Reduction of phosphorylated α-synuclein through downregulation of casein kinase 2α alleviates dopaminergic-neuronal function

Potdar, Chandrakanta; Kaushal, Alka; Raj, Aditya; Mallick, Rathijit

doi:10.1016/j.bbrc.2022.05.023

Cited by 3 publications

(1 citation statement)

References 34 publications

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“…Several cellular studies have demonstrated the capacity for overexpressed or mutated α-syn to cause neuronal dysfunction as seen in PD, as follows: disruption of the ubiquitin-dependent proteolytic system in PC12 cells (an immortalized cell line of rat pheochromocytoma often used in neuroscience research [ 61 ]) with the A53T mutation [ 62 ], disruption in calcium signaling in SH-SY5Y cells with the A53T mutation [ 29 ], impaired dopamine (DA) release in stable PC12 cells expressing non-toxic amounts of A30P mutant or WT α-syn [ 63 ] as well as vesicular DA storage impairments in a human mesencephalic cell line (MESC2.10) expressing A53T mutant α-syn [ 64 ]. In addition to these immortalized cell models, murine primary neurons have also been broadly used to study the effects of α-syn overexpression.…”

Section: Modeling Alpha-synuclein Aggregation In Non-hipsc Lines: Wha...mentioning

confidence: 99%

Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study

et al. 2022

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Alpha-synuclein’s role in diseases termed “synucleinopathies”, including Parkinson’s disease, has been well-documented. However, after over 25 years of research, we still do not fully understand the alpha-synuclein protein and its role in disease. In vitro cellular models are some of the most powerful tools that researchers have at their disposal to understand protein function. Advantages include good control over experimental conditions, the possibility for high throughput, and fewer ethical issues when compared to animal models or the attainment of human samples. On the flip side, their major disadvantages are their questionable relevance and lack of a “whole-brain” environment when it comes to modeling human diseases, such as is the case of neurodegenerative disorders. Although now, with the advent of pluripotent stem cells and the ability to create minibrains in a dish, this is changing. With this review, we aim to wade through the recent alpha-synuclein literature to discuss how different cell culture setups (immortalized cell lines, primary neurons, human induced pluripotent stem cells (hiPSCs), blood–brain barrier models, and brain organoids) can help us understand aggregation pathology in Parkinson’s and other synucleinopathies.

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Section: Modeling Alpha-synuclein Aggregation In Non-hipsc Lines: Wha...mentioning

confidence: 99%

Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study

et al. 2022

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Impaired Sonic Hedgehog Responsiveness of Induced Pluripotent Stem Cell-Derived Floor Plate Cells Carrying the LRRK2-I1371V Mutation Contributes to the Ontogenic Origin of Lower Dopaminergic Neuron Yield

Potdar,

Jagtap,

Singh

et al. 2024

Stem Cells and Development

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Neuroprotective compounds from marine invertebrates

Rivai

Umar

2023

Beni-Suef Univ J Basic Appl Sci

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Background Neuroinflammation is a key pathological feature of a wide variety of neurological disorders, including Parkinson’s, multiple sclerosis, Alzheimer’s, and Huntington’s disease. While current treatments for these disorders are primarily symptomatic, there is a growing interest in developing new therapeutics that target the underlying neuroinflammatory processes. Main body Marine invertebrates, such as coral, sea urchins, starfish, sponges, and sea cucumbers, have been found to contain a wide variety of biologically active compounds that have demonstrated potential therapeutic properties. These compounds are known to target various key proteins and pathways in neuroinflammation, including 6-hydroxydopamine (OHDH), caspase-3 and caspase-9, p-Akt, p-ERK, p-P38, acetylcholinesterase (AChE), amyloid-β (Aβ), HSF-1, α-synuclein, cellular prion protein, advanced glycation end products (AGEs), paraquat (PQ), and mitochondria DJ-1. Short conclusion This review focuses on the current state of research on the neuroprotective effects of compounds found in marine invertebrates and the potential therapeutic implications of these findings for treating neuroinflammatory disorders. We also discussed the challenges and limitations of using marine-based compounds as therapeutics, such as sourcing and sustainability concerns, and the need for more preclinical and clinical studies to establish their efficacy and safety. Graphical abstract

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Reduction of phosphorylated α-synuclein through downregulation of casein kinase 2α alleviates dopaminergic-neuronal function

Cited by 3 publications

References 34 publications

Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study

Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study

Impaired Sonic Hedgehog Responsiveness of Induced Pluripotent Stem Cell-Derived Floor Plate Cells Carrying the LRRK2-I1371V Mutation Contributes to the Ontogenic Origin of Lower Dopaminergic Neuron Yield

Neuroprotective compounds from marine invertebrates

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