Calpain activity in plasma of patients with essential tremor and Parkinson’s disease: a pilot study

Muruzheva, Zamira M.; Traktirov, Dmitrii S.; Zubov, Alexander; Pestereva, Nina; Tikhomirova, Maria S.; Karpenko, Marina N.

doi:10.1080/01616412.2020.1854004

Cited by 6 publications

(5 citation statements)

References 28 publications

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“…Activation of Calpain 1 is considered to be a key pathogenic factor in neurodegenerative diseases such as AD [19,20]. It has been reported in the literature that when the steady state of calcium ions is disrupted, it leads to the activation of Calpain 1, which will lead to the occurrence of many diseases including neuroinflammation.…”

Section: Discussionmentioning

confidence: 99%

The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson’s Disease Model Mice

Han

Liu

Ren

et al. 2023

JPD

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Background: Endophilin A1 (EPA1) is encoded by the SH3GL2 gene, and SH3GL2 was designated as a Parkinson’s disease (PD) risk locus by genome-wide association analysis, suggesting that EPA1 may be involved in the occurrence and development of PD. Objective: To investigate the role of EPA1 in lipopolysaccharide (LPS)-induced PD model mice. Methods: The mice PD model was prepared by injecting LPS into the substantia nigra (SN), and the changes in the behavioral data of mice in each group were observed. The damage of dopaminergic neurons, activation of microglia, and reactive oxygen species (ROS) generation were detected by immunofluorescence method; calcium ion concentration was detected by calcium content detection kit; EPA1 and inflammation and its related indicators were detected by western blot method. EPA1 knockdown was performed by an adeno-associated virus vector containing EPA1-shRNA-eGFP infusion. Results: LPS-induced PD model mice developed behavioral dysfunction, SN dopaminergic nerve damage, significantly increased calcium ion, calpain 1, and ROS production, activated NLRP1 inflammasome and promoted pro-inflammatory cell release, and SN EPA1 knockdown improves behavioral disorders, alleviates dopaminergic neuron damage, reduces calcium, calpain 1, ROS generation, and blocks NLRP1 inflammasome-driven inflammatory responses. Conclusion: The expression of EPA1 in the SN of LPS-induced PD model mice was increased, and it played a role in promoting the occurrence and development of PD. EPA1 knockdown inhibited the NLRP1 inflammasome activation, decreased the release of inflammatory factors and ROS generation, and alleviated dopaminergic neuron damage. This indicated that EPA1 may participating in the occurrence and development of PD.

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Section: Discussionmentioning

confidence: 99%

The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson’s Disease Model Mice

Han

Liu

Ren

et al. 2023

JPD

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“…Overactivated calpain signalling triggers hyperactivation of Cdk5 by increasing binding of p35 to Cdk5 result in the formation of p25/Cdk5 complex which cause neurodegeneration 4 . A case–control study showed that plasma calpain activity is increased in PD patients 42 . Overactivated calpain signalling triggers hyperactivation of Cdk5 by increasing the binding of p35 to Cdk5 resulting in the formation of p25/Cdk5 complex and neurodegeneration 43 …”

Section: Role Of Cdk5 In Pdmentioning

confidence: 99%

“…4 A case-control study showed that plasma calpain activity is increased in PD patients. 42 Overactivated calpain signalling triggers hyperactivation of Cdk5 by increasing the binding of p35 to Cdk5 resulting in the formation of p25/Cdk5 complex and neurodegeneration. 43 Taken together, aberrant activation of p29/p25/calpain/ Cdk5 signalling pathway is intricate in the pathogenesis of PD.…”

