Leucine-Rich Repeat Kinase 2 (LRRK2) için kapak resmi
Leucine-Rich Repeat Kinase 2 (LRRK2)
Başlık:
Leucine-Rich Repeat Kinase 2 (LRRK2)
ISBN:
9783319499697
Edition:
1st ed. 2017.
Yayın Bilgileri:
Cham : Springer International Publishing : Imprint: Springer, 2017.
Fiziksel Tanımlama:
XVII, 271 p. 27 illus., 17 illus. in color. online resource.
Series:
Advances in Neurobiology, 14
Contents:
Part I: Clinical and Genetic Considerations of LRRK2 Associated Parkinson's Disease -- Leucine-rich repeat kinase (LRRK2) genetics and Parkinson's disease -- Clinical features of LRRK2 carriers with Parkinson's disease -- Part II: Fundamentals of LRRK2 Biology -- LRRK2 phosphorylation -- Understanding the GTPase activity of LRRK2: regulation, function and neurotoxicity -- LRRK2 and autophagy -- Molecular insights and functional implication of LRRK2 dimerization -- LRRK2 and the immune system -- Regulation of LRRK2 by phosphatases -- Part III: LRRK2 Neurodegeneration, Modeling, and Therapeutic Options -- Animal models of LRRK2-associated Parkinson's disease -- LRRK2 and the "LRRKtosome" at the crossroads of programmed cell death: Clues from RIP kinase relatives -- Interaction of LRRK2 and α-synuclein in Parkinson's disease -- Mechanisms of mutant LRRK2 neurodegeneration -- Small molecule inhibitors of LRRK2.
Abstract:
This is the first book to assemble the leading researchers in the field of LRRK2 biology and neurology and provide a snapshot of the current state of knowledge, encompassing all major aspects of its function and dysfunction. The contributors are experts in cell biology and physiology, neurobiology, and medicinal chemistry, bringing a multidisciplinary perspective on the gene and its role in disease. The book covers the identification of LRRK2 as a major contributor to the pathogenesis of Parkinson's Disease. It also discusses the current state of the field after a decade of research, putative normal physiological roles of LRRK2, and the various pathways that have been identified in the search for the mechanism(s) of its induction of neurodegeneration.
Added Author:
Dil:
English