Precuneal Thickness and Depression in Parkinson Disease

Zanigni, Stefano; Sambati, Luisa; Evangelisti, Stefania; Testa, Claudia; Calandra-Buonaura, Giovanna; Manners, David Neil; Terlizzi, Rossana; Poda, Roberto; Oppi, Federico; Lodi, Raffaele; Cortelli, Pietro; Tonon, Caterina

doi:10.1159/000450614

Cited by 16 publications

(12 citation statements)

References 25 publications

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“…Anxiety and depressive disorders are common in PD, which are associated with structural and functional changes of multiple brain regions (Schrag and Taddei, 2017;Carey et al, 2021). In PD with mild to moderate depression, cortical thickness of the precuneus cortex was also significantly increased (Zanigni et al, 2017). However, in our cohort, we did not observe any significant correlations.…”

Section: Discussioncontrasting

confidence: 80%

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Xuan

Wang

Zhang

et al. 2022

Front. Aging Neurosci.

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Parkinson’s disease (PD) is a common neurodegenerative disease with progressive gait, cognition, and overall functional decline. Surface area changes are frequently seen with aging. In neurodegenerative diseases, the changes can be evident with disease progression. The current study aimed to study the regional microstructural alterations using surface-based morphometry to correlate with gait measures of the pace and rhythm domains in PD patients. We hypothesize that specific regional surface changes can be associated with PD gait impairments. Surface analysis might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker in conjunction with other imaging markers. Twenty-seven PD patients and 37 healthy controls were included. The clinical assessment included Mini-Mental State Exanimation, PD motor assessment, clinical gait testing, and objective/quantitative gait assessment. For patients with PD, all motor and gait testing were performed during both OFF and ON medication states. Three Tesla MRI and high-resolution 3D structural images were acquired with an MP-RAGE pulse sequence. Structural image data preprocessing was performed using the DPABISurf toolbox. Clinical characteristics between PD and control group were compared, and correlation between the surface area and behavioral data were analyzed. At the left lateral temporal cortex (LTC) and right inferior parietal cortex (IPC), PD patients have significantly larger surface areas when compared to controls (P < 0.05) using surface-based morphometry. The surface area changes of the left LTC and right IPC were associated with the worse performance of gait assessed by Berg Balance Scale and Timed Up and Go during OFF (P < 0.01). The left LTC area changes significantly correlated with the number of steps, velocity, and the stride length of the pace domain in the ON state. Our findings suggest that PD is associated with a characteristic regional pattern of larger surface area in the left LTC and right IPC. These regional changes were associated with the pace domain of the gait in the ON state. Overall, surface-based analyses might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker.

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Section: Discussioncontrasting

confidence: 80%

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Xuan

Wang

Zhang

et al. 2022

Front. Aging Neurosci.

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“…In addition to the regions in the corticolimbic system, we identified postcentral gyrus, precuneus, and temporal pole. These regions were also reported to be related to DPD patients [7,12,58]. The alteration in postcentral gyrus was associated with the cortical-basal ganglia circuit that is known as an important system that controls motor symptoms in PD patients [59].…”

Section: Discussionmentioning

confidence: 99%

Effectiveness of imaging genetics analysis to explain degree of depression in Parkinson’s disease

et al. 2019

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Depression is one of the most common and important neuropsychiatric symptoms in Parkinson’s disease and often becomes worse as Parkinson’s disease progresses. However, the underlying mechanisms of depression in Parkinson’s disease are not clear. The aim of our study was to find genetic features related to depression in Parkinson’s disease using an imaging genetics approach and to construct an analytical model for predicting the degree of depression in Parkinson’s disease. The neuroimaging and genotyping data were obtained from an openly accessible database. We computed imaging features through connectivity analysis derived from tractography of diffusion tensor imaging. The imaging features were used as intermediate phenotypes to identify genetic variants according to the imaging genetics approach. We then constructed a linear regression model using the genetic features from imaging genetics approach to describe clinical scores indicating the degree of depression. As a comparison, we constructed other models using imaging features and genetic features based on references to demonstrate the effectiveness of our imaging genetics model. The models were trained and tested in a five-fold cross-validation. The imaging genetics approach identified several brain regions and genes known to be involved in depression, with the potential to be used as meaningful biomarkers. Our proposed model using imaging genetic features predicted and explained the degree of depression in Parkinson’s disease appropriately (adjusted R2 larger than 0.6 over five training folds) and with a lower error and higher correlation than with other models over five test folds.

