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Sub-cellular Biochemistry 2019Proper functioning of the brain is dependent on integrity of the cerebral vasculature. During ageing, a number of factors including aortic or arterial stiffness,... (Review)
Review
Proper functioning of the brain is dependent on integrity of the cerebral vasculature. During ageing, a number of factors including aortic or arterial stiffness, autonomic dysregulation, neurovascular uncoupling and blood-brain barrier (BBB) damage will define the dynamics of brain blood flow and local perfusion. The nature and extent of ageing-related cerebrovascular changes, the degree of involvement of the heart and extracranial vessels and the consequent location of tissue pathology may vary considerably. Atheromatous disease retarding flow is a common vascular insult, which increases exponentially with increasing age. Arteriolosclerosis characterized as a prominent feature of small vessel disease is one of the first changes to occur during the natural history of cerebrovascular pathology. At the capillary level, the cerebral endothelium, which forms the BBB undergoes changes including reduced cytoplasm, fewer mitochondria, loss of tight junctions and thickened basement membranes with collagenosis. Astrocyte end-feet protecting the BBB retract as part of the clasmatodendrotic response whereas pericyte coverage is altered. The consequences of these microvascular changes are lacunar infarcts, cortical and subcortical microinfarcts, microbleeds and diffuse white matter disease, which involves myelin loss and axonal abnormalities. The deeper structures are particularly vulnerable because of the relatively reduced density of the microvascular network formed by perforating and penetrating end arteries. Ultimately, the integrity of both the neurovascular and gliovascular units is compromised such that there is an overall synergistic effect reflecting on ageing associated cerebral perfusion and permeability. More than one protagonist appears to be involved in ageing-related cognitive dysfunction characteristically associated with the neurocognitive disorders.
Topics: Aging; Blood-Brain Barrier; Brain; Humans; Neurocognitive Disorders
PubMed: 30888663
DOI: 10.1007/978-981-13-3681-2_17 -
The Journal of Pathology and... 1955
Topics: Arteriolosclerosis; Arteriosclerosis; Cardiovascular System; Humans; Hyalin; Kidney
PubMed: 13243182
DOI: 10.1002/path.1700690121 -
Cardiovascular Pathology : the Official... 2015Arterial vascular diseases comprise the leading cause of death in the industrialized world. Every physician learns about the pathology of these diseases in medical... (Review)
Review
Arterial vascular diseases comprise the leading cause of death in the industrialized world. Every physician learns about the pathology of these diseases in medical school. All pathologists evaluate arterial disease in surgical pathology and/or autopsy specimens. All clinicians encounter patients with clinical manifestations of these diseases. With such a common and clinically-important group of entities one would think there would be a general understanding of the "known" information that exists. That is, physicians and scientists should be able to separate what is fact and what is fancy. This review article is intended to generate thought in this regard.
Topics: Arteries; Arteriosclerosis; Biopsy; Humans; Monckeberg Medial Calcific Sclerosis; Plaque, Atherosclerotic; Predictive Value of Tests; Prognosis; Risk Factors; Rupture, Spontaneous; Severity of Illness Index; Terminology as Topic
PubMed: 26365806
DOI: 10.1016/j.carpath.2015.07.007 -
Stroke Jan 2020
Review
Topics: Brain; Cerebral Amyloid Angiopathy; Cerebral Small Vessel Diseases; Cognitive Dysfunction; Hemorrhage; Humans; Magnetic Resonance Imaging
PubMed: 31752615
DOI: 10.1161/STROKEAHA.119.027969 -
Transactions of the American... 1966
Topics: Adolescent; Adult; Aged; Aging; Arteriosclerosis; Biopsy; Blood Pressure Determination; Child; Diabetic Nephropathies; Diabetic Retinopathy; Eye Diseases; Female; Humans; Hypertension; Kidney Diseases; Male; Middle Aged; Omentum; Ophthalmoscopy; Retinal Vessels; Skin
PubMed: 5964940
DOI: No ID Found -
Acta Neuropathologica Nov 2021
Limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC) is independently associated with dementia and strongly associated with arteriolosclerosis in the oldest-old.
