Gene Expression Profiles of Entorhinal Cortex in Alzheimer’s Disease

Ding, Bingqian; Yan, Xin; Gao, Ming; Li, Zhenjiang; Xu, Chenyang; Fan, Shaokang; He, Weichun

doi:10.1177/1533317514523487

Cited by 26 publications

(23 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The glycolysis pathway is related to VaD, and genes involved in this pathway, such as GPI and GAPD, are significantly downregulated in the AD hippocampus [31,35]. In addition, PFKM, PGM1, ALDOA, and ALDOC are also downregulated in the entorhinal cortex of AD patients [32,36,37]. Our study showed that downregulated proteins were significantly enriched in the subpathways of the ‘glycolysis/gluconeogenesis' pathway.…”

Section: Discussionmentioning

confidence: 89%

“…The downregulated ATP5B in the AD hippocampus leads to a reduction in the levels of energy metabolism [31]. In addition, Ding et al [32] proved that the ATP metabolism network comprises many downregulated genes such as ATP5B, ATP5C1, and ATP5G1 in the entorhinal cortex of AD. In this study, ‘metabolic pathways' and the ‘Alzheimer's disease' pathway were the significant pathways identified in the pathway crosstalk network.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of Pivotal Markers in Vascular Dementia Based on Proteomics Data

Wang¹,

Zhao²,

Xu³

et al. 2015

Dement Geriatr Cogn Disord

View full text Add to dashboard Cite

Objective: The aim of this study was to analyze protein expression profiles of vascular dementia (VaD) subjects for investigating the underlying therapeutic markers. Methods: Protein expression profile data were acquired from a quantitative clinical proteomic study, including 10 nondemented elderly controls and 10 age-matched VaD subjects. Differentially expressed proteins (DEPs) were identified between VaD subjects and controls, followed by function prediction using DAVID (Database for Annotation, Visualization, and Integrated Discovery). Then, a protein-protein interaction (PPI) network was constructed by comparing it with the STRING (Search Tool for the Retrieval of Interacting Genes) database, and the pathway crosstalk analysis was conducted based on overlapping PPI network and enriched pathways. Furthermore, the subpathway was screened and analyzed by the iSubpathwayMiner package in R. Results: A total of 144 DEPs were screened from VaD subjects and the controls. They were significantly enriched in many pathways. High-degree proteins were detected in the PPI network, such as ATP5B (ATP synthase subunit β). Furthermore, ‘metabolic pathways' and ‘Alzheimer's disease' were the significant pathways screened in the crosstalk analysis. At last, upregulated proteins were enriched in 2 subpathways of 1 pathway, while downregulated proteins were enriched in 162 subpathways of 36 pathways. Conclusion: By analyzing the differential expressions of proteins, the potential underlying therapeutic markers and mechanism of VaD might be elucidated.

show abstract

Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Identification of Pivotal Markers in Vascular Dementia Based on Proteomics Data

Wang¹,

Zhao²,

Xu³

et al. 2015

Dement Geriatr Cogn Disord

View full text Add to dashboard Cite

show abstract

“…the transcriptional response associated with its onset and progression (29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). These studies have revealed that this transcriptional response involves genes corresponding to proteins that can cause the disease and those associated with the cellular processes engaged in combating it (29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

“…These studies have revealed that this transcriptional response involves genes corresponding to proteins that can cause the disease and those associated with the cellular processes engaged in combating it (29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

A transcriptional signature of Alzheimer’s disease is associated with a metastable subproteome at risk for aggregation

Ciryam

Kundra

Freer

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

It is well-established that widespread transcriptional changes accompany the onset and progression of Alzheimer’s disease. Because of the multifactorial nature of this neurodegenerative disorder and its complex relationship with aging, however, it remains unclear whether such changes are the result of nonspecific dysregulation and multisystem failure or instead are part of a coordinated response to cellular dysfunction. To address this problem in a systematic manner, we performed a meta-analysis of about 1,600 microarrays from human central nervous system tissues to identify transcriptional changes upon aging and as a result of Alzheimer’s disease. Our strategy to discover a transcriptional signature of Alzheimer’s disease revealed a set of down-regulated genes that encode proteins metastable to aggregation. Using this approach, we identified a small number of biochemical pathways, notably oxidative phosphorylation, enriched in proteins vulnerable to aggregation in control brains and encoded by genes down-regulated in Alzheimer’s disease. These results suggest that the down-regulation of a metastable subproteome may help mitigate aberrant protein aggregation when protein homeostasis becomes compromised in Alzheimer’s disease.

show abstract

“…However, this concept has been recently challenged111213. In fact, in addition to mitochondrial respiratory enzyme defects, increasing evidence implicates the dysfunction of mitochondrial F1FO-ATP synthase in AD14151617.…”

mentioning

confidence: 99%

Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer’s disease

Beck¹,

Guo²,

Phensy³

et al. 2016

Nat Commun

144

185

View full text Add to dashboard Cite

F1FO-ATP synthase is critical for mitochondrial functions. The deregulation of this enzyme results in dampened mitochondrial oxidative phosphorylation (OXPHOS) and activated mitochondrial permeability transition (mPT), defects which accompany Alzheimer’s disease (AD). However, the molecular mechanisms that connect F1FO-ATP synthase dysfunction and AD remain unclear. Here, we observe selective loss of the oligomycin sensitivity conferring protein (OSCP) subunit of the F1FO-ATP synthase and the physical interaction of OSCP with amyloid beta (Aβ) in the brains of AD individuals and in an AD mouse model. Changes in OSCP levels are more pronounced in neuronal mitochondria. OSCP loss and its interplay with Aβ disrupt F1FO-ATP synthase, leading to reduced ATP production, elevated oxidative stress and activated mPT. The restoration of OSCP ameliorates Aβ-mediated mouse and human neuronal mitochondrial impairments and the resultant synaptic injury. Therefore, mitochondrial F1FO-ATP synthase dysfunction associated with AD progression could potentially be prevented by OSCP stabilization.

show abstract

Gene Expression Profiles of Entorhinal Cortex in Alzheimer’s Disease

Cited by 26 publications

References 34 publications

Identification of Pivotal Markers in Vascular Dementia Based on Proteomics Data

Identification of Pivotal Markers in Vascular Dementia Based on Proteomics Data

A transcriptional signature of Alzheimer’s disease is associated with a metastable subproteome at risk for aggregation

Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer’s disease

Contact Info

Product

Resources

About