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Special Issue "Small Vessel Disease: New Perspectives on an Emerging Reality"

Special Issue Editor

Prof. Dr. Rita Moretti
Guest Editor

Special Issue Information

Dear Colleagues,

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
Guest Editor

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  • biological markers
  • vitamin
  • endothelium
  • blood brain barrier
  • CAA
  • astrocytes
  • neurovascular coupling
  • neuro-inflammation
  • glymphatic system

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Published Papers (1 paper)

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Open AccessReview
Sleep as a Novel Biomarker and a Promising Therapeutic Target for Cerebral Small Vessel Disease: A Review Focusing on Alzheimer’s Disease and the Blood-Brain Barrier
Int. J. Mol. Sci. 2020, 21(17), 6293; https://doi.org/10.3390/ijms21176293 - 31 Aug 2020
Cerebral small vessel disease (CSVD) is a leading cause of cognitive decline in elderly people and development of Alzheimer’s disease (AD). Blood–brain barrier (BBB) leakage is a key pathophysiological mechanism of amyloidal CSVD. Sleep plays a crucial role in keeping health of the [...] Read more.
Cerebral small vessel disease (CSVD) is a leading cause of cognitive decline in elderly people and development of Alzheimer’s disease (AD). Blood–brain barrier (BBB) leakage is a key pathophysiological mechanism of amyloidal CSVD. Sleep plays a crucial role in keeping health of the central nervous system and in resistance to CSVD. The deficit of sleep contributes to accumulation of metabolites and toxins such as beta-amyloid in the brain and can lead to BBB disruption. Currently, sleep is considered as an important informative platform for diagnosis and therapy of AD. However, there are no effective methods for extracting of diagnostic information from sleep characteristics. In this review, we show strong evidence that slow wave activity (SWA) (0–0.5 Hz) during deep sleep reflects glymphatic pathology, the BBB leakage and memory deficit in AD. We also discuss that diagnostic and therapeutic targeting of SWA in AD might lead to be a novel era in effective therapy of AD. Moreover, we demonstrate that SWA can be pioneering non-invasive and bed–side technology for express diagnosis of the BBB permeability. Finally, we review the novel data about the methods of detection and enhancement of SWA that can be biomarker and a promising therapy of amyloidal CSVD and CSVD associated with the BBB disorders. Full article
(This article belongs to the Special Issue Small Vessel Disease: New Perspectives on an Emerging Reality)
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