Blood-Brain Barrier Permeability Correlates with Medial Temporal Lobe Atrophy but Not with Amyloid-β Protein Transport across the Blood-Brain Barrier in Alzheimer’s Disease

Matsumoto, Y.; Yanase, Daisuke; Noguchi‐Shinohara, Moeko; Ono, Kenjiro; Yoshita, Mitsuhiro; Yamada, Masahito

doi:10.1159/000100019

Cited by 35 publications

(27 citation statements)

References 57 publications

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“…Previously, we reported that BBB permeability also shows a positive correlation with MTA in AD [20] . However, the correlation was not significant between BBB permeability and the IgG index ( fig.…”

Section: Discussionmentioning

confidence: 71%

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Cerebrospinal Fluid/Serum IgG Index Is Correlated with Medial Temporal Lobe Atrophy in Alzheimer’s Disease

Matsumoto

Yanase

Noguchi‐Shinohara

et al. 2007

Dement Geriatr Cogn Disord

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Background/Aim: Intrathecal inflammation has been suggested to play an important role in the pathogenesis of Alzheimer’s disease (AD). However, there is little clinical evidence in support of this hypothesis in AD patients. We previously reported that the blood-brain barrier permeability represented by the cerebrospinal fluid/serum albumin ratio correlates with medial temporal lobe atrophy (MTA) in AD.The aim of this study was to elucidate the relationship between intrathecal inflammation and the severity of AD. Methods: We investigated the correlations between the cerebrospinal fluid/serum IgG index and the indices of AD severity, including Clinical Dementia Rating and Mini-Mental State Examination, and MTA on magnetic resonance imaging in 42 AD patients. Further, the number of apolipoprotein E isoforms and the blood-brain barrier permeability were also examined for the correlation with the IgG index. Results: The IgG index showed a positive correlation with the severity of MTA but not with the other parameters examined. Conclusion: Our results suggest that intrathecal inflammation increases in association with the severity of MTA in AD.

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Section: Discussionmentioning

confidence: 71%

“…In contrast to previous studies [15][16][17][18][19][20] , the present study included only AD patients fulfilling the AD criteria [21] with no significant vascular lesions as determined on MRI. Further, we used not only CDR and MMSE as dementia scales but also MTA on MRI as an indicator of the severity of AD.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid/Serum IgG Index Is Correlated with Medial Temporal Lobe Atrophy in Alzheimer’s Disease

Matsumoto

Yanase

Noguchi‐Shinohara

et al. 2007

Dement Geriatr Cogn Disord

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“…The maintenance of the BBB is critical for neuronal functions, and its breakdown will alter the transport of molecules between blood and brain and may also result in progressive synaptic and neuronal dysfunction and loss in disorders such as Alzheimer's disease and Parkinson's disease (56)(57)(58)(59). Our findings provide insights into the mechanistic link between the elaborate regulation of Hippo signaling and BBB functions and may also shed light on the relationship between neurodegenerative disorders and dysregulation of Hippo signaling and BBB.…”

Section: Discussionmentioning

confidence: 99%

miR-285– Yki/Mask double-negative feedback loop mediates blood–brain barrier integrity in Drosophila

Liu

Pei

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The Hippo signaling pathway is highly conserved from Drosophila to mammals and plays a central role in maintaining organ size and tissue homeostasis. The blood-brain barrier (BBB) physiologically isolates the brain from circulating blood or the hemolymph system, and its integrity is strictly maintained to perform sophisticated neuronal functions. Until now, the underlying mechanisms of subperineurial glia (SPG) growth and BBB maintenance during development are not clear. Here, we report an miR-285-Yorkie (Yki)/Multiple Ankyrin repeats Single KH domain (Mask) double-negative feedback loop that regulates SPG growth and BBB integrity. Flies with a loss of miR-285 have a defective BBB with increased SPG ploidy and disruptive septate junctions. Mechanistically, miR-285 directly targets the Yki cofactor Mask to suppress Yki activity and down-regulates the expression of its downstream target cyclin E, a key regulator of cell cycle. Disturbance of cyclin E expression in SPG causes abnormal endoreplication, which leads to aberrant DNA ploidy and defective septate junctions. Moreover, the expression of miR-285 is increased by knockdown of yki or mask and is decreased with yki overexpression, thus forming a double-negative feedback loop. This regulatory loop is crucial for sustaining an appropriate Yki/Mask activity and cyclin E level to maintain SPG ploidy and BBB integrity. Perturbation of this signaling loop, either by dysregulated miR-285 expression or Yki activity, causes irregular SPG ploidy and BBB disruption. Furthermore, ectopic expression of miR-285 promotes canonical Hippo pathwaymediated apoptosis independent of the p53 or JNK pathway. Collectively, these results reveal an exquisite regulatory mechanism for BBB maintenance through an miR-285-Yki/Mask regulatory circuit.Hippo | Mask | miR-285 | blood-brain barrier | subperineurial glia

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“…Matsumoto et al [68] Alzheimer's disease CSF markers, MRI and clinical assessment Increased albumin ratio, indication of increased BBB permeability, correlated with medial temporal lobe atrophy in AD patients. There was no correlation between BBB function and Ab peptides in the CSF.…”

Section: Blood-brain Barriersmentioning

confidence: 99%

Review: Role of developmental inflammation and blood–brain barrier dysfunction in neurodevelopmental and neurodegenerative diseases

Stolp

Dziegielewska

2009

Neuropathology Appl Neurobio

220

161

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The causes of most neurological disorders are not fully understood. Inflammation and blood–brain barrier dysfunction appear to play major roles in the pathology of these diseases. Inflammatory insults that occur during brain development may have widespread effects later in life for a spectrum of neurological disorders. In this review, a new hypothesis suggesting a mechanistic link between inflammation and blood–brain barrier function (integrity), which is universally important in both neurodevelopmental and neurodegerative diseases, is proposed. The role of inflammation and the blood–brain barrier will be discussed in cerebral palsy, schizophrenia, Parkinson's disease, Alzheimer's disease and multiple sclerosis, conditions where both inflammation and blood–brain barrier dysfunction occur either during initiation and/or progression of the disease. We suggest that breakdown of normal blood–brain barrier function resulting in a short‐lasting influx of blood‐born molecules, in particular plasma proteins, may cause local damage, such as reduction of brain white matter observed in some newborn babies, but may also be the mechanism behind some neurodegenerative diseases related to underlying brain damage and long‐term changes in barrier properties.

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Blood-Brain Barrier Permeability Correlates with Medial Temporal Lobe Atrophy but Not with Amyloid-β Protein Transport across the Blood-Brain Barrier in Alzheimer’s Disease

Cited by 35 publications

References 57 publications

Cerebrospinal Fluid/Serum IgG Index Is Correlated with Medial Temporal Lobe Atrophy in Alzheimer’s Disease

Cerebrospinal Fluid/Serum IgG Index Is Correlated with Medial Temporal Lobe Atrophy in Alzheimer’s Disease

miR-285– Yki/Mask double-negative feedback loop mediates blood–brain barrier integrity in Drosophila

Review: Role of developmental inflammation and blood–brain barrier dysfunction in neurodevelopmental and neurodegenerative diseases

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