Neuroinflammation as a Link Between Atherosclerosis and Neurodegenerative Conditions
Neuroinflammation, chronic and unresolved inflammation of brain tissue, is important in the progression of neurodegenerative diseases. It disrupts the normal maintenance and function of cells and tissue. As researchers note here, it is well know that the progression of atherosclerosis correlates with the progression of neurodegenerative disease. Atherosclerosis is the formation of fatty lesions that narrow and weaken blood vessels. It is an inflammatory condition, and atherosclerotic lesions are localized sites of inflammatory signaling and immune cell dysfunction. So it may well be that, in addition to more structural concerns around blood flow and rupture of vessels in the brain, that inflammatory signaling originating in blood vessel walls to some degree links these two conditions.
Neuroinflammation comprises inflammation-like processes inside the parenchyma of the central nervous system (CNS). Neuroinflammation is currently considered as a driving force in progression and likely etiology of numerous neurological diseases, including neurodegenerative ones. Atherosclerosis is a chronic disease characterized by progressive development of lipid-rich fibrotic deposits (atheroma plaques) inside the intima of large- and medium-sized arteries. Increasing evidence points to the chronic inflammation, occurring either locally or at the systemic level, as a key factor in progression of atherosclerotic lesions and related acute cardiovascular events.
Given the growing evidence pointing to the impact of systemic inflammation as a trigger of neuroinflammation, and the fact that neuroinflammation is recognized as being associated with neurodegenerative diseases such as Alzheimer's disease, it is important to assess neuroinflammation in the specific context of atherosclerosis in future studies. Indeed, the mechanistic link between atherosclerosis and neuroinflammation has barely been addressed so far, except in one experimental study on the animal model of atherosclerosis: the ApoE-knockout (ApoE-/-) adult mouse fed for 2 months with a hyperlipidic diet. In the brain of this atherosclerosis mouse model, reactive microglial cells and CD45+ infiltrated leukocytes significantly outnumbered microglia and leukocytes seen in age-matched, wild-type mice.
In this light, the mechanisms behind the atherosclerosis-related neuroinflammation still remain poorly understood, since the phenotypes of effector cells and the transcriptomic variations of inflammatory mediators have not been addressed so far.