Progressive brain changes in Parkinson’s disease: A meta-analysis of structural magnetic resonance imaging studies

He, Hanwei; Liang, Ling; Tang, Tao; Luo, Jie-Kun; Wang, Yan; Cui, Hanjin

doi:10.1016/j.brainres.2020.146847

Cited by 18 publications

(13 citation statements)

References 49 publications

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“…Effects between visits were most pronounced in the right caudate and these changes in normalized FDOPA uptake correlated with both the increasing disease duration and worsening in UPDRS-III scores. Consistent with our findings, the caudate nucleus’ significance for disease progression is underpinned by associated atrophy 34 , increased iron content 28 and gradual dopamine depletion 35 as detailed in previous studies. Considering the latter studies, our results highlight the inestimable value of combining different imaging techniques for capturing direct consequences of degeneration in a “disease hub” such as the SN.…”

Section: Discussionsupporting

confidence: 91%

Longitudinal trimodal imaging of midbrain-associated network degeneration in Parkinson’s disease

Steidel

Ruppert

Greuel

et al. 2022

npj Parkinsons Dis.

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The prevailing network perspective of Parkinson’s disease (PD) emerges not least from the ascending neuropathology traceable in histological studies. However, whether longitudinal in vivo correlates of network degeneration in PD can be observed remains unresolved. Here, we applied a trimodal imaging protocol combining 18F-fluorodeoxyglucose (FDG)- and 18F-fluoro-L-Dopa- (FDOPA)-PET with resting-state functional MRI to assess longitudinal changes in midbrain metabolism, striatal dopamine depletion and striatocortical dysconnectivity in 17 well-characterized PD patients. Whole-brain (un)paired-t-tests with focus on midbrain or striatum were performed between visits and in relation to 14 healthy controls (HC) in PET modalities. Resulting clusters of FDOPA-PET comparisons provided volumes for seed-based functional connectivity (FC) analyses between visits and in relation to HC. FDG metabolism in the left midbrain decreased compared to baseline along with caudatal FDOPA-uptake. This caudate cluster exhibited a longitudinal FC decrease to sensorimotor and frontal areas. Compared to healthy subjects, dopamine-depleted putamina indicated stronger decline in striatocortical FC at follow-up with respect to baseline. Increasing nigrostriatal deficits and striatocortical decoupling were associated with deterioration in motor scores between visits in repeated-measures correlations. In summary, our results demonstrate the feasibility of in-vivo tracking of progressive network degeneration using a multimodal imaging approach. Specifically, our data suggest advancing striatal and widespread striatocortical dysfunction via an anterior-posterior gradient originating from a hypometabolic midbrain cluster within a well-characterized and only mild to moderately affected PD cohort during a relatively short period.

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Section: Discussionsupporting

confidence: 91%

Longitudinal trimodal imaging of midbrain-associated network degeneration in Parkinson’s disease

Steidel

Ruppert

Greuel

et al. 2022

npj Parkinsons Dis.

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“…Gray matter atrophy of cortical structures extending to the subcortical areas (e.g., insula and cerebellum) presents in the PD patients with MCI [ 11 , 74 ]. The subcortical structural deficits are functionally related to widespread cognitive functions [ 75 , 76 ]. The results confirmed that MCI was associated with widespread brain atrophy and indicated that the decreased gray matter volume or cortical thickness in these brain structures could be biomarkers for cognitive impairments in PD.…”

Section: Discussionmentioning

confidence: 99%

The structural changes of gray matter in Parkinson disease patients with mild cognitive impairments

