Role of connexins in neurodegenerative diseases (Review)

Xing, Juping; Xu, Chao-Jiang

doi:10.3892/mmr.2021.12034

Cited by 2 publications

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“… 56 , 57 Another significantly enriched pathway is the gap junction that is involved in the pathogenesis of AD and PD. 58 , 59 For instance, Angeli et al, 2020, demonstrated the altered expression of glial gap junction proteins, namely, Cx43, Cx30, and Cx47, in the 5XFAD model of AD, 60 whereas Maulik et al, 2020, concluded that Aβ regulates the gap junction protein connexin 43 in cultured primary astrocytes. 61 Consistent with this, the results demonstrated the importance of CDC42, TUBB4B, and FGFR1 in the pathogenesis of AD and PD.…”

Section: Results and Discussionmentioning

confidence: 99%

“…Similarly, a study concluded that the balance between dopamine and adenosine signals regulates the PKA/Rap1 pathway in spiny neurons, where D1R and A2AR agonist enhanced PKA-mediated Rap1 phosphorylation in vivo and in vitro . Further, studies demonstrated that impaired GnRH production is directly linked to oxidative stress and mitochondrial dysfunction in neurons. , Another significantly enriched pathway is the gap junction that is involved in the pathogenesis of AD and PD. , For instance, Angeli et al, 2020, demonstrated the altered expression of glial gap junction proteins, namely, Cx43, Cx30, and Cx47, in the 5XFAD model of AD, whereas Maulik et al, 2020, concluded that Aβ regulates the gap junction protein connexin 43 in cultured primary astrocytes . Consistent with this, the results demonstrated the importance of CDC42, TUBB4B, and FGFR1 in the pathogenesis of AD and PD.…”

Section: Results and Discussionmentioning

confidence: 99%

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CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

Gupta

Kumar

2021

ACS Omega

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Integration of omics data and deciphering the mechanism of a biological regulatory network could be a promising approach to reveal the molecular mechanism involved in the progression of complex diseases, including Alzheimer’s and Parkinson’s. Despite having an overlapping mechanism in the etiology of Alzheimer’s disease (AD) and Parkinson’s disease (PD), the exact mechanism and signaling molecules behind them are still unknown. Further, the acetylation mechanism and histone deacetylase (HDAC) enzymes provide a positive direction toward studying the shared phenomenon between AD and PD pathogenesis. For instance, increased expression of HDACs causes a decrease in protein acetylation status, resulting in decreased cognitive and memory function. Herein, we employed an integrative approach to analyze the transcriptomics data that established a potential relationship between AD and PD. Data preprocessing and analysis of four publicly available microarray datasets revealed 10 HUB proteins, namely, CDC42, CD44, FGFR1, MYO5A, NUMA1, TUBB4B, ARHGEF9, USP5, INPP5D, and NUP93, that may be involved in the shared mechanism of AD and PD pathogenesis. Further, we identified the relationship between the HUB proteins and transcription factors that could be involved in the overlapping mechanism of AD and PD. CREB1 and HINFP were the crucial regulatory transcription factors that were involved in the AD and PD crosstalk. Further, lysine acetylation sites and HDAC enzyme prediction revealed the involvement of 15 and 27 potential lysine residues of CREB1 and HINFP, respectively. Our results highlighted the importance of HDAC1(K292) and HDAC6(K330) association with CREB1 and HINFP, respectively, in the AD and PD crosstalk. However, different datasets with a large number of samples and wet lab experimentation are required to validate and pinpoint the exact role of CREB1 and HINFP in the AD and PD crosstalk. It is also possible that the different datasets may or may not affect the results due to analysis parameters. In conclusion, our study potentially highlighted the crucial proteins, transcription factors, biological pathways, lysine residues, and HDAC enzymes shared between AD and PD at the molecular level. The findings can be used to study molecular studies to identify the possible relationship in the AD–PD crosstalk.

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Section: Results and Discussionmentioning

confidence: 99%

Section: Results and Discussionmentioning

confidence: 99%

CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

Gupta

Kumar

2021

ACS Omega

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Pharmacological effects of Astragalus polysaccharides in treating neurodegenerative diseases

Shi,

2024

Front. Pharmacol.

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Astragalus membranaceus widely used in traditional Chinese medicine, exhibits multiple pharmacological effects, including immune stimulation, antioxidation, hepatoprotection, diuresis, antidiabetes, anticancer, and expectorant properties. Its main bioactive compounds include flavonoids, triterpene saponins, and polysaccharides. Astragalus polysaccharides (APS), one of its primary bioactive components, have been shown to possess a variety of pharmacological activities, such as antioxidant, immunomodulatory, anti-inflammatory, antitumor, antidiabetic, antiviral, hepatoprotective, anti-atherosclerotic, hematopoietic, and neuroprotective effects. This review provides a comprehensive summary of the molecular mechanisms and therapeutic effects of APS in treating neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). It discusses how APS improve insulin resistance, reduce blood glucose levels, enhance cognitive function, and reduce Aβ accumulation and neuronal apoptosis by modulating various pathways such as Nrf2, JAK/STAT, Toll, and IMD. For PD, APS protect neurons and stabilize mitochondrial function by inhibiting ROS production and promoting autophagy through the PI3K/AKT/mTOR pathway. APS also reduce oxidative stress and neurotoxicity induced by 6-hydroxydopamine, showcasing their neuroprotective effects. In MS, APS alleviate symptoms by suppressing T cell proliferation and reducing pro-inflammatory cytokine expression via the PD-1/PD-Ls pathway. APS promote myelin regeneration by activating the Sonic hedgehog signaling pathway and fostering the differentiation of neural stem cells into oligodendrocytes. This article emphasizes the significant antioxidant, anti-inflammatory, immunomodulatory, and neuroprotective pharmacological activities of APS, highlighting their potential as promising candidates for the treatment of neurodegenerative diseases.

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Role of connexins in neurodegenerative diseases (Review)

Cited by 2 publications

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CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

Pharmacological effects of Astragalus polysaccharides in treating neurodegenerative diseases

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Role of connexins in neurodegenerative diseases (Review)

Cited by 2 publications

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CREB1K292 and HINFPK330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

CREB1K292 and HINFPK330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

Pharmacological effects of Astragalus polysaccharides in treating neurodegenerative diseases

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Product

Resources

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CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease

CREB1^K292 and HINFP^K330 as Putative Common Therapeutic Targets in Alzheimer’s and Parkinson’s Disease