About this Research Topic
Cerebral Small Vessel Diseases (cSVD) is a group of age-related neurological diseases related to small blood vessels in the brain. Sporadic cSVD, which accounts for most of the cSVD, can be typically categorized into two forms: Arteriolosclerosis-related cSVD and sporadic Cerebral amyloid angiopathy (CAA). Pathogenic mechanisms of sporadic cSVD may include endothelia failure, smooth muscle damage, blood-brain-barrier (BBB) damage, Aβ-induced cellular toxicity, inflammatory reaction and oxidative stress.
Arteriolosclerosis-related cSVD, as a very common form of sporadic cSVD, have been referred as arteriolosclerosis, age-related or vascular risk factor related SVD, or degenerative microangiopathy. However, the association between arteriolosclerosis-related cSVD and vascular risk factors are incompletely understood because the arteriolosclerosis-related cSVD may also be associated with a range of other factors including genetic susceptibility, thrombo-inflammation, autonomic and hemodynamic disorders (both arterial and venous), migraine and chronic stress. Due to the complexity of the pathogenic mechanisms of sporadic cSVD, it lacks evidence in terms of whether the pharmacological and non-pharmacological approaches are effective for arteriolosclerosis-related cSVD.
Sporadic CAA is a degenerative disease characterized by progressive deposition and decreased elimination of amyloid-beta (Aβ) in the walls of leptomeningeal of small arteries, arterioles, and sometimes capillaries in the cerebral cortex and small arteries, arterioles, and venules in central nervous system. The pathogenic mechanism of Aβ deposition is still unclear. The CAA related vasculopathy may cause ischemic or hemorrhagic parenchymal brain injury and dementia. However, some of the ischemic brain lesions caused by CAA are not detectable by conventional MRI and hence their prevalence and significance in CAA have been underestimated. Due to the microbleeds caused by CAA, there is a challenge in making treatment decisions in ischemic stroke. Although CAA may benefit from anti-amyloid treatment, effective preventive and therapeutic options for CAA and its clinical outcomes (dementia and vasculopathy) still remain very limited.
In this Research Topic, we welcome Original Research Articles, Review Articles, Methods, Theory and Hypothesis, and Brief/Case Reports contributing to advance our understanding to the pathogenic mechanisms and therapeutic approaches for sporadic cSVD. We are particularly interested in papers describing the processes involved in arteriolosclerosis, vascular amyloidosis, cSVD-related dementia and vascular diseases and thus their important therapeutic implications. Papers providing critical theory and hypothesis is welcome. Innovative techniques, e.g. new neuroimaging methods are also of great interest to this topic.
Arteriolosclerosis-related cSVD, as a very common form of sporadic cSVD, have been referred as arteriolosclerosis, age-related or vascular risk factor related SVD, or degenerative microangiopathy. However, the association between arteriolosclerosis-related cSVD and vascular risk factors are incompletely understood because the arteriolosclerosis-related cSVD may also be associated with a range of other factors including genetic susceptibility, thrombo-inflammation, autonomic and hemodynamic disorders (both arterial and venous), migraine and chronic stress. Due to the complexity of the pathogenic mechanisms of sporadic cSVD, it lacks evidence in terms of whether the pharmacological and non-pharmacological approaches are effective for arteriolosclerosis-related cSVD.
Sporadic CAA is a degenerative disease characterized by progressive deposition and decreased elimination of amyloid-beta (Aβ) in the walls of leptomeningeal of small arteries, arterioles, and sometimes capillaries in the cerebral cortex and small arteries, arterioles, and venules in central nervous system. The pathogenic mechanism of Aβ deposition is still unclear. The CAA related vasculopathy may cause ischemic or hemorrhagic parenchymal brain injury and dementia. However, some of the ischemic brain lesions caused by CAA are not detectable by conventional MRI and hence their prevalence and significance in CAA have been underestimated. Due to the microbleeds caused by CAA, there is a challenge in making treatment decisions in ischemic stroke. Although CAA may benefit from anti-amyloid treatment, effective preventive and therapeutic options for CAA and its clinical outcomes (dementia and vasculopathy) still remain very limited.
In this Research Topic, we welcome Original Research Articles, Review Articles, Methods, Theory and Hypothesis, and Brief/Case Reports contributing to advance our understanding to the pathogenic mechanisms and therapeutic approaches for sporadic cSVD. We are particularly interested in papers describing the processes involved in arteriolosclerosis, vascular amyloidosis, cSVD-related dementia and vascular diseases and thus their important therapeutic implications. Papers providing critical theory and hypothesis is welcome. Innovative techniques, e.g. new neuroimaging methods are also of great interest to this topic.
Keywords: Sporadic Cerebral Small Vessel Diseases, Arteriolosclerosis, Cerebral Amyloid Angiopathy，Pathogenic Mechanism, Treatment
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