Asset Details
Do you wish to reserve the book?
Anti‐interleukin‐17A and anti‐interleukin‐23 antibodies may be effective against Alzheimer's disease: Role of neutrophils in the pathogenesis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Anti‐interleukin‐17A and anti‐interleukin‐23 antibodies may be effective against Alzheimer's disease: Role of neutrophils in the pathogenesis
Do you wish to request the book?
Anti‐interleukin‐17A and anti‐interleukin‐23 antibodies may be effective against Alzheimer's disease: Role of neutrophils in the pathogenesis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Anti‐interleukin‐17A and anti‐interleukin‐23 antibodies may be effective against Alzheimer's disease: Role of neutrophils in the pathogenesis
2020
Overview
Introduction Despite the remarkable progress achieved in the research on Alzheimer's disease (AD), its exact pathogenesis is not fully understood and effective therapies do not currently exist. In order to find effective therapy for AD, I ranged extensively over the literature and found an important paper by Tiffany and colleagues. Results and Conclusion Neuroinflammation has been proposed as a possible cause or driving force of AD. The discovery by Tiffany et al. that amyloid β (Aβ) is a formylpeptide receptor 2 agonist indicated that Aβ is a potent chemoattractant for phagocytic leukocytes. Therefore, in all likelihood Aβ attracts peripheral blood neutrophils, monocytes, as well as microglia cells in brain parenchyma, and activates them. However, the role of microglia cells and their precursor monocytes in AD pathogenesis remains elusive. Recently, neutrophils were found to be present in areas with Aβ deposits in AD brain and in transgenic AD model mice. Because brain is vulnerable to the effects of reactive oxygen species (ROS) and neutrophils secrete a large amount of ROS, neutrophils look like a driving force of AD. Therefore, a possibility arises that anti‐IL‐17A and anti‐IL‐23 antibodies are effective against AD, because these antibodies can be thought to interfere with neutrophil trafficking from the bone marrow to the blood circulation and thus inhibit neutrophil infiltration into AD brain. Clinical studies using anti‐IL‐17A and anti‐IL‐23 antibodies in patients with AD are required. IL‐17A mediates neutrophil migration from the bone marrow. Anti‐IL‐17A antibody inhibits it.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc,Wiley
