Imaging Brain Networks in Neurodegenerative Diseases

He, Yong

doi:10.1111/cns.12466

Cited by 3 publications

(1 citation statement)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Parkinson's disease (PD) is a multifactorial disorder, characterized by the deposition of Lewy bodies and loss of dopaminergic neurons in the substantia nigra pars compacta (SNc) . The enhanced oxidative stress , protein misfolding and aggregation , and dysfunction of the ubiquitin–proteasome system are involved in the pathogenesis of PD, but the exact mechanisms that contribute to dopaminergic neuronal degeneration remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Atp13a2 Deficiency Aggravates Astrocyte‐Mediated Neuroinflammation via NLRP3 Inflammasome Activation

Qiao

Yin

et al. 2016

CNS Neurosci Ther

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Atp13a2 Deficiency Aggravates Astrocyte‐Mediated Neuroinflammation via NLRP3 Inflammasome Activation

Qiao

Yin

et al. 2016

CNS Neurosci Ther

View full text Add to dashboard Cite

show abstract

Application of Graph Theory to Assess Static and Dynamic Brain Connectivity: Approaches for Building Brain Graphs

Chen

et al. 2018

Proc. IEEE

View full text Add to dashboard Cite

Human brain connectivity is complex. Graph theory based analysis has become a powerful and popular approach for analyzing brain imaging data, largely because of its potential to quantitatively illuminate the networks, the static architecture in structure and function, the organization of dynamic behavior over time, and disease related brain changes. The first step in creating brain graphs is to define the nodes and edges connecting them. We review a number of approaches for defining brain nodes including fixed versus data-driven nodes. Expanding the narrow view of most studies which focus on static and/or single modality brain connectivity, we also survey advanced approaches and their performances in building dynamic and multi-modal brain graphs. We show results from both simulated and real data from healthy controls and patients with mental illnesse. We outline the advantages and challenges of these various techniques. By summarizing and inspecting recent studies which analyzed brain imaging data based on graph theory, this article provides a guide for developing new powerful tools to explore complex brain networks.

show abstract

The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson’s Disease

2019

Med Sci Monit

View full text Add to dashboard Cite

Background The purpose of this study was to investigate the role and mechanism of steroid receptor coactivator-interacting protein (SIP) in an astrocyte model of 1-methyl-4-phenylpyridinium (MPP + )-induced Parkinson’s disease. Material/Methods To perform our study, a Parkinson’s disease cell model was established by treating the rat glioblastoma cell line C6 with MPP + . SIP was overexpressed in C6 cells using SIP-plasmid. Cell viability and apoptosis were analyzed using MTT assay and flow cytometer respectively. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels were detected using enzyme linked immunosorbent assay and quantitative reverse transcription PCR. Besides, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production, and superoxide dismutase (SOD) enzyme activity were determined in the present study. For protein and mRNA detection, western blot assay, and qRT-PCR were performed respectively. Results SIP was decreased in MPP + -induced C6 cells. SIP overexpression relieved MPP + -induced cytotoxicity of C6 cells, displayed as increased cell viability and reduced cell apoptosis and reduced LDH release. Besides, SIP inhibited MPP + -induced inflammatory response and oxidative stress, evidenced by decreased levels of inflammatory factors (TNF-α and IL-1β), reduced ROS generation and enhanced SOD activity. Moreover, MPP + -induced nuclear factor-κB activation was inhibited by SIP overexpression. Conclusions SIP was downregulated in Parkinson’s disease and it played a protective role in the development Parkinson’s disease, thus may be a promising target for Parkinson’s disease treatment.

show abstract

Imaging Brain Networks in Neurodegenerative Diseases

Cited by 3 publications

References 15 publications

Atp13a2 Deficiency Aggravates Astrocyte‐Mediated Neuroinflammation via NLRP3 Inflammasome Activation

Atp13a2 Deficiency Aggravates Astrocyte‐Mediated Neuroinflammation via NLRP3 Inflammasome Activation

Application of Graph Theory to Assess Static and Dynamic Brain Connectivity: Approaches for Building Brain Graphs

The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson’s Disease

Contact Info

Product

Resources

About