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Cerebral small vessel disease: Capillary pathways to stroke and cognitive decline.

Østergaard L, Engedal TS, Moreton F, Hansen MB, Wardlaw JM, Dalkara T, Markus HS, Muir KW - J. Cereb. Blood Flow Metab. (2015)

Bottom Line: Capillary flow patterns were, however, recently shown to limit the extraction efficacy of oxygen in tissue and capillary dysfunction therefore proposed as a source of stroke-like symptoms and neurodegeneration, even in the absence of physical flow-limiting vascular pathology.In this review, we examine whether capillary flow disturbances may be a shared feature of conditions that represent risk factors for SVD.We then discuss aspects of capillary dysfunction that could be prevented or alleviated and therefore might be of general benefit to patients at risk of SVD, stroke or cognitive decline.

View Article: PubMed Central - PubMed

Affiliation: Center of Functionally Integrative Neuroscience and MINDLab, Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark Department of Neuroradiology, Aarhus University Hospital, Aarhus, Denmark leif@cfin.au.dk.

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Panel (a) illustrates the organization of endothelial cells, basement membrane and pericytes in the vessel wall. Capillaries are ensheathed by astrocytic endfeet, and neuronal terminals are closely apposed to capillaries and pericytes.66 Source: Reproduced from Hamilton et al.66 according to the Creative Commons terms. Panel (b) shows a cross section of normal capillary with a thin basement membrane (arrow) and normal appearing endothelial cell (e). In ageing (Panel (c)), thickened basement membranes (arrows), pericapillary fibrosis and pericyte loss are often found. Source: Panels (b) and (c) are reproduced from Farkas et al.188 Panel (d) shows a capillary cross section from the skin of a patient with Fabry’s disease. Note the lamellar sphingolipid inclusions in the capillary endothelium (arrow). These inclusions disappear upon enzyme replacement therapy. Source: Reproduced from Eng et al.189 Panel (e) shows typical cerebral capillary wall pathology in human AD. The arrow indicates pericyte degeneration. The symbols denote lumen (l), endothelial cell (e), basement membrane (*) and pericyte (p). Source: Reproduced from Farkas et al.190 Panel (f) shows a cross section of a muscle capillary from a patient with MELAS. Note the thickened basement membrane and increased number and size of mitochondria in the pericyte. Source: Reproduced from Sakuta and Nonaka.191 Panel (g) shows a cross section of a cerebral capillary from the motor cortex of a MELAS patient with accumulation of mitochondria in the endothelial cell. Source: Reproduced from Ohama et al.192 with permission from the publisher. AD: Alzheimer’s disease; MELAS: mitochondrial encephalopathy with lactic acidosis and stroke-like episodes.
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fig2-0271678X15606723: Panel (a) illustrates the organization of endothelial cells, basement membrane and pericytes in the vessel wall. Capillaries are ensheathed by astrocytic endfeet, and neuronal terminals are closely apposed to capillaries and pericytes.66 Source: Reproduced from Hamilton et al.66 according to the Creative Commons terms. Panel (b) shows a cross section of normal capillary with a thin basement membrane (arrow) and normal appearing endothelial cell (e). In ageing (Panel (c)), thickened basement membranes (arrows), pericapillary fibrosis and pericyte loss are often found. Source: Panels (b) and (c) are reproduced from Farkas et al.188 Panel (d) shows a capillary cross section from the skin of a patient with Fabry’s disease. Note the lamellar sphingolipid inclusions in the capillary endothelium (arrow). These inclusions disappear upon enzyme replacement therapy. Source: Reproduced from Eng et al.189 Panel (e) shows typical cerebral capillary wall pathology in human AD. The arrow indicates pericyte degeneration. The symbols denote lumen (l), endothelial cell (e), basement membrane (*) and pericyte (p). Source: Reproduced from Farkas et al.190 Panel (f) shows a cross section of a muscle capillary from a patient with MELAS. Note the thickened basement membrane and increased number and size of mitochondria in the pericyte. Source: Reproduced from Sakuta and Nonaka.191 Panel (g) shows a cross section of a cerebral capillary from the motor cortex of a MELAS patient with accumulation of mitochondria in the endothelial cell. Source: Reproduced from Ohama et al.192 with permission from the publisher. AD: Alzheimer’s disease; MELAS: mitochondrial encephalopathy with lactic acidosis and stroke-like episodes.

Mentions: Type 1: Arteriolosclerosis (age- and vascular risk-factor-related SVD). Type 2: CAA, sporadic or hereditary.


Cerebral small vessel disease: Capillary pathways to stroke and cognitive decline.

