intracranial volume, lifestyle factors, cardiovascular risk factors, depressive symptoms, and cognitive functioning.Results.Total number of negative life events and of late-life events, but not of early-life, early-adulthood, or middle-adulthood events, was related to larger amygdala volume. There were interactions of early-life events with age and gender. Participants who reported two or more early-life events had significantly smaller amygdala and hippocampal volumes with increasing age. Furthermore, smaller hippocampal volume was found in men who reported two or more early-life events, but not in women.Conclusions.These results suggest that the effect of negative life events on the brain depends on the time when the events occurred, with the strongest effects observed during the critical time periods of early and late life.

Association between hippocampal volume change and change in memory following electroconvulsive therapy in late‐life depression

2019 ◽  
Vol 140 (5) ◽  
pp. 435-445 ◽  
Author(s):  
M. Laroy ◽  
F. Bouckaert ◽  
K. Vansteelandt ◽  
J. Obbels ◽  
A. Dols ◽  
...  
Keyword(s):  
Electroconvulsive Therapy ◽  
Volume Change ◽  
Late Life ◽  
Hippocampal Volume ◽  
Late Life Depression

scholarly journals Structural brain changes and neuroticism in late-life depression: a neural basis for depression subtypes

2021 ◽  
pp. 1-6
Author(s):  
Chinaka Joseph ◽  
Lihong Wang ◽  
Rong Wu ◽  
Kevin J. Manning ◽  
David C. Steffens
Keyword(s):  
White Matter ◽  
Late Life ◽  
Hippocampal Volume ◽  
Late Life Depression ◽  
Frontal Pole ◽  
Neural Basis ◽  
Prior Literature ◽  
Brain Changes ◽  
And Gender ◽  
Depression Subtypes

ABSTRACT The neurobiological basis of neuroticism in late-life depression (LLD) is understudied. We hypothesized that older depressed subjects scoring high in measures of neuroticism would have smaller hippocampal and prefrontal volumes compared with non-neurotic older depressed subjects and with nondepressed comparison subjects based on previous research. Non-demented subjects were recruited and were either depressed with high neuroticism (n = 65), depressed with low neuroticism (n = 36), or never depressed (n = 27). For imaging outcomes focused on volumetric analyses, we found no significant between-group differences in hippocampal volume. However, we found several frontal lobe regions for which depressed subjects with high neuroticism scores had smaller volumes compared with non-neurotic older depressed subjects and with nondepressed comparison subjects, controlling for age and gender. These regions included the frontal pole, medial orbitofrontal cortex, and left pars orbitalis. In addition, we found that non-neurotic depressed subjects had a higher volume of non-white matter hypointensities on T1-weighted images (possibly related to cerebrovascular disease) than did neurotic depressed subjects. Our finding that depressed subjects low in neuroticism had higher volumes of non-white matter hypointensities is consistent with prior literature on “vascular depression.” In contrast, the finding that those high in neuroticism had smaller frontal volume than depressed subjects low in neuroticism and never-depressed subjects highlight the importance of frontal circuitry in the subgroup of older depressed individuals with comorbid neuroticism. Together, these results implicate different neural mechanisms in older neurotic and non-neurotic depressed groups and suggest that multiple biological pathologies may lead to different clinical expressions of LLD.

scholarly journals A missense variant in SHARPIN mediates Alzheimer’s disease-specific brain damages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jun Young Park ◽  
Dongsoo Lee ◽  
Jang Jae Lee ◽  
Jungsoo Gim ◽  
Tamil Iniyan Gunasekaran ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Thickness ◽  
Association Studies ◽  
Brain Magnetic Resonance Imaging ◽  
Amyloid Β ◽  
Missense Variant ◽  
Hippocampal Volume ◽  
Genome Wide Association Studies ◽  
Increased Risk

AbstractEstablished genetic risk factors for Alzheimer’s disease (AD) account for only a portion of AD heritability. The aim of this study was to identify novel associations between genetic variants and AD-specific brain atrophy. We conducted genome-wide association studies for brain magnetic resonance imaging measures of hippocampal volume and entorhinal cortical thickness in 2643 Koreans meeting the clinical criteria for AD (n = 209), mild cognitive impairment (n = 1449) or normal cognition (n = 985). A missense variant, rs77359862 (R274W), in the SHANK-associated RH Domain Interactor (SHARPIN) gene was associated with entorhinal cortical thickness (p = 5.0 × 10−9) and hippocampal volume (p = 5.1 × 10−12). It revealed an increased risk of developing AD in the mediation analyses. This variant was also associated with amyloid-β accumulation (p = 0.03) and measures of memory (p = 1.0 × 10−4) and executive function (p = 0.04). We also found significant association of other SHARPIN variants with hippocampal volume in the Alzheimer’s Disease Neuroimaging Initiative (rs3417062, p = 4.1 × 10−6) and AddNeuroMed (rs138412600, p = 5.9 × 10−5) cohorts. Further, molecular dynamics simulations and co-immunoprecipitation indicated that the variant significantly reduced the binding of linear ubiquitination assembly complex proteins, SHPARIN and HOIL-1 Interacting Protein (HOIP), altering the downstream NF-κB signaling pathway. These findings suggest that SHARPIN plays an important role in the pathogenesis of AD.

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