A population study on blood-brain barrier function in 85-year-olds

Skoog, Ingmar; Wallin, Anders; Fredman, Pam; Hesse, Camilla; Aevarsson, Olafur; Karlsson, Ingvar; Gottfries, C. G.; Blennow, Kaj

doi:10.1212/wnl.50.4.966

Cited by 220 publications

(181 citation statements)

References 34 publications

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“…However, a growing body of evidence addresses alterations in BBB permeability (typically to large molecules). For example, increases in BBB permeability have been reported to accompany aging (Shah and Mooradian, 1997), Alzheimers dementia (Skoog et al, 1998;Ujiie et al, 2003), type II diabetes (Starr et al, 2003), and hypertension (Mooradian, 1988;Mayhan, 1990;Ueno et al, 2004). BBB permeability also increases with increasing plasma osmolarity (Tamaki et al, 1984), and after the administration of certain drugs (Boertje et al, 1992).…”

Section: Central Nervous Systemmentioning

confidence: 99%

Consensus meeting: monosodium glutamate – an update

et al. 2006

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Objective: Update of the Hohenheim consensus on monosodium glutamate from 1997: Summary and evaluation of recent knowledge with respect to physiology and safety of monosodium glutamate. Design: Experts from a range of relevant disciplines received and considered a series of questions related to aspects of the topic. Setting: University of Hohenheim, Stuttgart, Germany. Method: The experts met and discussed the questions and arrived at a consensus. Conclusion: Total intake of glutamate from food in European countries is generally stable and ranged from 5 to 12 g/day (free: ca. 1 g, protein-bound: ca. 10 g, added as flavor: ca. 0.4 g). L-Glutamate (GLU) from all sources is mainly used as energy fuel in enterocytes. A maximum intake of 16.000 mg/kg body weight is regarded as safe. The general use of glutamate salts (monosodium-L-glutamate and others) as food additive can, thus, be regarded as harmless for the whole population. Even in unphysiologically high doses GLU will not trespass into fetal circulation. Further research work should, however, be done concerning the effects of high doses of a bolus supply at presence of an impaired blood brain barrier function. In situations with decreased appetite (e.g., elderly persons) palatability can be improved by low dose use of monosodium-L-glutamate.

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Section: Central Nervous Systemmentioning

confidence: 99%

Consensus meeting: monosodium glutamate – an update

et al. 2006

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“…41 Permeability of the BBB augments with advancing age and in the presence of cerebral SVD. Increased cerebrospinal fluid/serum albumin ratio, a marker of BBB breakdown, has been documented in vascular dementia, 42,43 and in patients with white-matter changes on neuroimaging. 44 More recently, contrast-enhanced MRI has been used to study BBB permeability, documenting an increased permeability in the white matter of patients with lacunar stroke compared with patients with cortical stroke.…”

Section: Evidence Of Endothelial Dysfunction/ Damage In Small Vessel mentioning

confidence: 99%

Circulating biologic markers of endothelial dysfunction in cerebral small vessel disease: A review

