Effect of aging on the blood-brain barrier

Mooradian, Arshag D.

doi:10.1016/s0197-4580(88)80013-7

Cited by 281 publications

(163 citation statements)

References 117 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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“…Because the integrity of the blood–brain barrier (BBB) gradually decreases in aging58, 59 and amyloid deposition in cerebral blood vessels is almost universal in AD, leakage of plasma protein has long been postulated as causative of disease 60. In this context, leakage of plasma APN into the brain parenchyma may result in sequestration of amyloidogenic proteins, such as tau and α ‐syn, leading to stimulation of neurodegeneration.…”

Section: Apn May Promote Neurodegeneration In Ad Through Novel Mechanmentioning

confidence: 99%

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Waragai

Ho²,

Takamatsu

et al. 2017

Ann Clin Transl Neurol

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A recent study suggested that insulin resistance may play a central role in the pathogenesis of Alzheimer's disease (AD). In this regard, it is of note that upregulation of plasma adiponectin (APN), a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation, has recently been associated with the severities of amyloid deposits and cognitive deficits in the elderly, suggesting that APN may enhance the risk of AD. These results are unanticipated because AD has been linked to type II diabetes and other metabolic disorders in which hypoadiponectinemia has been firmly established, and because APN ameliorated neuropathological features in a mouse model of neurodegeneration. Therefore, the objective of this study is to discuss the possible mechanisms underlying the biological actions of APN in the context of AD. Given that insulin receptor signaling is required for normal function of the nervous system, we predict that APN may be upregulated to compensate for compromised activity of the insulin receptor signaling pathway. However, increased APN might be sequestered by tau in the brain, leading to neurotoxic protein aggregation in AD. Alternatively, misfolding of APN may result in downregulation of the insulin/APN signal transduction network, leading to decreased neuroprotective and neurotrophic activities. Thus, it is possible that both ‘gain of function’ and ‘loss of function’ of APN may underlie synaptic dysfunction and neuronal cell death in AD. Such a unique biological mechanism underlying APN function in AD may require a novel therapeutic strategy that is distinct from previous treatment for metabolic disorders.

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“…Regarding the first aspect, aging, the cerebral vasculature is prone to pathological changes during the aging process similar to peripheral vessels (29,30). Amyloid deposits have been observed on the walls of cerebral vessels as well as in the choroidal epithelia, and are sometimes associated with Alzheimer-type lesions (31)(32)(33).…”

Section: Role Of Altered Brain Barriers In Alzheimer's Diseasementioning

confidence: 99%

Neurotoxicology of the Brain Barrier System: New Implications

Zheng

2001

Journal of Toxicology: Clinical Toxicology

100

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The concept of a barrier system in the brain has existed for nearly a century. The barrier that separates the blood from the cerebral interstitial fluid is defined as the blood-brain barrier, while the one that discontinues the circulation between the blood and cerebrospinal fluid is named the blood-cerebrospinal fluid barrier. Evidence in the past decades suggests that brain barriers are subject to toxic insults from neurotoxic chemicals circulating in blood. The aging process and some disease states render barriers more vulnerable to insults arising inside and outside the barriers. The implication of brain barriers in certain neurodegenerative diseases is compelling, although the contribution of chemical-induced barrier dysfunction in the etiology of any of these disorders remains poorly understood. This review examines what is currently understood about brain barrier systems in central nervous system disorders by focusing on chemical-induced neurotoxicities including those associated with nitrobenzenes, N-methyl-D-aspartate, cyclosporin A, pyridostigmine bromide, aluminum, lead, manganese, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and 3-nitropropionic acid. Contemporary research questions arising from this growing understanding show enormous promises for brain researchers, toxicologists, and clinicians.

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Effect of aging on the blood-brain barrier

Cited by 281 publications

References 117 publications

Consensus meeting: monosodium glutamate – an update

Consensus meeting: monosodium glutamate – an update

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Neurotoxicology of the Brain Barrier System: New Implications

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