Involvement of the cerebellum in Parkinson disease and dementia with Lewy bodies

Seidel, Kay; Bouzrou, Mohamed; Heidemann, Nina; Krüger, Rejko; Schöls, Lüdger; Dunnen, Wilfred F. A. den; Korf, Horst‐Werner; Rüb, Udo

doi:10.1002/ana.24937

Cited by 59 publications

(43 citation statements)

References 20 publications

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“…To determine if this localization was maintained in differentiated progeny, we next studied NSCs with mutant LRRK2 and observed increased expression of dysregulated genes in the cerebellum (Seidel et al , ), mesencephalon, and myelencephalon (Qamhawi et al , ), where significant PD pathology is observed, particularly in the substantia nigra pars compacta, in the prenatal and adult brain heatmaps. Interestingly, this dysregulated gene expression localizes in the late months and years of the developmental transcriptome, consistent with the degenerative component of Parkinson's pathology (Fig A–C).…”

Section: Resultsmentioning

confidence: 99%

iPhemap: an atlas of phenotype to genotype relationships of human iPSC models of neurological diseases

et al. 2017

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Disease modeling with induced pluripotent stem cells (iPSCs) is creating an abundance of phenotypic information that has become difficult to follow and interpret. Here, we report a systematic analysis of research practices and reporting bias in neurological disease models from 93 published articles. We find heterogeneity in current research practices and a reporting bias toward certain diseases. Moreover, we identified 663 CNS cell‐derived phenotypes from 243 patients and 214 controls, which varied by mutation type and developmental stage in vitro. We clustered these phenotypes into a taxonomy and characterized these phenotype–genotype relationships to generate a phenogenetic map that revealed novel correlations among previously unrelated genes. We also find that alterations in patient‐derived molecular profiles associated with cellular phenotypes, and dysregulated genes show predominant expression in brain regions with pathology. Last, we developed the iPS cell phenogenetic map project atlas (iPhemap), an open submission, online database to continually catalog disease phenotypes. Overall, our findings offer new insights into the phenogenetics of iPSC‐derived models while our web tool provides a platform for researchers to query and deposit phenotypic information of neurological diseases.

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Section: Resultsmentioning

confidence: 99%

iPhemap: an atlas of phenotype to genotype relationships of human iPSC models of neurological diseases

et al. 2017

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“…Finally, the current study was limited to the SN, but it is known that pathology in PS is more widespread. As such, evaluation of other regions is necessary in order to gain a more holistic view of MRI‐pathology correlates, such as a recent study demonstrating α‐synuclein pathology in cerebellum‐related structures in PD and DLB patients …”

Section: Discussionmentioning

confidence: 99%

“…As such, evaluation of other regions is necessary in order to gain a more holistic view of MRI-pathology correlates, such as a recent study demonstrating a-synuclein pathology in cerebellum-related structures in PD and DLB patients. 58 17. Lee JH, Han YH, Kang BM, Mun CW, Lee SJ, Baik SK.…”

Section: Limitations Of Our Study and Future Directionsmentioning

confidence: 99%

Susceptibility MRI captures nigral pathology in patients with parkinsonian syndromes

Lewis

Baccon

et al. 2018

Movement Disorders

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Susceptibility MRI measurements capture nigral pathologies associated with parkinsonian syndromes. Whereas quantitative susceptibility mapping is more sensitive to iron, R2* may reflect pathological aspects of the disorders beyond iron such as α-synuclein. They may be invaluable tools in diagnosing differential parkinsonian syndromes, and tracking in living patients the dynamic changes associated with the pathological progression of these disorders. © 2018 International Parkinson and Movement Disorder Society.

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“…This kind of gait is characteristic feature of Parkinson's disease and is a useful indicator of altered functioning of basal ganglia (Fathalla et al, 2016). Depleted levels of dopamine due to loss of dopaminergic neurons has been associated with altered, planning, control over movements, cortical function and cerebellar dysfunction (Georgiev et al, 2016;Seidel et al, 2017). Polydatin+rotenone treated animals displayed significantly longer stride lengths than parkinsonian rats.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Potential of Polydatin Against Motor Abnormalities and Dopaminergic Neuronal Loss in Rotenone Induced Parkinson Model

Ahmed¹,

Shaikh²,

Baloch³

et al. 2018

Int. J. Morphol.

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SUMMARY:Among the neurodegenerative disorders, Parkinson disease (PD) is ranked as second most common. The pathological hallmark is selective degeneration of the dopaminergic neurons in the nigro-striatal regions of brain with appearance of the Lewy bodies. Present study explores the neuro-protective potential of polydatin in terms of amelioration of degeneration of dopaminergic neurons in nigro-striatal regions of brain and distorted neuromotor behavior in the rotenone model of Parkinson's disease. Thirty-six male Sprague Dawley rats were divided into three groups. Group A (control), Group B (rotenone treated) and Group C (rotenone+polydatin treated). Rotenone was administrated intraperitoneally (i.p) at a dose of 3 mg/kg/body weight while polydatin was given i.p. at a dose of 50 mg/ kg/body weight for four weeks. Then, animals were sacrificed; substantia nigra (SN) & striatum isolated from brain and five micron thick sections were prepared. Cresyl violet (CV), H&E and Immuno-histochemical staining using anti-TH antibody was done. Motor behavior was assessed weekly throughout the experiment using five different methods. Rotenone treated parkinsonian animals showed deterioration of motor behavior, weight loss, loss of dopaminergic neurons and diminished immune-reactivity in the sections from the nigrostriatal regions of these animals Polydatin+rotenone treatment showed contradicting effects to parkinsonism, with amelioration in weight loss, neuro-motor behavior, dopaminergic loss and immune-reactivity against dopaminergic neurons. Present study revealed a neuro-protective potential of polydatin in animal model of PD by ameliorating the neuro-motor abnormalities and degeneration of dopaminergic neurons in nigrostriatal regions.

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Involvement of the cerebellum in Parkinson disease and dementia with Lewy bodies

Cited by 59 publications

References 20 publications

iPhemap: an atlas of phenotype to genotype relationships of human iPSC models of neurological diseases

iPhemap: an atlas of phenotype to genotype relationships of human iPSC models of neurological diseases

Susceptibility MRI captures nigral pathology in patients with parkinsonian syndromes

Neuroprotective Potential of Polydatin Against Motor Abnormalities and Dopaminergic Neuronal Loss in Rotenone Induced Parkinson Model

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