Fig. 1: The deep interactions between aging, inflammaging, and age-related CSVD.
From: Age-related cerebral small vessel disease and inflammaging
As aging, several cellular and molecular mechanisms lead to chronic inappropriate activation of the immune system. This complex interaction between genetic susceptibility and risk stimuli (both exogenous and endogenous) contributes to the continuous activation of a limited range of confounding sensors which triggers inflammaging (upper part of the box). The resulting synthesis and release of different inflammatory mediators are related to the common pathophysiological mechanisms of age-related diseases. For age-related CSVD, regional analyses showed that blood markers of vascular inflammation were associated with deep perforating arteriopathy (DPA), while blood markers of systemic inflammation were associated with cerebral amyloid angiopathy (CAA), both of which were closely related to the critical pathophysiological mechanisms of blood-brain barrier leakage and endothelial dysfunction (lower part of the box).