Poggesi

Pasi

Pescini

et al. 2015

J Cereb Blood Flow Metab

220

183

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The term cerebral small vessel disease (SVD) refers to a group of pathologic processes with various etiologies that affect small arteries, arterioles, venules, and capillaries of the brain. Magnetic resonance imaging (MRI) correlates of SVD are lacunes, recent small subcortical infarcts, white-matter hyperintensities, enlarged perivascular spaces, microbleeds, and brain atrophy. Endothelial dysfunction is thought to have a role in the mechanisms leading to SVD-related brain changes, and the study of endothelial dysfunction has been proposed as an important step for a better comprehension of cerebral SVD. Among available methods to assess endothelial function in vivo, measurement of molecules of endothelial origin in peripheral blood is currently receiving selective attention. These molecules include products of endothelial cells that change when the endothelium is activated, as well as molecules that reflect endothelial damage and repair. This review examines the main molecular factors involved in both endothelial function and dysfunction, and the evidence linking endothelial dysfunction with cerebral SVD, and gives an overview of clinical studies that have investigated the possible association between endothelial circulating biomarkers and SVD-related brain changes. KeywordsCerebral small vessel disease, endothelium, inflammation, lacunar infarcts, white-mater hyperintensities The term cerebral small vessel disease (SVD) refers to a group of pathologic processes with various etiologies that affect the small arteries, arterioles, venules, and capillaries of the brain.1 Age/hypertension-related SVDs and cerebral amyloid angiopathy are the most common sporadic forms of SVD. Among a few genetic forms of SVD, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), caused by NOTCH3 gene mutations, is the most frequent one. It is a systemic arteriopathy although the clinical symptoms are those caused by brain dysfunction. The effects of both sporadic and inherited SVD on the brain parenchyma are represented by lesions mainly located in the subcortical structures, and include lacunar infarcts, ischemic white-matter lesions, and intracerebral hemorrhage. An international working group has recently published the STRIVE (STandards for ReportIng Vascular changes on nEuroimaging) to provide definitions and imaging standards for markers and consequences of SVD.2 According to this consensus, changes currently seen on neuroimaging related to SVD include lacunes, recent small subcortical infarcts, white-matter hyperintensities (WMH), perivascular spaces (PVS), microbleeds (MB), and brain atrophy.Over the last few decades, evidence has being accumulated regarding prevalence, clinical significance, and

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“…The blood–brain barrier (BBB) hinders the entry of most molecules into the brain and enables active transportation of penetrated molecules to the brain (Zlokovic, 2011). Dysfunction of the BBB has been demonstrated in the pathogenesis and progression of AD (Kalaria, 2010), even before dementia onset (Skoog et al, 1998) and also in the aging human hippocampus, which worsens with mci, a condition preceding AD (Montagne et al, 2015). Changes in plasma glucose levels have been associated with altered BBB transport functions, with paracellular integrity (tight junction disruption) and with oxidative stress in the CNS microcapillaries (Prasad, Sajja, Naik, & Cucullo, 2014).…”

Section: Introductionmentioning

confidence: 99%

High‐fat diet protects the blood–brain barrier in an Alzheimer's disease mouse model

et al. 2018

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Type 2 diabetes (T2D) is associated with increased risk of Alzheimer's disease (AD). There is evidence for impaired blood–brain barrier (BBB) in both diseases, but its role in the interplay between them is not clear. Here, we investigated the effects of high‐fat diet (HFD), a model for T2D, on the Tg2576 mouse model of AD, in regard to BBB function. We showed that HFD mice had higher weight, more insulin resistance, and higher serum HDL cholesterol levels, primarily in Tg2576 mice, which also had higher brain lipids content. In terms of behavior, Tg2576 HFD mice were less active and more anxious, but had better learning in the Morris Water Maze compared to Tg2576 on regular diet. HFD had no effect on the level of amyloid beta 1–42 in the cortex of Tg2576 mice, but increased the transcription level of insulin receptor in the hippocampus. Tg2576 mice on regular diet demonstrated more BBB disruption at 8 and 12 months accompanied by larger lateral ventricles volume in contrast to Tg2576 HFD mice, whose BBB leakage and ventricular volume were similar to wild‐type (WT) mice. Our results suggest that in AD, HFD may promote better cognitive function through improvements of BBB function and of brain atrophy but not of amyloid beta levels. Lipid metabolism in the CNS and peripheral tissues and brain insulin signaling may underlie this protection.

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A population study on blood-brain barrier function in 85-year-olds

Cited by 220 publications

References 34 publications

Consensus meeting: monosodium glutamate – an update

Consensus meeting: monosodium glutamate – an update

Circulating biologic markers of endothelial dysfunction in cerebral small vessel disease: A review

High‐fat diet protects the blood–brain barrier in an Alzheimer's disease mouse model

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