Topics: Aged, 80 and over; Arteriolosclerosis; Dementia; Female; Humans; Limbic Lobe; Male; TDP-43 Proteinopathies
PubMed: 34415381
DOI: 10.1007/s00401-021-02360-w -
Seminars in Nephrology Jan 2005Prolonged hyperuricemia is associated with the development of hypertension, renal arteriolosclerosis, glomerulosclerosis, and tubulointerstitial injury. It confers a... (Review)
Review
Prolonged hyperuricemia is associated with the development of hypertension, renal arteriolosclerosis, glomerulosclerosis, and tubulointerstitial injury. It confers a greater risk than proteinuria for developing chronic renal disease and is associated with the development of hypertension. Mild chronic hyperuricemia without intrarenal crystal deposition was induced in rats by inhibiting uricase with oxonic acid. Hyperuricemic rats developed hypertension, afferent arteriolar thickening, and mild renal interstitial fibrosis. Additionally, hyperuricemia accelerated renal damage and vascular disease in rats undergoing renal ablation. To better understand the role of hyperuricemia in the kidney, micropuncture studies were performed. Hyperuricemia resulted in renal cortical vasoconstriction (single nephron glomerular filtration rate (SNGFR) 35%, P < .05) and glomerular hypertension (P < .05). The possibility that hyperuricemia could modify renal hemodynamic disturbances during progression of renal disease was tested in rats with 5/6 nephrectomy. Hyperuricemia accentuated the renal vascular damage and caused cortical vasoconstriction (SNGFR 40%, P < .05) and persistent glomerular hypertension. In conclusion, hyperuricemia impairs the autoregulatory response of preglomerular vessels, resulting in glomerular hypertension. Lumen obliteration induced by vascular wall thickening results in severe vasoconstriction. The resulting ischemia is a potent stimulus that induces tubulointerstitial inflammation and fibrosis as well as arterial hypertension.
Topics: Animals; Blood Pressure; Chronic Disease; Disease Progression; Glomerular Filtration Rate; Humans; Hypertension; Hyperuricemia; Kidney Cortex; Vasoconstriction
PubMed: 15660330
DOI: 10.1016/j.semnephrol.2004.09.004 -
Neurology Nov 1999To investigate whether internal carotid artery (ICA) occlusive disease-induced hemodynamic disturbance is associated with extensive white matter high-intensity lesions...
OBJECTIVE
To investigate whether internal carotid artery (ICA) occlusive disease-induced hemodynamic disturbance is associated with extensive white matter high-intensity lesions (WMLs) on T2-weighted MR images in the hemisphere with lacunar infarct in the basal ganglia.
BACKGROUND
Hemodynamic disturbance in the brain with arteriolosclerosis may be one of the mechanisms by which ischemic injury induces extensive WMLs.
METHODS
The authors used MRI and PET to study 21 patients with unilateral ICA occlusion or stenosis and lacunar infarct in the bilateral basal ganglia. In hemispheres with ICA disease, the association of WMLs with the mean hemispheric values of oxygen extraction fraction (OEF)-an index of hemodynamic compromise-measured with the 15O-labeled gas steady-state technique was analyzed. Twenty-five patients with ICA occlusive disease without lacunar infarct were studied as control subjects.
RESULTS
In the hemispheres with ICA disease, patients with lacunar infarct had a significantly greater severity of WMLs than control subjects, although the mean hemispheric values of the OEF showed no significant difference. The severity of WMLs correlated significantly with the mean hemispheric values of the OEF in patients with lacunar infarct, but not in control subjects. Multivariate analysis revealed that lacunar infarcts and increased OEF were independent predictors of extensive WMLs, with lacunar infarcts the most heavily weighted factor.
