Brain degeneration in Parkinson’s disease patients with cognitive decline: a coordinate-based meta-analysis

Mihaescu, Alexander; Masellis, Mario; Graff‐Guerrero, Ariel; Kim, Jinhee; Criaud, Marion; Cho, Sang Soo; Ghadery, Christine; Valli, Mikaeel; Strafella, Antonio P.

doi:10.1007/s11682-018-9922-0

Cited by 40 publications

(29 citation statements)

References 81 publications

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“…Memory problems are frequently the first subjective cognitive complaint in Parkinson’s disease (Noe et al , 2004) and are a prominent component of PD dementia (Whittington et al , 2000; Bronnick et al , 2007; Muslimovic et al , 2007; Reid et al , 2011; Wang et al , 2015), forming part of the diagnostic criteria for PD dementia (Emre et al , 2007). In patients with PD dementia the hippocampus shows a higher density of Lewy pathology (Harding and Halliday, 2001; Apaydin et al , 2002; Arnold et al , 2013; Hall et al , 2014), reduction in cholinergic activity (Hall et al , 2014) and progressive atrophy with disease progression (Aybek et al , 2009; Weintraub et al , 2011, 2012; Morales et al , 2013; Kandiah et al , 2014; Mak et al , 2015; Gee et al , 2017; Mihaescu et al , 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Neuroimaging studies of PD dementia have been particularly heterogeneous (Lanskey et al , 2018), with atrophy or hypometabolism reported in frontal (Song et al , 2011; Melzer et al , 2012), temporal (Melzer et al , 2012; Pagonabarraga et al , 2013), parietal (Melzer et al , 2012; Pereira et al , 2014), occipital (Melzer et al , 2012) and insular cortices (Mak et al , 2014) as well as numerous subcortical regions (Melzer et al , 2012; Foo et al , 2017; Schneider et al , 2017). Different meta-analyses of the coordinates reported by these studies have also been inconsistent (Minkova et al , 2017; Mihaescu et al , 2018).…”

Section: Introductionmentioning

confidence: 99%

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Neuroimaging in Parkinson’s disease dementia: connecting the dots

Weil

Hsu

Darby

et al. 2019

Brain Communications

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Abstract Dementia is a common and devastating symptom of Parkinson’s disease but the anatomical substrate remains unclear. Some evidence points towards hippocampal involvement but neuroimaging abnormalities have been reported throughout the brain and are largely inconsistent across studies. Here, we test whether these disparate neuroimaging findings for Parkinson’s disease dementia localize to a common brain network. We used a literature search to identify studies reporting neuroimaging correlates of Parkinson’s dementia (11 studies, 385 patients). We restricted our search to studies of brain atrophy and hypometabolism that compared Parkinson’s patients with dementia to those without cognitive involvement. We used a standard coordinate-based activation likelihood estimation meta-analysis to assess for consistency in the neuroimaging findings. We then used a new approach, coordinate-based network mapping, to test whether neuroimaging findings localized to a common brain network. This approach uses resting-state functional connectivity from a large cohort of normative subjects (n = 1000) to identify the network of regions connected to a reported neuroimaging coordinate. Activation likelihood estimation meta-analysis failed to identify any brain regions consistently associated with Parkinson’s dementia, showing major heterogeneity across studies. In contrast, coordinate-based network mapping found that these heterogeneous neuroimaging findings localized to a specific brain network centred on the hippocampus. Next, we tested whether this network showed symptom specificity and stage specificity by performing two further analyses. We tested symptom specificity by examining studies of Parkinson’s hallucinations (9 studies, 402 patients) that are frequently co-morbid with Parkinson’s dementia. We tested for stage specificity by using studies of mild cognitive impairment in Parkinson’s disease (15 studies, 844 patients). Coordinate-based network mapping revealed that correlates of visual hallucinations fell within a network centred on bilateral lateral geniculate nucleus and correlates of mild cognitive impairment in Parkinson’s disease fell within a network centred on posterior default mode network. In both cases, the identified networks were distinct from the hippocampal network of Parkinson’s dementia. Our results link heterogeneous neuroimaging findings in Parkinson’s dementia to a common network centred on the hippocampus. This finding was symptom and stage-specific, with implications for understanding Parkinson’s dementia and heterogeneity of neuroimaging findings in general.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroimaging in Parkinson’s disease dementia: connecting the dots

Weil

Hsu

Darby

et al. 2019

Brain Communications

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“…It has been noted that the incidence of dementia is nearly 100 per 100,000 patient-years in prevalence samples of PD [7]. In addition, the bilateral insula and right hippocampus were identified as regions of structural atrophy in PD patients with dementia (PDD) [8].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 prevents MPTP-induced changes in hippocampal memory via regulation of the α-synuclein/PSD-95 pathway

