Mechanism of protein phosphatase-2Aregulating phosphorylation of amyloid precursor proteosome and Aβ generation

Zhang, J W; Jing, Liang; Ge, Jian; Dong, Guofa

doi:10.4149/bll_2015_037

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…3). Decreased activity and expression of PP2A-C subunit in AD were not only reported to be involved in tau hyperphosphorylation, but also suggested to be responsible for the activation of c-jun N-terminal kinase (JNK), which could lead to Aβ overproduction [255,256]. Accordingly, two endogenous inhibitors of PP2A, I1(PP2A) and I2(PP2A), were upregulated in the neocortex by in situ hybridization in AD brains, and were suggested to be involved in the hyperphosphorylation of tau in AD [257].…”

Section: Pp2amentioning

confidence: 99%

Molecular crosstalk between cancer and neurodegenerative diseases

Seo

Park

2019

Cell. Mol. Life Sci.

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The progression of cancers and neurodegenerative disorders is largely defined by a set of molecular determinants that are either complementarily deregulated, or share remarkably overlapping functional pathways. A large number of such molecules have been demonstrated to be involved in the progression of both diseases. In this review, we particularly discuss our current knowledge on p53, cyclin D, cyclin E, cyclin F, Pin1 and protein phosphatase 2A, and their implications in the shared or distinct pathways that lead to cancers or neurodegenerative diseases. In addition, we focus on the interdependent regulation of brain cancers and neurodegeneration, mediated by intercellular communication between tumor and neuronal cells in the brain through the extracellular microenvironment. Finally, we shed light on the therapeutic perspectives for the treatment of both cancer and neurodegenerative disorders. Keywords Age-related diseases • Cell death • Cell survival • Redox system • Glioma • Neurotoxicity Abbreviations Aβ Amyloid-β AD Alzheimer's disease ALS Amyotrophic lateral sclerosis AMPA α-Amino-3-hydroxy-5-methyl-4isoxazolepropionate APC/C Anaphase promoting complex/ cyclosome APP Amyloid precursor protein ATRA All-trans retinoic acid APL Acute promyelocytic leukemia Bax Bcl-2 associated X BH3 Bcl-2 homology 3 Bim Bcl-2-interacting mediator of cell death BimEL Bim-extra long CDK Cyclin-dependent kinase Cellular and Molecular Life Sciences

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Section: Pp2amentioning

confidence: 99%

Molecular crosstalk between cancer and neurodegenerative diseases

Seo

Park

2019

Cell. Mol. Life Sci.

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“…Aβ peptides are proteolytic fragments of the transmembrane APP and work with down‐stream protein tau to drive neurons into diseased state (Bloom, ). It is ascertained that protein phosphatase 2A (PP‐2A) is capable of regulating the Aβ level by regulating APP phosphorylation level and β and γ‐secretase activity (J. W. Zhang, Jing, Jian, & Dong, ). BBR may be a promising multitarget drug to prevent and protect against AD by regulating AD‐associated products such as PP‐2A, APP, amyloid‐β, and tau.…”

Section: Other Neuroprotective Pathwaysmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

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Berberine, an isoquinoline alkaloid, is demonstrated to have a variety of pharmacologic effects. Widely used as nonprescription drug for diarrhea, berberine has also broadened its applications in therapies of cardiovascular diseases, diabetes mellitus, tumor, and so forth. However, researches about berberine's protective effects on nervous system are still so insufficient that clinical uses cannot popularize and underlying molecules mechanisms are confused and incomplete. Well-known pathways such as Pl3K/Akt/Bcl-2 pathway, Nrf2/HO-1 pathway, and MAPK signaling pathway help berberine to protect neurons through antiapoptotic, antioxidative, and anti-inflammatory activities. New hypotheses have been raised consistently to explore more possible ways of berberine preventing nerves from injuries as attention on its neuroprotective properties is increasing. Therefore, this review is trying to analyze these mechanisms, which actually play roles in neuronal disease models such as brain ischemia, Alzheimer's disease, and experimental autoimmune encephalomyelitis. Much more understanding about how berberine mediates these pathways provides novel insights into the clinical treatment of neurological disorders.

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“…The observed enhancement in spatial cognitive function due to berberine may primarily result from attenuated hippocampal Aβ. Protein phosphatase 2A (PP-2A) modulates Aβ levels by regulating APP phosphorylation and β- and γ-secretase activities ( Zhang et al, 2015 ). It suggesting that berberine may be a good multi-targeted drug that can modulate AD related substances tau, PP-2A, Aβ, APP, or BACE-2.…”

Section: Discussionmentioning

confidence: 99%

Effect of berberine on cognitive function and β-amyloid precursor protein in Alzheimer’s disease models: a systematic review and meta-analysis

Liu,

Dai,

et al. 2024

Front. Pharmacol.

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Introduction: Berberine is an isoquinoline alkaloid extracted from Berberis vulgaris, which possesses a variety of pharmacological activities. Alzheimer’s disease (AD) is a complex disease with multiple pathologic factors, with cognitive decline being the main manifestation of AD. The neuroprotective effects of berberine in animal models of Alzheimer’s disease (AD) have been widely reported, exhibiting protective effects against risk factors associated with AD. In this study, we summarize and evaluate the effects of berberine on cognitive function and β-amyloid precursor protein in animal models of AD.Material and methods: Eligible studies were retrieved from PubMed, MEDLINE, EMBASE, Web of Science, and Cochrane Library databases up to 1 June 2023. Risk of bias was assessed by the Systematic Review Center for Laboratory Animal Experiments (SYRCLE). Statistical analyses were performed using STATA 14.0 and Review Manger 5.4 software to calculate weighted standardized mean difference (SMD) and 95% confidence intervals (CI), Morris water maze (MWM) test and β-amyloid precursor protein as outcome measures. Heterogeneity was tested using the I2 test. Sensitivity analysis and publication bias were also assessed.Results: 19 studies involving 360 animals met the inclusion criteria, and the results of the meta-analysis showed that berberine decreased escape latency (SMD = −2.19, 95% CI: (−2.50, −1.88), p < 0.00001), increased the number of platform crossings (SMD = 4.27, 95% CI (3.38, 5.17), p < 0.00001), time in the target quadrant (SMD = 5.92, 95% CI (4.43, 7.41), p < 0.00001) and APP expression (SMD = 0.73, 95% CI: (0.25, 1.21), p = 0.003).Conclusion: Berberine can regulate APP expression and improve cognitive function in animal models of AD, and the mechanism may be related to the involvement of berberine in APP processing and influence the expression of its related factors.Systematic review registration: PROSPERO, CRD42023437445

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Mechanism of protein phosphatase-2Aregulating phosphorylation of amyloid precursor proteosome and Aβ generation

Cited by 5 publications

References 24 publications

Molecular crosstalk between cancer and neurodegenerative diseases

Molecular crosstalk between cancer and neurodegenerative diseases

Berberine: Pathways to protect neurons

Effect of berberine on cognitive function and β-amyloid precursor protein in Alzheimer’s disease models: a systematic review and meta-analysis

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