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Palsamy Periyasamy

Researcher at University of Nebraska Medical Center

Publications -  47
Citations -  2500

Palsamy Periyasamy is an academic researcher from University of Nebraska Medical Center. The author has contributed to research in topics: Neuroinflammation & Autophagy. The author has an hindex of 18, co-authored 37 publications receiving 1145 citations.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Interplay of endoplasmic reticulum stress and autophagy in neurodegenerative disorders

TL;DR: This review highlights recent advances in the field on the role of ER stress and autophagy in AD, prion diseases, PD, ALS and HAND with the involvement of key signaling pathways in these processes and implications for future development of therapeutic strategies.
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HIV-1 Tat Primes and Activates Microglial NLRP3 Inflammasome-Mediated Neuroinflammation

TL;DR: A novel role of Tat is demonstrated in priming and activating NLR family pyrin domain containing 3 (NLRP3) inflammasomes in microglial cells and in HIV-Tg rats administered lipopolysaccharide, which suggests NLRP3 can be envisioned as a therapeutic target for ameliorating Tat-mediated neuroinflammation.
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Cocaine-mediated microglial activation involves the ER stress-autophagy axis

TL;DR: It is demonstrated that cocaine exposure induced autophagy in both BV-2 and primary rat microglial cells as demonstrated by a dose- and time-dependent induction of autophile-signature proteins such as BECN1/Beclin 1, ATG5, and MAP1LC3B.
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Age-Related Cataracts: Role of unfolded protein response, Ca2+ mobilization, epigenetic DNA modifications, and loss of Nrf2/Keap1 dependent cytoprotection

TL;DR: The overall view of ER stress, increases in Ca2+ levels, protein cleavage, and loss of the well‐established stress protection in somatic lens cells are summarized.