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Siva Sundara Kumar Durairajan

Researcher at Central University of Tamil Nadu

Publications -  58
Citations -  1976

Siva Sundara Kumar Durairajan is an academic researcher from Central University of Tamil Nadu. The author has contributed to research in topics: Autophagy & Amyloid precursor protein. The author has an hindex of 19, co-authored 53 publications receiving 1545 citations. Previous affiliations of Siva Sundara Kumar Durairajan include Hong Kong Baptist University & Central University, India.

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Baicalein Inhibits Formation of α-Synuclein Oligomers within Living Cells and Prevents Aβ Peptide Fibrillation and Oligomerisation

TL;DR: Zhang et al. as discussed by the authors showed that Baicalein, a flavonoid extracted from the Chinese herbal medicine Scutellaria baicalensis Georgi ("huang qin" in Chinese), is a potent inhibitor of α-syn oligomerization both in cell-free and cellular systems.
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Isorhynchophylline, a natural alkaloid, promotes the degradation of alpha-synuclein in neuronal cells via inducing autophagy.

TL;DR: Data from this study raise the possibility that oxindole alkaloid derivatives may serve as a means to stimulate autophagy in neuronal cells, thereby exerting preventive and therapeutic values against neurodegenerative diseases such as Parkinson disease by reducing pathogenic protein aggregates in neurons.
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Salvianolic acid B inhibits Aβ fibril formation and disaggregates preformed fibrils and protects against Aβ-induced cytotoxicty

TL;DR: Sal B is a better aggregation inhibitor than ferulic acid but less active than curcumin in the inhibition of Aβ1–40 aggregation, and has therapeutic potential in the treatment of AD, and warrants its study in animal models.
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A novel curcumin analog binds to and activates TFEB in vitro and in vivo independent of MTOR inhibition

TL;DR: Curcumin derivative C1 is identified as a novel MTOR-independent activator of TFEB, which enhances autophagy and lysosome biogenesis in vitro and in vivo and is a potential therapeutic agent for the treatment of neurodegenerative diseases.