A role for spinal cord hypoxia in neurodegeneration
The vascular system of the spinal cord is particularly complex and vulnerable. Damage to the main vessels or alterations to the regulation of blood flow will result in a reduction or temporary cessation of blood supply. The resulting tissue hypoxia may be brief: acute, or long lasting: chronic. Dama...
Saved in:
Published in | Cell death & disease Vol. 10; no. 11; pp. 861 - 8 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
13.11.2019
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | The vascular system of the spinal cord is particularly complex and vulnerable. Damage to the main vessels or alterations to the regulation of blood flow will result in a reduction or temporary cessation of blood supply. The resulting tissue hypoxia may be brief: acute, or long lasting: chronic. Damage to the vascular system of the spinal cord will develop after a traumatic event or as a result of pathology. Traumatic events such as road traffic accidents, serious falls and surgical procedures, including aortic cross-clamping, will lead to an immediate cessation of perfusion, the result of which may not be evident for several days, but may have long-term consequences including neurodegeneration. Pathological events such as arterial sclerosis, venous occlusion and spinal cord compression will result in a progressive reduction of blood flow, leading to chronic hypoxia. While in some situations the initial pathology is exclusively vascular, recent research in neurodegenerative disease has drawn attention to concomitant vascular anomalies in disorders, including amyotrophic lateral sclerosis, spinal muscular atrophy and muscular sclerosis. Understanding the role of, and tissue response to, chronic hypoxia is particularly important in these cases, where inherent neural damage exacerbates the vulnerability of the nervous system to stressors including hypoxia. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 2041-4889 2041-4889 |
DOI: | 10.1038/s41419-019-2104-1 |