tetano
Editor, Senior Moderator
ACS Appl Mater Interfaces
. 2023 Aug 16.
doi: 10.1021/acsami.3c09815. Online ahead of print. Spike Protein Fragments Promote Alzheimer's Amyloidogenesis
Sujian Cao[SUP] 1 [/SUP], Zhiyuan Song[SUP] 2 [/SUP], Jinyu Rong[SUP] 3 [/SUP], Nicholas Andrikopoulos[SUP] 1 4 [/SUP], Xiufang Liang[SUP] 1 5 [/SUP], Yue Wang[SUP] 1 5 [/SUP], Guotao Peng[SUP] 3 [/SUP], Feng Ding[SUP] 2 [/SUP], Pu Chun Ke[SUP] 1 4 [/SUP]
Affiliations
Alzheimer's disease (AD) is a major cause of dementia inducing memory loss, cognitive decline, and mortality among the aging population. While the amyloid aggregation of peptide Aβ has long been implicated in neurodegeneration in AD, primarily through the production of toxic polymorphic aggregates and reactive oxygen species, viral infection has a less explicit role in the etiology of the brain disease. On the other hand, while the COVID-19 pandemic is known to harm human organs and function, its adverse effects on AD pathobiology and other human conditions remain unclear. Here we first identified the amyloidogenic potential of [SUP]1058[/SUP]HGVVFLHVTYV[SUP]1068[/SUP], a short fragment of the spike protein of SARS-CoV-2 coronavirus. The peptide fragment was found to be toxic and displayed a high binding propensity for the amyloidogenic segments of Aβ, thereby promoting the aggregation and toxicity of the peptide in vitro and in silico, while retarding the hatching and survival of zebrafish embryos upon exposure. Our study implicated SARS-CoV-2 viral infection as a potential contributor to AD pathogenesis, a little explored area in our quest for understanding and overcoming Long Covid.
Keywords: Alzheimer’s disease; SARS-CoV-2; amyloid β; spike protein; virus.
. 2023 Aug 16.
doi: 10.1021/acsami.3c09815. Online ahead of print. Spike Protein Fragments Promote Alzheimer's Amyloidogenesis
Sujian Cao[SUP] 1 [/SUP], Zhiyuan Song[SUP] 2 [/SUP], Jinyu Rong[SUP] 3 [/SUP], Nicholas Andrikopoulos[SUP] 1 4 [/SUP], Xiufang Liang[SUP] 1 5 [/SUP], Yue Wang[SUP] 1 5 [/SUP], Guotao Peng[SUP] 3 [/SUP], Feng Ding[SUP] 2 [/SUP], Pu Chun Ke[SUP] 1 4 [/SUP]
Affiliations
- PMID: 37585091
- DOI: 10.1021/acsami.3c09815
Alzheimer's disease (AD) is a major cause of dementia inducing memory loss, cognitive decline, and mortality among the aging population. While the amyloid aggregation of peptide Aβ has long been implicated in neurodegeneration in AD, primarily through the production of toxic polymorphic aggregates and reactive oxygen species, viral infection has a less explicit role in the etiology of the brain disease. On the other hand, while the COVID-19 pandemic is known to harm human organs and function, its adverse effects on AD pathobiology and other human conditions remain unclear. Here we first identified the amyloidogenic potential of [SUP]1058[/SUP]HGVVFLHVTYV[SUP]1068[/SUP], a short fragment of the spike protein of SARS-CoV-2 coronavirus. The peptide fragment was found to be toxic and displayed a high binding propensity for the amyloidogenic segments of Aβ, thereby promoting the aggregation and toxicity of the peptide in vitro and in silico, while retarding the hatching and survival of zebrafish embryos upon exposure. Our study implicated SARS-CoV-2 viral infection as a potential contributor to AD pathogenesis, a little explored area in our quest for understanding and overcoming Long Covid.
Keywords: Alzheimer’s disease; SARS-CoV-2; amyloid β; spike protein; virus.