Exploring the Role of CLU in the Pathogenesis of Alzheimer’s Disease
Authors: Md Sahab Uddin
Mst Marium Begum
Ghulam Md Ashraf
Md Tanvir Kabir
Tapan Behl
Md Siddiqul Islam
Journal: Neurotoxicity Research (2021)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: APOJ; Alzheimer’s disease; Amyloid beta; Clusterin; Neuroinflammation
Affiliations: Department of Pharmacy, Southeast University, Dhaka, Bangladesh. ., Pharmakon Neuroscience Research Network, Dhaka, Bangladesh. ., Department of Pharmacy, Brac University, Dhaka, Bangladesh., Department of Pharmacy, East West University, Dhaka, Bangladesh., Department of Pharmacy, Southeast University, Dhaka, Bangladesh., Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, India., King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia., Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.

Abstract:  Alzheimer's disease (AD) is a chronic and devastating neurodegenerative disorder that is affecting elderly people at an increasing rate. Clusterin (CLU), an extracellular chaperone, is an ubiquitously expressed protein that can be identified in various body fluids and tissues. Expression of CLU can lead to various processes including suppression of complement system, lipid transport, chaperone function, and also controlling neuronal cell death and cell survival mechanisms. Studies have confirmed that the level of CLU expression is increased in AD. Furthermore, CLU also decreased the toxicity and aggregation of amyloid beta (Aβ). However when the Aβ level was far greater than CLU, then the amyloid generation was increased. CLU was also found to incorporate in the amyloid aggregates, which were more harmful as compared with the Aβ42 aggregates alone. Growing evidence indicates that CLU plays roles in AD pathogenesis via various processes, including aggregation and clearance of Aβ, neuroinflammation, lipid metabolism, Wnt signaling, copper homeostasis, and regulation of neuronal cell cycle and apoptosis. In this article, we represent the critical interaction of CLU and AD based on recent advances. Furthermore, we have also focused on the Aβ-dependent and Aβ-independent mechanisms by which CLU plays a role in AD pathogenesis. 

Retracted: No

PubPeer comments:
 Plagiarism of paper previously published in Frontiers of Neuroscience: https: doi.org 10.3389 fnins.2019.00164. Following the use of plagiarism software by Springer, a retraction wording was granted by EiC but a year later no retraction notice on the article. A closer look at the first author reveals a large number of papers across multiple fields disciplines and evidence of plagiarism of other articles. , 
 Retracted [19 May 2022](10.1007 s12640-022-00519-1). ------ The Editors have retracted this article because a significant part of the content was paraphrased from another article by different authors (Foster et al. 2019). All authors agree with this retraction. ----- Dr. Evangeline Foster, first author of the paraphrased article commented on Twitter: https: twitter.com evangeline_mf status 1527592780494786563 , 
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