Special Issue "Small Vessel Disease: New Perspectives on an Emerging Reality"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 30 April 2021.
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Small vessel disease (SVD) is an umbrella term that starts in para-physiological healthy aging and ends into related subcortical vascular dementia (sVAD). SVD and white matter abnormalities related to age could be accelerated and potentiated by different vascular risk factors. Vascular function changes can be heavily influenced by genetic and epigenetic factors, which are mostly unknown to the best of our knowledge. Metabolic demands, active neurovascular coupling, correct glymphatic process, and adequate oxidative and inflammatory responses could be bulwarks in defense of the correct aging process; their impairments lead to a potentially catastrophic and non‐reversible condition.
The arteriosclerosis‐dependent alteration of brain perfusion is one of the major determinants in small vessel disease, with degeneration of the smooth muscle layer and replacement by hyaline fibrosis, leading to a subtotal luminal occlusion, but also since small vessels have a pivotal role in the brain’s autoregulation. Nevertheless, as far as we know, endothelium distress can potentiate the flow dysregulation and lead to subcortical vascular dementia that is related to SVD, also being defined as subcortical vascular dementia, as well as microglia activation, chronic hypoxia and hypoperfusion, vessel‐tone dysregulation, altered astrocytes, and pericyte functioning blood–brain barrier disruption. The molecular basis of this pathology remains controversial. The apparent consequence is the macroscopic alteration of neurovascular coupling. SVD is an ongoing process, which begins with altered microvessels and pial arteries and ends in subcortical dementia; CBF regional selective decrease seems to be one of the critical factors for the progression from small vessel disease to small vessel disease‐related dementia. The most relevant aspects still under debate are the modality of changing from typical aging small vessel disease toward dementia; the impact of aging and age–gene interactions in arteriolosclerosis, endothelium dysfunction, pericyte alterations, and astrocyte modifications, which are caused, promoted, or potentiated by hypoperfusion and metabolic disruption; altered neurovascular coupling, a secondary or a causative (primary) defect in SVD; and potential clinical rescue from SVD, knowing different times of its development, probably by acting precociously, simultaneously via various strategies (anti‐inflammatory, anti‐oxidant, anti‐thrombotic, and perhaps via nutraceutical promotions, acting as co‐enzymatic promoters).
This Special Issue will aim to shed some light on these fascinating aspects.
Prof. Dr. Rita Moretti
Manuscript Submission Information
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- biological markers
- blood brain barrier
- neurovascular coupling
- glymphatic system