Section: Role Of Cdk5 In Pdmentioning

confidence: 99%

Cyclin‐dependent kinase 5 (CDK5) inhibitors in Parkinson disease

Alrouji,

Al‐kuraishy,

Al‐Gareeb

et al. 2024

J Cellular Molecular Medi

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Cyclin‐dependent kinase 5 (Cdk5) is a protein expressed in postmitotic neurons in the central nervous system (CNS). Cdk5 is activated by p35 and p39 which are neuron regulatory subunits. Cdk5/p35 complex is activated by calpain protease to form Cdk5/p35 which has a neuroprotective effect by regulating the synaptic plasticity and memory functions. However, exaggerated Cdk5 is implicated in different types of neurodegenerative diseases including Parkinson disease (PD). Therefore, modulation of Cdk5 signalling may mitigate PD neuropathology. Therefore, the aim of the present review was to discuss the critical role of Cdk5 in the pathogenesis of PD, and how Cdk5 inhibitors are effectual in the management of PD. In conclusion, overactivated Cdk5 is involved the development of neurodegeneration, and Cdk5/calpain inhibitors such as statins, metformin, fenofibrates and rosiglitazone can attenuate the progression of PD neuropathology.

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“…Activation of Calpain 1 is considered to be a key pathogenic factor in neurodegenerative diseases such as et al 2019; Muruzheva et al 2021). It has been reported in the literature that when the steady state of calcium ions is disrupted, it leads to the activation of Calpain 1, which will lead to the occurrence of many diseases including neuroin ammation.…”

Section: Epa1 Knockdown Analysismentioning

confidence: 99%

The role and Mechanism of Endophilin A1 in LPS-induced Parkinson's disease model mice

Han

Liu

Oiu

et al. 2022

Preprint

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Background: Neuroinflammation and oxidative stress are closely related to the pathogenesis of Parkinson's disease (PD), and PD is pathologically characterized by progressive loss of dopaminergic neurons in the SN pars compacta and excessive accumulation of α-synuclein. Endophilin A1(EPA1) is a cytoplasmic protein that is widely expressed in presynaptic nerve terminals in the brain and regulates synaptic vesicle cycling. EPA1 is encoded by the SH3GL2 gene, and SH3GL2 was designated as a PD risk locus by genome-wide association analysis, suggesting that EPA1 may be involved in the occurrence and development of PD. However, the role of EPA1 in PD remains unclear.Methods: The mice PD model was prepared by injecting LPS into the SN, and the changes in the behavioral data of mice in each group were observed through grasping force and open-field behavioral experiments. The damage of DA neurons, activation of microglia, and reactive oxygen species (ROS) generation were detected by immunofluorescence method; calcium ion concentration was detected by calcium content detection kit; EPA1 and inflammation and its related indicators (NLRP1, ASC, Caspase-1, IL-1β, IL-18, IL-6, TNF-α) were detected by Western blot method. EPA1 knockdown was performed by an adeno-associated virus (AAV) vector containing EPA1-shRNA-eGFP infusion.Results: LPS-induced PD model mice developed behavioral dysfunction, SN dopaminergic nerve damage, significantly increased calcium ion, calpain 1, and ROS production, activated NLRP1 inflammasome and promoted pro-inflammatory cell release, and SN EPA1 knockdown improves behavioral disorders, alleviates dopaminergic neuron damage, reduces calcium, calpain 1, ROS generation, and blocks NLRP1 inflammasome-driven inflammatory responses.Conclusions: The expression of EPA1 in the SN of LPS-induced PD model mice was increased, and it played a role in promoting the occurrence and development of PD. EPA1 activates the NLRP1 inflammasome to promote the release of inflammatory factors by regulating calcium ion homeostasis and ROS generation, and induces DA neuron damage through an inflammatory mechanism, thereby participating in the occurrence and development of PD.

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Calpain activity in plasma of patients with essential tremor and Parkinson’s disease: a pilot study

Cited by 6 publications

References 28 publications

The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson’s Disease Model Mice

The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson’s Disease Model Mice

Cyclin‐dependent kinase 5 (CDK5) inhibitors in Parkinson disease

The role and Mechanism of Endophilin A1 in LPS-induced Parkinson's disease model mice

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