Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
Full metadata record
|dc.identifier.citation||Human Molecular Genetics, 2018; 27(R2):108-118||en|
|dc.description.abstract||The notion that one common pathogenic pathway could account for the various clinically distinguishable, typically late-onset neurodegenerative diseases might appear unlikely given the plethora of diverse primary causes of neurodegeneration. On the contrary, an autoinflammatory pathogenic mechanism allows diverse genetic and environmental factors to converge into a common chain of causality. Inflammation has long been known to correlate with neurodegeneration. Until recently this relationship was seen as one of consequence rather than cause - with inflammatory cells and events acting to "clean up the mess" after neurological injury. This explanation is demonstrably inadequate and it is now clear that inflammation is at the very least, rate-limiting for neurodegeneration (and more likely, a principal underlying cause in most if not all neurodegenerative diseases), protective in its initial acute phase, but pernicious in its latter chronic phase.||en|
|dc.description.statementofresponsibility||Robert I. Richards, Sarah A. Robertson and Daniel L. Kastner||en|
|dc.publisher||Oxford University Press||en|
|dc.rights||© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For permissions, please email: email@example.com||en|
|dc.subject||Humans; Neurodegenerative Diseases; Autoimmune Diseases; Inflammation||en|
|dc.title||Neurodegenerative diseases have genetic hallmarks of autoinflammatory disease||en|
|pubs.library.collection||Medical Sciences publications||en|
|dc.identifier.orcid||Robertson, S. [0000-0002-9967-0084]||en|
|Appears in Collections:||Medical Sciences publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.