Blood–brain barrier permeability in Alzheimer's disease: a case–control MRI study

Starr, John M.; Farrall, Andrew; Armitage, Paul A.; McGurn, Brian; Wardlaw, Joanna M.

doi:10.1016/j.pscychresns.2008.04.003

Cited by 163 publications

(129 citation statements)

References 40 publications

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“…The T 1 -mapping method as applied in this study, with a sampling time of 3.5 min, lacks the temporal resolution to assess leakage rates that are fast on a time scale of a few minutes. A short total sampling interval as applied by Larsson et al, on the other hand, is inadequate for measuring slower rates of leakage, which may be of interest in studies on pathologies with suspected low rates of BBB leakage, such as Alzheimer's Disease (20), lacunar stroke (19), and Binswanger's disease (21). Both types of measurements, therefore, have the potential to provide useful information on the degree of pathology involving the BBB.…”

Section: Discussionmentioning

confidence: 99%

“…Prior DCEMRI studies of BBB permeability in humans measure pixel intensity changes in T 1 -or T 2 * -weighted images over a short time course after contrast agent injection (14,15,18,19) and are sensitive only to relatively high rates of contrast agent leakage. Slower rates of BBB leakage appear to be important in chronic diseases, such as Alzheimer's disease (20) and Binswanger's disease (21), as shown in qualitative studies of changes in T 1 -weighted image intensities that were monitored for longer periods after contrast agent injection. Quantitative T 1 measurements in animal models show slow rates of BBB leakage (see Ewing et al, 2006 and references therein).…”

Section: Introductionmentioning

confidence: 99%

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Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping

Taheri

Gasparovic

Shah

et al. 2011

Magnetic Resonance in Med

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Breakdown of the blood-brain barrier (BBB), occurring in many neurological diseases, has been difficult to measure noninvasively in humans. Dynamic contrast-enhanced magnetic resonance imaging measures BBB permeability. However, important technical challenges remain and normative data from healthy humans is lacking. We report the implementation of a method for measuring BBB permeability, originally developed in animals, to estimate BBB permeability in both healthy subjects and patients with white matter pathology. Fast T 1 mapping was used to measure the leakage of contrast agent Gadolinium diethylene triamine pentaacetic acid (Gd-DTPA) from plasma into brain. A quarter of the standard Gd-DTPA dose for dynamic contrastenhanced magnetic resonance imaging was found to give both sufficient contrast-to-noise and high T 1 sensitivity. The Patlak graphical approach was used to calculate the permeability from changes in 1/T 1 . Permeability constants were compared with cerebrospinal fluid albumin index. The upper limit of the 95% confidence interval for white matter BBB permeability for normal subjects was 3 × 10 −4 L/g min. MRI measurements correlated strongly with levels of cerebrospinal fluid albumin in those subjects undergoing lumbar puncture. Dynamic contrast-enhanced magnetic resonance imaging with low dose Gd-DTPA and fast T 1 imaging is a sensitive method to measure subtle differences in BBB permeability in humans and may have advantages over techniques based purely on the measurement of pixel contrast changes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping

Taheri

Gasparovic

Shah

et al. 2011

Magnetic Resonance in Med

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show abstract

“…A limitation of these imaging studies with regard to AD is the fact that these were normal animals. BBB abnormalities may occur in AD [101,102]. The effects of any such abnormalities on the distribution of etanercept are not presently known.…”

Section: Experimental Evidence: Radionuclide Pet and Single Proton-emismentioning

confidence: 99%

Perispinal etanercept: a new therapeutic paradigm in neurology

Tobinick

2010

Expert Review of Neurotherapeutics

107

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“…Using the AD model Tg2576 mice a higher BBB permeability for albumin was measured in cerebral cortex, which preceded senile plaque formation [14]. Even if extensive BBB damage or substantial increases in BBB permeability in AD can not be found in some animal studies [48] or clinical evaluations [49], considering all available data focal and transient loss of integrity of the BBB in AD seems probable [50].…”

Section: Changes In Blood-brain Barrier Function and Morphology In Admentioning

confidence: 99%

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Deli

Veszelka

Csiszár

et al. 2010

JAD

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Abstract. Endothelial cells of brain capillaries forming the blood-brain barrier play an important role in the pathogenesis and therapy of Alzheimer's disease. Amyloid-β (Aβ) peptides are key pathological elements in the development of the disease. A blood-brain barrier model, based on primary rat brain endothelial cells was used in which the barrier properties were induced by glial cells. The effects of amyloid peptides have been tested on cell viability and barrier functions. Aβ showed toxic effects on primary rat brain endothelial cells measured by MTT dye conversion and the lactate dehydrogenase release. Morphologically cytoplasmic vacuolization, disruption of the structure of cytoplasmic organelles and tight junctions could be observed in brain endothelial cells. Treatment with Aβ1−42 decreased the electrical resistance, and increased the permeability of brain endothelial cell monolayers for both fluorescein and albumin. Serum amyloid P component which stabilizes Aβ fibrils in cortical amyloid plaques and cerebrovascular amyloid deposits significantly potentiated the barrier-weakening effect of Aβ1−42. Sulfated polysaccharide pentosan could decrease the toxic effects of Aβ peptides in brain endothelial cells. It could also significantly protect the barrier integrity of monolayers from damaging actions of peptides. Pentosan modified the size, and significantly decreased the number of amyloid aggregates demonstrated by atomic force microscopy. The present data further support the toxic effects of amyloid peptides on brain endothelial cells, and can contribute to the development of molecules protecting the blood-brain barrier in Alzheimer's disease.

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Blood–brain barrier permeability in Alzheimer's disease: a case–control MRI study

Cited by 163 publications

References 40 publications

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping

Perispinal etanercept: a new therapeutic paradigm in neurology

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

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Blood–brain barrier permeability in Alzheimer's disease: a case–control MRI study

Cited by 163 publications

References 40 publications

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T1 mapping

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T1 mapping

Perispinal etanercept: a new therapeutic paradigm in neurology

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Contact Info

Product

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Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping

Quantitative measurement of blood‐brain barrier permeability in human using dynamic contrast‐enhanced MRI with fast T₁ mapping