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Contains fulltext : 244253.pdf (Publisher’s version ) (Open Access), BACKGROUND: Brain structure abnormalities throughout the course of Parkinson's disease have yet to be fully elucidated. OBJECTIVE: Using a multicenter approach and harmonized analysis methods, we aimed to shed light on Parkinson's disease stage-specific profiles of pathology, as suggested by in vivo neuroimaging. METHODS: Individual brain MRI and clinical data from 2357 Parkinson's disease patients and 1182 healthy controls were collected from 19 sources. We analyzed regional cortical thickness, cortical surface area, and subcortical volume using mixed-effects models. Patients grouped according to Hoehn and Yahr stage were compared with age- and sex-matched controls. Within the patient sample, we investigated associations with Montreal Cognitive Assessment score. RESULTS: Overall, patients showed a thinner cortex in 38 of 68 regions compared with controls (d(max) = -0.20, d(min) = -0.09). The bilateral putamen (d(left) = -0.14, d(right) = -0.14) and left amygdala (d = -0.13) were smaller in patients, whereas the left thalamus was larger (d = 0.13). Analysis of staging demonstrated an initial presentation of thinner occipital, parietal, and temporal cortices, extending toward rostrally located cortical regions with increased disease severity. From stage 2 and onward, the bilateral putamen and amygdala were consistently smaller with larger differences denoting each increment. Poorer cognition was associated with widespread cortical thinning and lower volumes of core limbic structures. CONCLUSIONS: Our findings offer robust and novel imaging signatures that are generally incremental across but in certain regions specific to disease stages. Our findings highlight the importance of adequately powered multicenter collaborations. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Contains fulltext : 218611.pdf (Publisher’s version ) (Closed access), The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder.

Objective The current study aimed to examine the neural correlates of processing genuine compared with posed emotional expressions, in depressed and healthy subjects using a novel functional magnetic resonance imaging (fMRI) paradigm Method During fMRI scanning, sixteen depressed patients and ten healthy controls performed an Emotion Categorisation Task, whereby participants were asked to distinguish between genuine and non-genuine (posed or neutral) facial displays of happiness and sadness. Results Compared to controls, the depressed group showed greater activation whilst processing genuine versus posed facial displays of sadness, in the left medial orbitofrontal cortex, caudate and putamen. The depressed group also showed greater activation whilst processing genuine facial displays of sadness relative to neutral displays, in the bilateral medial frontal/orbitofrontal cortex, left dorsolateral prefrontal cortex, right dorsal anterior cingulate, bilateral posterior cingulate, right superior parietal lobe, left lingual gyrus and cuneus. No differences were found between the two groups for happy facial displays. Limitations Relatively small sample sizes and due to the exploratory nature of the study, no correction was made for multiple comparisons. Conclusion The findings of this exploratory study suggest that depressed individuals may show a different pattern of brain activation in response to genuine versus posed facial displays of sadness, compared to healthy individuals. This may have important implications for future studies that wish to examine the neural correlates of facial emotion processing in depression.