The vascular factor in Alzheimer's disease: A study in Golgi technique and electron microscopy

Baloyannis, Stavros J.; Baloyannis, Ioannis S.

doi:10.1016/j.jns.2012.07.010

Cited by 129 publications

(142 citation statements)

References 52 publications

(58 reference statements)

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“…93 Pericytes demonstrate large numbers of intracellular inclusions, pinocytotic vesicles, large lipid granules and mitochondrial abnormalities suggesting cellular dysfunction and/or degeneration. 94,95 Also, pericyte degenerative changes are associated with capillary reductions and gross dilatation and tortuosity of surviving vessels. 95 In post-mortem tissue of individual AD subjects, reductions in pericyte coverage inversely correlate with evidence of BBB disruption, such as leakage of the plasma proteins including immunoglobulin G and fibrin.…”

Section: Astrocytesmentioning

confidence: 99%

Age-associated physiological and pathological changes at the blood–brain barrier: A review

Erdő

Dénès

Lange

2016

J Cereb Blood Flow Metab

345

260

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The age-associated decline of the neurological and cognitive functions becomes more and more serious challenge for the developed countries with the increasing number of aged populations. The morphological and biochemical changes in the aging brain are the subjects of many extended research projects worldwide for a long time. However, the crucial role of the blood-brain barrier (BBB) impairment and disruption in the pathological processes in age-associated neurodegenerative disorders received special attention just for a few years. This article gives an overview on the major elements of the blood-brain barrier and its supporting mechanisms and also on their alterations during development, physiological aging process and age-associated neurodegenerative disorders (Alzheimer's disease, multiple sclerosis, Parkinson's disease, pharmacoresistant epilepsy). Besides the morphological alterations of the cellular elements (endothelial cells, astrocytes, pericytes, microglia, neuronal elements) of the BBB and neurovascular unit, the changes of the barrier at molecular level (tight junction proteins, adheres junction proteins, membrane transporters, basal lamina, extracellular matrix) are also summarized. The recognition of new players and initiators of the process of neurodegeneration at the level of the BBB may offer new avenues for novel therapeutic approaches for the treatment of numerous chronic neurodegenerative disorders currently without effective medication. KeywordsAging, blood-brain barrier, endothelial cells, neurodegenerative disorders, transport systems Structure of the blood-brain barrier (BBB)Homeostasis of the extracellular microenvironment in the neural tissue of the brain as well as its protection against neurotoxic compounds and variations in the composition of the blood are important for normal function of the neurons. It is warranted by a structure formed between blood and brain, which is therefore called the BBB.1 Clear evidence for the existence of this permeability barrier in the brain emerged in 1909 with the demonstration by Edwin Goldman (a South African-German) that a dye injected into the blood stream of a rat stained the whole body -except for the brain and spinal cord. The opposite was also true: injection of the dye into the cerebral ventricles stained the brain and spinal cord but not the rest of the body. 2,3 This occurs because most organs of the body are perfused by capillaries lined with endothelial cells (ECs) that have small pores (fenestrations) to allow for the rapid movement of small molecules into the organ interstitial fluid from the circulation. However, the capillary endothelium of the brain and spinal cord lack these pores because the ECs of brain capillary are connected to each other by continuous tight junctions (TJs), produced by the interaction of several transmembrane proteins that project into and seal the paracellular pathway.3-5 The interaction of these junctional proteins effectively blocks the free diffusion of

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Section: Astrocytesmentioning

confidence: 99%

Age-associated physiological and pathological changes at the blood–brain barrier: A review

Erdő

Dénès

Lange

2016

J Cereb Blood Flow Metab

345

260

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“…Despite the hypoperfusion, the density of capillaries in the cerebral cortex is unchanged or reduced in AD (8,15,17,45,60,134), and more of them show degenerative changes in AD than in age-matched controls (7,20,51,123). Both endothelial cells and pericytes are affected, their degeneration eventually leaving residual 'string' vessels consisting solely of tubes of collagen.…”

Section: Capillary Damagementioning

confidence: 99%

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

Love

Miners

2016

Brain Pathology

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“…Supporting this view, experimental studies suggest that the BBB dysfunction diminishes clearance of the soluble brain ȕ-amyloid, leading to its accumulation as neurotoxic ȕ-amyloid oligomers in parenchyma and vessel walls (Iadecola, 2010;Sagare et al, 2013;Stanimirovic and Friedman, 2012;Zlokovic, 2008aZlokovic, , 2008bZlokovic et al, 1996). ȕ-amyloid has been shown to be toxic to pericytes (Baloyannis and Baloyannis, 2012;Verbeek et al, 1997;Wilhelmus et al, 2007Wilhelmus et al, , 2007. Indeed, amyloid deposits within degenerating pericytes have been observed in the brains of patients with Alzheimer's disease (Szpak et al, 2007;Wisniewski et al, 1992).…”

Section: -Microvascular Dysfunction As a Cause Of Neurodegenerativementioning

confidence: 99%

Cerebral microvascular pericytes and neurogliovascular signaling in health and disease

2015

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The vascular factor in Alzheimer's disease: A study in Golgi technique and electron microscopy

Cited by 129 publications

References 52 publications

Age-associated physiological and pathological changes at the blood–brain barrier: A review

Age-associated physiological and pathological changes at the blood–brain barrier: A review

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

Cerebral microvascular pericytes and neurogliovascular signaling in health and disease

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