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“…It was also associated with cortical thinning in left temporal, anterior cingulate, right posterior cingulate and hippocampal cortices as well as thalamus volume shrinking over time, and higher scores of depressive symptoms at baseline correlated with a higher rate of cortical thinning longitudinally (Goto et al 2018 ; Hanganu et al 2017 ). Precuneus thinning was evident in PD patients with mild-moderate depression in early stages of disease (Zanigni et al 2017 ). Others reported smaller amygdala volumes but intact limbic connectivity (Surdhar et al 2012 ), and GM decrease in bilateral orbitofrontal, right temporal region and the limbic system (Feldmann et al 2008 ).…”

Section: Brain Structural Correlates Of Dpdmentioning

confidence: 99%

“…Both the dorsal raphe nucleus (serotonergic) and LC (noradrenergic) involved in premotor PD stages can lead to depletion of monoaminergic transporter systems in the basal ganglia-cortical loop linked to emotional control. These and changes of precuneal cortex thickness have been associated with depression in early PD (Borgonovo et al 2017 ; Zanigni et al 2017 ). Higher prevalence of pathological features in depressed vs non-depressed PD patients particularly in the catecholaminergic brain areas, LC (neuronal loss p = 0.08; gliosis p = 0.008), dorsal raphe nuclei (neuronal loss p < 0.05) and SNc (ns), but differences in amygdala and cortical regions suggested that DPD is more related to catecholaminergic than to serotonergic dysfunction (Frisina et al 2009 ), whereas LBs in the dorsal raphe nuclei in early PD implicated a serotonergic pathology in early DPD (Tan et al 2011 ), without a prominent role of dopaminergic degeneration (Maillet et al 2016 ).…”

Section: Combined Neurotransmitter Deficitsmentioning

confidence: 99%

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Ka¹

2022

J Neural Transm

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Depression, with an estimated prevalence of about 40% is a most common neuropsychiatric disorder in Parkinson disease (PD), with a negative impact on quality of life, cognitive impairment and functional disability, yet the underlying neurobiology is poorly understood. Depression in PD (DPD), one of its most common non-motor symptoms, can precede the onset of motor symptoms but can occur at any stage of the disease. Although its diagnosis is based on standard criteria, due to overlap with other symptoms related to PD or to side effects of treatment, depression is frequently underdiagnosed and undertreated. DPD has been related to a variety of pathogenic mechanisms associated with the underlying neurodegenerative process, in particular dysfunction of neurotransmitter systems (dopaminergic, serotonergic and noradrenergic), as well as to disturbances of cortico-limbic, striato-thalamic-prefrontal, mediotemporal-limbic networks, with disruption in the topological organization of functional mood-related, motor and other essential brain network connections due to alterations in the blood–oxygen-level-dependent (BOLD) fluctuations in multiple brain areas. Other hypothetic mechanisms involve neuroinflammation, neuroimmune dysregulation, stress hormones, neurotrophic, toxic or metabolic factors. The pathophysiology and pathogenesis of DPD are multifactorial and complex, and its interactions with genetic factors, age-related changes, cognitive disposition and other co-morbidities awaits further elucidation.

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Precuneal Thickness and Depression in Parkinson Disease

Cited by 16 publications

References 25 publications

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Effectiveness of imaging genetics analysis to explain degree of depression in Parkinson’s disease

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

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