Blood-Cerebrospinal Fluid Barrier Dysfunction for High Molecular Weight Proteins in Alzheimer Disease and Major Depression

Hampel, Harald; Kotter, H. U.; Möller, H.-J.

doi:10.1097/00002093-199706000-00004

Cited by 59 publications

(33 citation statements)

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“…The relationship of plasma arginase to brain arginase activity remains unclear. However, this decrease in plasma arginase activity may be the reflection of reduced CNS arginase activity [28]. Since all the groups were medically healthy, it seems possible that the altered activity of the arginine-NO pathway in our patients may reflect a disorder in the CNS.…”

Section: Discussionmentioning

confidence: 83%

Is the Arginine-Nitric Oxide Pathway Involved in the Pathogenesis of Schizophrenia?

Yanik¹,

Vural

Koçyiğit

et al. 2003

Neuropsychobiology

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The reciprocal regulation of arginase and nitric oxide synthase (NOS) in L-arginine-metabolizing pathways has been demonstrated. There are various evidences of the role of the nitric oxide (NO) in several neuropsychiatric disorders including schizophrenia. However, there is no study which has investigated the role of arginase as an important part of the arginine regulatory system affecting NOS activity in schizophrenia. This study aims to investigate arginase, manganese (Mn) and total nitrite levels (a metabolite of NO) and their relationship to the arginine-NO pathway in patients with schizophrenia. Arginase activities, Mn and total nitrite levels were measured in plasma from 46 patients with schizophrenia and 32 healthy control subjects. Plasma arginase activities and Mn were found to be significantly lower and total nitrite level higher in patients with schizophrenia compared with controls. Our results suggest that the arginine-NO pathway is involved in the pathogenesis of schizophrenia.

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Section: Discussionmentioning

confidence: 83%

Is the Arginine-Nitric Oxide Pathway Involved in the Pathogenesis of Schizophrenia?

Yanik¹,

Vural

Koçyiğit

et al. 2003

Neuropsychobiology

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“…Another possibility is an increase of sPLA2 synthesis/secretion from the choroidal epithelium which in turn is involved in the BCB breakdown process. Corroborating this hypothesis, Hampel H. et al proposed that an altered BCB function in neurodegenerative disorders may result from immune mediated events initiated, for example by increased levels of circulating inflammatory mediators [12]. In return, these inflammatory cytokines can induce the secretory PLA2 expression [26] followed by an increase of arachidonic acid synthesis.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid secretory Ca2+-dependent phospholipase A2 activity: A biomarker of blood–cerebrospinal fluid barrier permeability

Chalbot

Zetterberg

Blennow

et al. 2010

Neuroscience Letters

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The blood-brain barrier, the blood-cerebrospinal fluid barrier (BCB) and other specialized brain barriers are increasingly recognized as a major obstacle to the treatment of most brain disorders. The impairment of these barriers has been implicated in neuropathology of several diseases, such as autism, ischemia, multiple sclerosis and Alzheimer disease. This dual function of the blood-neural barriers points out the importance and need for the development of techniques that can evaluate the nature and level of their integrity. Here we report the discovery of CSF secretory Ca 2+ -dependent phospholipase A2 (sPLA2) activity as a measure of BCB permeability. Lumbar CSF from BCBimpaired (n=26), multiple sclerosis (n=18) and healthy control (n=32) cases was analyzed using both a newly developed continuous fluorescence assay for CSF sPLA2 activity and CSF/Serum albumin ratio (Q Alb ), the most common and established method to evaluate BCB permeability. While both measurements showed no significant differences between multiple sclerosis and age-matched normal healthy cases, they were highly correlated. Though the CSF sPLA2 activity and Q Alb had over 95 % agreement, the former was found to be more sensitive than the latter in measuring low levels of BCB impairment.

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“…This assumption is supported by studies showing reduced volumes [6,7], and diminished densities of glial cells [8,21,22] in several brain regions in mood disorders. Further, the blood-brain barrier is disrupted in depression as measured with the cerebrospinal fluid/serum ratio for albumin [23]. Because astrocytes induce and maintain the proper function of the blood-brain barrier [24,25], injury of astrocytes may lead to its disruption.…”

Section: Discussionmentioning

confidence: 99%

S100B is increased in mood disorders and may be reduced by antidepressive treatment

Abdul-Khaliq²,

et al. 2002

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Previous studies have reported alterations of glial cells and particularly astrocytes in mood disorders. Therefore, serum concentration of the astrocytic marker S100B was ascertained with an immunoluminometric assay in 20 patients with mood disorder and 12 healthy age-matched controls. Serum S100B was elevated in major depression (median after admission 410 ng/l, at discharge o 100 ng/l) and mania (130,160 ng/l), when compared with controls (o 100 ng/l; p o 0.01). Antidepressive treatment reduced S100B in conjunction with severity of depressive symptoms (p o 0.01). The severity of depression (Hamilton Depression Rating Scale) was positively correlated with S100B (r s ¼ 0.51, p o 0.005). Elevated serum S100B during depressive and manic episodes of mood disorders may indicate alterations of astrocytes, which are reversed by antidepressive treatment. NeuroReport 13:1675^1678

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Blood-Cerebrospinal Fluid Barrier Dysfunction for High Molecular Weight Proteins in Alzheimer Disease and Major Depression

Cited by 59 publications

References 0 publications

Is the Arginine-Nitric Oxide Pathway Involved in the Pathogenesis of Schizophrenia?

Is the Arginine-Nitric Oxide Pathway Involved in the Pathogenesis of Schizophrenia?

Cerebrospinal fluid secretory Ca2+-dependent phospholipase A2 activity: A biomarker of blood–cerebrospinal fluid barrier permeability

S100B is increased in mood disorders and may be reduced by antidepressive treatment

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