title: Age-related hypoxia in CNS pathology.
abstract: Although neuropathological conditions differ in the etiology of the inflammatory response, cellular and molecular mechanisms of neuroinflammation are probably similar in aging, hypertension, depression and cognitive impairment. Moreover, a number of common risk factors such as obesity, hypertension, diabetes and atherosclerosis are increasingly understood to act as "silent contributors" to neuroinflammation and can underlie the development of disorders such as cerebral small vessel disease (cSVD) and subsequent dementia. On the other hand, acute neuroinflammation, such as in response to traumatic or cerebral ischemia, aggravates the acute damage and can lead to a number of pathological such as depression, post-stroke dementia and potentially neurodegeneration. All of those sequelae impair recovery and most of them provide the ground for further cerebrovascular events and a vicious cycle develops. Therefore, understanding the mechanisms associated with vascular dementia, stroke and related complications is of paramount importance in improving current preventive and therapeutic interventions. Likewise, understanding of molecular factors and pathways associated with neuroinflammation will eventually enable the discovery and implementation of new diagnostic and therapeutic strategies indicated in a wide range of neurological conditions.
authors.affiliation: Department of Psychiatry, University of Medicine Rostock, Germany; aurel.popa-wagner@med.uni-rostock.de.
authors.forename: George Mihai
authors.initials: GM
authors.lastname: Bădescu
authors.forename: Mădălina
authors.initials: M
authors.lastname: Fîlfan
authors.forename: Ovidiu
authors.initials: O
authors.lastname: Ciobanu
authors.forename: DănuŢ Adrian
authors.initials: DA
authors.lastname: Dumbravă
authors.forename: Aurel
authors.initials: A
authors.lastname: Popa-Wagner
mesh_terms: D000375:Aging / Q000473:pathology*; D002490:Central Nervous System / Q000473:pathology*; D006801:Humans; D000860:Hypoxia / Q000473:pathology*; D007249:Inflammation / Q000473:pathology; D008954:Models, Biological; D010477:Perfusion