Hippocampal and anterior cingulate activation deficits in patients with geriatric depression. S., Pan, H., Van Gorp, W., Blumberg, H., … Silbersweig, D. Cortical thickness and VBM-DARTEL in late-life depression. Early and late onset, first-episode, treatment-naive depression: Same clinical symptoms, different regional neural activities. Association of cerebral amyloidosis, blood pressure, and neuronal injury with late-life onset depression. Power failure: Why small sample size undermines the reliability of neuroscience. Dialogues in Clinical Neuroscience, 10(3), 345–357. Pathways linking late-life depression to persistent cognitive impairment and dementia. American Journal of Geriatric Psychiatry, 23(3), 304–313.
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Age and gender modulate the neural circuitry supporting facial emotion processing in adults with major depressive disorder. Variability in the analysis of a single neuroimaging dataset by many teams. F., Dreber, A., Huber, J., Johannesson, M., … Schonberg, T. īotvinik-Nezer, R., Holzmeister, F., Camerer, C.
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Neuroanatomy of Alzheimer’s disease and late-life depression: a coordinate-based meta-analysis of MRI studies. American Journal of Geriatric Psychiatry, 20(12), 1057–1069. Neural correlates of successful response inhibition in unmedicated patients with late-life depression. Data-driven biological subtypes of depression: Systematic review of biological approaches to depression subtyping. American Journal of Psychiatry, 157(1), 89–95. Anxiety and depression in later life: co-occurrence and communality of risk factors. Neuroscience and Biobehavioral Reviews, 30(6), 791–807. The correlative triad among aging, dopamine, and cognition: Current status and future prospects. īäckman, L., Nyberg, L., Lindenberger, U., Li, S.-C., & Farde, L. Mechanisms and treatment of late-life depression.
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Journal of Affective Disorders, 210, 49-56. Attention bias in older women with remitted depression is associated with enhanced amygdala activity and functional connectivity. Vascular depression consensus report-A critical update. J., Baskys, A., Boldrini, M., Butters, M. Our findings highlight the importance of clinical/biological heterogeneity of late-life depression, in addition to the need for more reproducible research by using pre-registered and standardized protocols on more homogenous populations to identify potential consistent brain abnormalities in late-life depression.Īizenstein, H. This inconsistency might be due to clinical and biological heterogeneity of LLD, as well as experimental (e.g., choice of tasks, image modalities) and analytic flexibility (e.g., preprocessing and analytic parameters), and distributed patterns of neural abnormalities. Our sufficiently powered analysis on all the experiments, and more homogenous subsections of the data (patients > controls, controls > patients, and functional imaging experiments) revealed no significant convergent regional abnormality in late-life depression. The peak coordinates of group comparisons between the patients and the controls were extracted and then analyzed using activation likelihood estimation method. Our search revealed 3252 unique records, among which we identified 32 eligible whole-brain neuroimaging publications comparing 674 patients with 568 controls. Here, we provide a quantitative consolidation of neuroimaging in late-life depression using coordinate-based meta-analysis by searching multiple databases up to March 2020.
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Several neuroimaging studies have investigated localized aberrations in brain structure, function or connectivity in late-life depression, but the ensuing results are equivocal and often conflicting.