Meng

Liu

et al. 2019

Aging

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Memory deficiency is a common non-motor symptom of Parkinson’s disease (PD), and conventionally, α-synuclein is considered to be an important biomarker for both motor and cognitive characteristics attributed to PD. However, the role of physiological α-synuclein in cognitive impairment remains undetermined. Ginsenoside Rb1 has been shown to protect dopaminergic neurons (DA) from death and inhibit α-synuclein fibrillation and toxicity in vitro . Our recent study also revealed that ginsenoside Rb1 ameliorates motor deficits and prevents DA neuron death via upregulating glutamate transporter GLT-1 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Whether Rb1 can improve memory deficiency and the underlying mechanism is still unknown. In this study, we found that Rb1 can prevent the spatial learning and memory deficits, increase long-term potentiation (LTP) and hippocampal glutamatergic transmission in the MPTP mouse model. The underlying neuroprotective mechanism of Rb1-improved synaptic plasticity involves Rb1 promoting hippocampal CA3 α-synuclein expression, restoring the glutamate in the CA3-schaffer collateral-CA1 pathway, and sequentially increasing postsynaptic density-95 (PSD-95) expression. Thus, we provide evidence that Rb1 modulates memory function, synaptic plasticity, and excitatory transmission via the trans-synaptic α-synuclein/PSD-95 pathway. Our findings suggest that Rb1 may serve as a functional drug in treating the memory deficiency in PD.

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“…In addition, resting-state functional MRI revealed a reduced connectivity specifically in the default mode network (left precuneus, right median cingulate gyrus, left superior frontal gyrus, and right precentral gyrus) in PD-MCI patients (34). Interestingly, another recent metaanalysis found differences in several brain regions (left insula, bilateral dorsolateral prefrontal cortex, left angular gyrus, midcingulate cortex, and right supramarginal gyrus) between PD-MCI and PD-NC patients (35), which was not entirely consistent with our findings. This could be due to the fact that the earlier meta-analysis was biased as it pooled multiple studies that employed both VBM and cortical thickness measures, which may have reduced the sensitivity of detecting structural changes in subcortical regions such as the basal ganglia (35).…”

Section: Discussionmentioning

confidence: 97%

Voxel-wise meta-analysis of structural changes in gray matter of Parkinson’s disease patients with mild cognitive impairment

Qin

Yang

Gao

et al. 2020

Braz J Med Biol Res

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Evidence from previous voxel-based morphometry (VBM) studies indicates that widespread brain regions are involved in Parkinson's disease with mild cognitive impairment (PD-MCI). However, the spatial localization reported for gray matter (GM) abnormalities is heterogeneous. The aim of the present study was to quantitatively integrate studies on GM abnormalities observed in PD-MCI in order to determine whether a pattern exists. Eligible whole-brain VBM studies were identified by a systematic search of articles in PubMed and EMBASE databases spanning from 1995 to January 1, 2019. A meta-analysis was performed to investigate regional GM abnormalities in PD-MCI. The anisotropic effect size version of seed-based d mapping (AES-SDM) meta-analysis was conducted to explore the GMV differences of PD-MCI compared with PD patients with normal cognitive function (PD-NC). A total of 12 studies comprising 243 PD-MCI patients and 326 PD-NC were included in the metaanalysis. PD-MCI patients showed a robust GM decrease in the left insula and left superior temporal gyrus. Moreover, meta-regression analysis demonstrated that age, PD duration and stage, and Unified Parkinson's Disease Rating Scale III and Mini-Mental State Examination scores might be partly correlated with the GM abnormalities observed in PD-MCI patients. The convergent findings of this quantitative meta-analysis revealed a characteristic neuroanatomical pattern in PD-MCI. The findings provide some evidence that MCI in PD may result in the breakdown of the insula and temporal gyrus, which may serve as specific regions of interest for further investigations.

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Brain degeneration in Parkinson’s disease patients with cognitive decline: a coordinate-based meta-analysis

Cited by 40 publications

References 81 publications

Neuroimaging in Parkinson’s disease dementia: connecting the dots

Neuroimaging in Parkinson’s disease dementia: connecting the dots

Ginsenoside Rb1 prevents MPTP-induced changes in hippocampal memory via regulation of the α-synuclein/PSD-95 pathway

Voxel-wise meta-analysis of structural changes in gray matter of Parkinson’s disease patients with mild cognitive impairment

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