CONCLUSION
Internal carotid artery occlusive disease-induced hemodynamic disturbance is associated with extensive WMLs in hemispheres with lacunar infarct. Hemodynamic disturbance may contribute to the development of extensive WMLs, although brain arteriolosclerosis may be a major contributing factor.
Topics: Aged; Basal Ganglia Cerebrovascular Disease; Brain Diseases; Carotid Artery Diseases; Carotid Artery, Internal; Cerebral Infarction; Cerebrovascular Circulation; Female; Hemodynamics; Humans; Intracranial Arteriosclerosis; Magnetic Resonance Imaging; Male; Middle Aged; Tomography, Emission-Computed
PubMed: 10563635
DOI: 10.1212/wnl.53.8.1833 -
Electrolyte & Blood Pressure : E & BP Dec 2015Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of... (Review)
Review
Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of hypertension. Hypertension in chronic GN is primarily volume dependent, and this increase in blood volume is not related to the deterioration of renal function. Patients with chronic GN become salt sensitive as renal damage including arteriolosclerosis progresses and the consequent renal ischemia causes the stimulation of the intrarenal renin-angiotensin-aldosterone system(RAAS). Overactivity of the sympathetic nervous system also contributes to hypertension in chronic GN. According to the KDIGO guideline, the available evidence indicates that the target BP should be ≤140mmHg systolic and ≤90mmHg diastolic in chronic kidney disease patients without albuminuria. In most patients with an albumin excretion rate of ≥30mg/24 h (i.e., those with both micro-and macroalbuminuria), a lower target of ≤130mmHg systolic and ≤80mmHg diastolic is suggested. The use of agents that block the RAAS system is recommended or suggested in all patients with an albumin excretion rate of ≥30mg/ 24 h. The combination of a RAAS blockade with a calcium channel blocker and a diuretic may be effective in attaining the target BP, and in reducing the amount of urinary protein excretion in patients with chronic GN.
PubMed: 26848302
DOI: 10.5049/EBP.2015.13.2.41 -
Journal of Neuropathology and... Nov 2014The blood-brain barrier protects brain tissue from potentially harmful plasma components. Small vessel disease (SVD; also termed arteriolosclerosis) is common in the...
The blood-brain barrier protects brain tissue from potentially harmful plasma components. Small vessel disease (SVD; also termed arteriolosclerosis) is common in the brains of older people and is associated with lacunar infarcts, leukoaraiosis, and vascular dementia. To determine whether plasma extravasation is associated with SVD, we immunolabeled the plasma proteins fibrinogen and immunoglobulin G, which are assumed to reflect blood-brain barrier dysfunction, in deep gray matter (DGM; anterior caudate-putamen) and deep subcortical white matter (DWM) in the brains of a well-characterized cohort of donated brains with minimal Alzheimer disease pathology (Braak Stages 0-II) (n = 84; aged 65 years or older). Morphometric measures of fibrinogen labeling were compared between people with neuropathologically defined SVD and aged control subjects. Parenchymal cellular labeling with fibrinogen and immunoglobulin G was detectable in DGM and DWM in many subjects (>70%). Quantitative measures of fibrinogen were not associated with SVD in DGM or DWM; SVD severity was correlated between DGM and DWM (p < 0.0001). Fibrinogen in DGM showed a modest association with a history of hypertension; DWM fibrinogen was associated with dementia and cerebral amyloid angiopathy (all p < 0.05). In DWM, SVD was associated with leukoaraiosis identified in life (p < 0.05), but fibrinogen was not. Our data suggest that, in aged brains, plasma extravasation and hence local blood-brain barrier dysfunction are common but do not support an association with SVD.
Topics: Aged; Aged, 80 and over; Arteriolosclerosis; Blood-Brain Barrier; Brain; Cerebral Small Vessel Diseases; Cohort Studies; Female; Humans; Male; Single-Blind Method
PubMed: 25289893
DOI: 10.1097/NEN.0000000000000124