Zhao

et al. 2022

PLoS ONE

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Objectives Parkinson disease (PD) is associated with cognitive impairments. However, the underlying neural mechanism of cognitive impairments in PD is still not clear. This study aimed to investigate the anatomic alternations of gray matter in PD patients with mild cognitive impairment (MCI) and their associations with neurocognitive measurements. Methods T1-weighted magnetic resonance imaging (MRI) data were acquired from 23 PD patients with MCI, 23 PD patients without MCI, and 23 matched healthy controls. The MRI data were analyzed using voxel-based morphometry (VBM) and surfaced-based morphometry (SBM) methods to assess the structural changes in gray matter volume and cortical thickness respectively. Receiver operating characteristic (ROC) analysis was used to examine the diagnostic accuracies of the indexes of interest. The correlations between the structural metrics and neurocognitive assessments (e.g., Montreal cognitive assessment, MOCA; Mini-mental state examination, MMSE) were further examined. Results PD patients with MCI showed reduced gray matter volume (GMV) in the frontal cortex (e.g., right inferior frontal gyrus and middle frontal gyrus) and extended to insula as well as cerebellum compared with the healthy controls and PD patients without MIC. Thinner of cortical thickens in the temporal lobe (e.g., left middle temporal gyrus and right superior temporal gyrus) extending to parietal cortex (e.g., precuneus) were found in the PD patients with MCI relative to the healthy controls and PD patients without MCI.ROC analysis indicated that the area under the ROC curve (AUC) values in the frontal, temporal, and subcortical structures (e.g., insula and cerebellum) could differentiate the PD patients with MCI and without MCI and healthy controls. Furthermore, GMV of the right middle frontal gyrus and cortical thickness of the right superior temporal gyrus were correlated with neurocognitive dysfunctions (e.g., MOCA and MMSE) in PD patients with MCI. Conclusion This study provided further evidence that PD with MCI was associated with structural alternations of brain. Morphometric analysis focusing on the cortical and subcortical regions could be biomarkers of cognitive impairments in PD patients.

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“…Although conventional MRI lacks specificity as a diagnostic aid for PD, 70 a large number of patients show structural microlesions in the basal ganglia, with progressive reductions in whole gray matter, and a volumetric decrease in the caudate, putamen, accumbens, and amygdala. 71,72 In our PD sample, over 80% of patients showed abnormal MRI.…”

Section: Psychometric Phenotypementioning

confidence: 74%

Atremorine in Parkinson's disease: From dopaminergic neuroprotection to pharmacogenomics

Cacabelos

Carrera

Martínez

et al. 2021

Medicinal Research Reviews

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Atremorine is a novel bioproduct obtained by nondenaturing biotechnological processes from a genetic species of Vicia faba.Atremorine is a potent dopamine (DA) enhancer with powerful effects on the neuronal dopaminergic system, acting as a neuroprotective agent in Parkinson's disease (PD). Over 97% of PD patients respond to a single dose of Atremorine (5 g, p.o.) 1 h after administration. This response is gender-, time-, dose-, and genotype-dependent, with optimal doses ranging from 5 to 20 g/day, depending upon disease severity and concomitant medication. Drug-free patients show an increase in DA levels from 12.14 ± 0.34 pg/ml to 6463.21 ± 1306.90 pg/ ml; and patients chronically treated with anti-PD drugs show an increase in DA levels from 1321.53 ± 389.94 pg/ml to 16,028.54 ± 4783.98 pg/ml, indicating that Atremorine potentiates the dopaminergic effects of conventional anti-PD drugs. Atremorine also influences the levels of other neurotransmitters (adrenaline, noradrenaline) and hormones which are regulated by DA (e.g., prolactin, PRL), with no effect on serotonin or histamine. The variability in Atremorine-induced DA response is highly attributable to pharmacogenetic factors.

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Progressive brain changes in Parkinson’s disease: A meta-analysis of structural magnetic resonance imaging studies

Cited by 18 publications

References 49 publications

Longitudinal trimodal imaging of midbrain-associated network degeneration in Parkinson’s disease

Longitudinal trimodal imaging of midbrain-associated network degeneration in Parkinson’s disease

The structural changes of gray matter in Parkinson disease patients with mild cognitive impairments

Atremorine in Parkinson's disease: From dopaminergic neuroprotection to pharmacogenomics

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