Both cerebral big artery disease and cerebral small vessel disease have been linked to cognitive decline and deterioration in brain health. Diseases of the big arteries and the tiny brain vessels have the same anatomical basis but are associated with distinct pathogenetic pathways. Previous research suggested a possible difference in the risk factor profile for these two forms of cerebrovascular illness.
Levels of lipoprotein in relation to cardiovascular disease
Apolipoprotein B100 and glycoapolipoprotein A(PO) are components of lipoprotein(a), often known as Lp(a) (a). Prolonged exposure to Lp(a) has been associated with an increased risk of atherosclerotic cardiovascular disease. In previous research, carotid atherosclerosis, ischemic stroke, and atherothrombotic stroke have all been linked to elevated Lp(a) levels. In contrast, Lp(a) level was associated with cerebral minor vascular disorders in just a few studies (cSVD). Some earlier investigations indicated a reduced Lp(a) level in patients with cSVD, but the findings were unclear because of the small sample sizes. Recent Mendelian randomization research has shown that lower Lp(a) levels are associated with an increased risk of minor vascular stroke. This suggests that Lp(a) concentrations may have various associations with disorders of the brain's significant and small blood vessels. However, the connections between Lp(a) and disorders of the big and small blood vessels in the brain remain poorly understood.
Results
Differential correlations of Lp(a) level with both major artery and small vessel disease in the brain were found by Pan et al., (2022) in this community-based sample. A high Lp(a) level was shown to be connected with the prevalence and severity of atherosclerosis in the brain, but to have the opposite effect on the risk of developing cSVD. These findings imply that high levels of Lp(a) may be harmful to cerebral big arteries but protective to cerebral small vessels. More research is necessary to understand the clinical significance and underlying mechanisms of the opposing effects of Lp(a) level on cerebral arteries.
This research has been posted in the BMJ journal for Stroke and Vascular Neurology