Concentrations of the water-soluble vitamins thiamin, ascorbic acid, and folic acid in serum and cerebrospinal fluid of healthy individuals

Tallaksen, Chantal; Bøhmer, Thomas; Bell, H.

doi:10.1093/ajcn/56.3.559

Cited by 49 publications

(22 citation statements)

References 20 publications

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“…1 when serum folate achieves high values ( 1 35 nmol/l). Among all 205 consecutive subjects, the lowest value of the R CSF/S was 0.0495 and the mean value of the folate gradient R CSF/S was 2.13 8 0.93, in agreement with previous study results [18,20,21] .…”

Section: Resultssupporting

confidence: 92%

“…It seems reasonable to presume that lack of folate can cause cerebral lesions also in adults [17] . There are a few other studies that have dealt with the concentration of folate in CSF [10,[18][19][20][21] and a few earlier works concerning the relation between CSF folate and dementia [22][23][24] . Shaw et al [22] found that CSF folate did not rise as serum folate did when severely demented, folate-deficient patients were substituted with folate, nor was there any clinical effect of the folate treatment.…”

Section: Csf/serum Folate Gradient In Different Dementiasmentioning

confidence: 99%

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CSF/Serum Folate Gradient: Physiology and Determinants with Special Reference to Dementia

Hagnelius

Wahlund

Nilsson

2008

Dement Geriatr Cogn Disord

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Background: Folate depletion has been implicated as a risk factor for neurodegenerative disorders. We hypothesized that transport of folate to the cerebrospinal fluid (CSF) compartment could be involved in the pathophysiology of these disorders. Methods: The CSF/serum folate gradient (R_CSF/S) was studied in 205 subjects with suspected cognitive disorder. Its relation to clinical and biochemical indices, including the integrity of the blood-CSF barrier, were characterized. Results: In subjects who were diagnosed as nondemented (ND) the mean R_CSF/S± SD was 2.46 ± 0.62 versus 2.09 ± 0.67 (p = 0.008) in the dementia subgroup with a vascular component (VaD + mixed). The ND subgroup had higher CSF folate (p = 0.001) and lower serum homocysteine values (p = 0.001) than the VaD + mixed subgroup. The folate gradient R_CSF/S was negatively correlated with serum folate (p < 0.001, R² = 0.518) and to the albumin ratio, a blood-CSF barrier biomarker (β = –0.235). The Alzheimer patients had R_CSF/S and albumin ratios similar to the ND subjects. Conclusion: The R_CSF/S was significantly lower in the VaD + mixed dementia subgroup, suggestive of a defect in the transport of folate over the choroid plexus that seems to be characteristic of, and limited to, the VaD + mixed dementia subgroup.

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Section: Resultssupporting

confidence: 92%

Section: Csf/serum Folate Gradient In Different Dementiasmentioning

confidence: 99%

CSF/Serum Folate Gradient: Physiology and Determinants with Special Reference to Dementia

Hagnelius

Wahlund

Nilsson

2008

Dement Geriatr Cogn Disord

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“…Of NAALADase's known substrates, only NAAG, ␥-glutamylglutamate, and folates have been detected in neural tissue, and the apparent affinity of ␥-glutamylglutamate for NAALADase and concentrations of folates in the extracellular space of the central nervous system are considerably lower than those of NAAG (1,20,47,48). NAALADase's regional and developmental expression in brain correlate with levels of NAAG, suggesting that the two are functionally related (8,21,49).…”

Section: Discussionmentioning

confidence: 99%

Isolation and expression of a rat brain cDNA encoding glutamate carboxypeptidase II

Lüthi-Carter

Berger

Barczak

et al. 1998

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

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“…[22][23][24][25] Plasma and tissue levels of total nitrite (NO 2 Ϫ ) plus nitrate (NO 3 Ϫ ), known as NOx, were measured by HPLC after reduction of total NOx to NO 2 Ϫ , as described previously. 26 Plasma levels of asymmetrical dimethyl arginine (ADMA), an endogenous NOS inhibitor, were determined by using HPLC as described previously.…”

Section: Plasma and Tissue Biochemical Measurementsmentioning

confidence: 99%

Hyperhomocysteinemia Impairs Angiogenesis in Response to Hindlimb Ischemia

Duan

Murohara

Ikeda

et al. 2000

ATVB

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Abstract-Hyperhomocysteinemia (HH) is an independent risk factor for atherosclerosis, including peripheral arterial occlusive disease (PAOD). Because angiogenesis and collateral vessel formation are important self-salvage mechanisms for ischemic PAOD, we examined whether HH modulates angiogenesis in vivo in a rat model of hindlimb ischemia. Rats were divided into 3 groups: the control group was given tap water, the HH group was given water containing, and the HHϩL-arg group was given water containing methionine (1 g ⅐ kg [1][2][3][4][5] Moreover, it has been established that modest HH occurs in up to 40% of patients with stroke, myocardial infarction, and/or peripheral arterial obstructive disease (PAOD). 1,6 HH may exert multiple adverse effects on cells composing the vascular wall. In particular, homocysteine induces endothelial dysfunction and thereby accelerates atherosclerosis. 7,8 Light-and electron-microscopic studies of arteries and arterioles from humans and animals have revealed that HH alters endothelial morphology. 5,7,9 HH has also been shown to attenuate endothelium-dependent vasodilatation, 8,10,11 presumably because of the inactivation of endothelium-derived NO (EDNO). 8 In addition, HH has been shown to produce oxygenderived free radicals that further inactivate EDNO. 12,13 We and others have recently reported that EDNO is an important endogenous modulator of angiogenesis. 14 -17 For example, angiogenesis induced by substance P, an endothelium-dependent vasodilator, 14 or vascular endothelial growth factor, 15,16 a potent angiogenic cytokine, was significantly attenuated by inhibitors of NO synthase (NOS). More recently, we showed that angiogenesis occurring after surgically induced hindlimb ischemia was severely impaired in mice lacking the gene for the endothelial constitutive NOS. 17 Although such adverse effects of HH on endothelial cells (ECs) have been documented in numerous studies, the effects of HH on angiogenesis and collateral vessel formation in response to tissue ischemia have not been examined as yet. This issue is clinically relevant inasmuch as HH is an independent risk factor for PAOD. In patients with PAOD, regional angiogenesis and collateral vessel formation from surrounding tissues are critical self-defense mechanisms for tissue survival. 18 Accordingly, we investigated the effects of HH on angiogenesis, collateral vessel formation, and regional blood flow in a rat model of surgically induced hindlimb ischemia. We also investigated whether oral supplementation of L-arginine, a substrate for NOS, had favorable effects on a potential HH-mediated impairment of angiogenesis.

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Concentrations of the water-soluble vitamins thiamin, ascorbic acid, and folic acid in serum and cerebrospinal fluid of healthy individuals

Cited by 49 publications

References 20 publications

CSF/Serum Folate Gradient: Physiology and Determinants with Special Reference to Dementia

CSF/Serum Folate Gradient: Physiology and Determinants with Special Reference to Dementia

Isolation and expression of a rat brain cDNA encoding glutamate carboxypeptidase II

Hyperhomocysteinemia Impairs Angiogenesis in Response to Hindlimb Ischemia

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