Østergaard L, Engedal TS, Moreton F, Hansen MB, Wardlaw JM, Dalkara T, Markus HS, Muir KW - J. Cereb. Blood Flow Metab. (2015)

Panel (a) illustrates the organization of endothelial cells, basement membrane and pericytes in the vessel wall. Capillaries are ensheathed by astrocytic endfeet, and neuronal terminals are closely apposed to capillaries and pericytes.66 Source: Reproduced from Hamilton et al.66 according to the Creative Commons terms. Panel (b) shows a cross section of normal capillary with a thin basement membrane (arrow) and normal appearing endothelial cell (e). In ageing (Panel (c)), thickened basement membranes (arrows), pericapillary fibrosis and pericyte loss are often found. Source: Panels (b) and (c) are reproduced from Farkas et al.188 Panel (d) shows a capillary cross section from the skin of a patient with Fabry’s disease. Note the lamellar sphingolipid inclusions in the capillary endothelium (arrow). These inclusions disappear upon enzyme replacement therapy. Source: Reproduced from Eng et al.189 Panel (e) shows typical cerebral capillary wall pathology in human AD. The arrow indicates pericyte degeneration. The symbols denote lumen (l), endothelial cell (e), basement membrane (*) and pericyte (p). Source: Reproduced from Farkas et al.190 Panel (f) shows a cross section of a muscle capillary from a patient with MELAS. Note the thickened basement membrane and increased number and size of mitochondria in the pericyte. Source: Reproduced from Sakuta and Nonaka.191 Panel (g) shows a cross section of a cerebral capillary from the motor cortex of a MELAS patient with accumulation of mitochondria in the endothelial cell. Source: Reproduced from Ohama et al.192 with permission from the publisher. AD: Alzheimer’s disease; MELAS: mitochondrial encephalopathy with lactic acidosis and stroke-like episodes.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2 - License 3
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getmorefigures.php?uid=PMC4759673&req=5

fig2-0271678X15606723: Panel (a) illustrates the organization of endothelial cells, basement membrane and pericytes in the vessel wall. Capillaries are ensheathed by astrocytic endfeet, and neuronal terminals are closely apposed to capillaries and pericytes.66 Source: Reproduced from Hamilton et al.66 according to the Creative Commons terms. Panel (b) shows a cross section of normal capillary with a thin basement membrane (arrow) and normal appearing endothelial cell (e). In ageing (Panel (c)), thickened basement membranes (arrows), pericapillary fibrosis and pericyte loss are often found. Source: Panels (b) and (c) are reproduced from Farkas et al.188 Panel (d) shows a capillary cross section from the skin of a patient with Fabry’s disease. Note the lamellar sphingolipid inclusions in the capillary endothelium (arrow). These inclusions disappear upon enzyme replacement therapy. Source: Reproduced from Eng et al.189 Panel (e) shows typical cerebral capillary wall pathology in human AD. The arrow indicates pericyte degeneration. The symbols denote lumen (l), endothelial cell (e), basement membrane (*) and pericyte (p). Source: Reproduced from Farkas et al.190 Panel (f) shows a cross section of a muscle capillary from a patient with MELAS. Note the thickened basement membrane and increased number and size of mitochondria in the pericyte. Source: Reproduced from Sakuta and Nonaka.191 Panel (g) shows a cross section of a cerebral capillary from the motor cortex of a MELAS patient with accumulation of mitochondria in the endothelial cell. Source: Reproduced from Ohama et al.192 with permission from the publisher. AD: Alzheimer’s disease; MELAS: mitochondrial encephalopathy with lactic acidosis and stroke-like episodes.
Mentions: Type 1: Arteriolosclerosis (age- and vascular risk-factor-related SVD). Type 2: CAA, sporadic or hereditary.

Bottom Line: Capillary flow patterns were, however, recently shown to limit the extraction efficacy of oxygen in tissue and capillary dysfunction therefore proposed as a source of stroke-like symptoms and neurodegeneration, even in the absence of physical flow-limiting vascular pathology.In this review, we examine whether capillary flow disturbances may be a shared feature of conditions that represent risk factors for SVD.We then discuss aspects of capillary dysfunction that could be prevented or alleviated and therefore might be of general benefit to patients at risk of SVD, stroke or cognitive decline.

View Article: PubMed Central - PubMed

Affiliation: Center of Functionally Integrative Neuroscience and MINDLab, Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark Department of Neuroradiology, Aarhus University Hospital, Aarhus, Denmark leif@cfin.au.dk.

Show MeSH
Related in: MedlinePlus