Vitamin B12, folic acid, and the nervous system

Reynolds, E. H.

doi:10.1016/s1474-4422(06)70598-1

Cited by 687 publications

(501 citation statements)

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“…Folic acid deficiency is well known for its role in learning and memory [56]. In the present study, we found that a FADD together with hypoperfusion induced impairments in spatial learning on the MWM only in Ung−/− mice.…”

Section: Discussionsupporting

confidence: 61%

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Jadavji

Farr

Lips

et al. 2015

Behavioural Brain Research

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(2015) Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment. Behavioural Brain Research, 283 . pp. 215-226. ISSN 1872-7549 Access from the University of Nottingham repository: http://eprints.nottingham.ac.uk/32983/9/UNG_FADD_20140826_manuscript_final.pdf Copyright and reuse:The Nottingham ePrints service makes this work by researchers of the University of Nottingham available open access under the following conditions. This article is made available under the Creative Commons Attribution Non-commercial No Derivatives licence and may be reused according to the conditions of the licence. For more details see: http://creativecommons.org/licenses/by-nc-nd/2.5/ A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription.For more information, please contact eprints@nottingham.ac.uk Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment. ABSTRACTDietary deficiencies in folic acid result in elevated levels of plasma homocysteine, which has been associated with the development of dementia and other neurodegenerative disorders.Previously, we have shown that elevated levels of plasma homocysteine in mice deficient for a DNA repair enzyme, uracil-DNA glycosylase (UNG), result in neurodegeneration. The goal of this study was to evaluate how deficiencies in folic acid and UNG along with elevated levels of homocysteine affect vascular cognitive impairment, via chronic hypoperfusion in an animal model. Ung+/+ and Ung−/− mice were placed on either control (CD) or folic acid deficient (FADD) diets. Six weeks later, the mice either underwent implantation of microcoils around both common carotid arteries. Post-operatively, behavioral tests began at 3-weeks, angiography was measured after 5-weeks using MRI to assess vasculature and at completion of study plasma and brain tissue was collected for analysis. Learning impairments in the Morris water maze (MWM) were observed only in hypoperfused Ung−/− FADD mice and these mice had significantly higher plasma homocysteine concentrations. Interestingly, Ung+/+ FADD produced significant remodeling of the basilar artery and arterial vasculature. Increased expression of GFAP was observed in the dentate gyrus of Ung−/− hypoperfused and FADD sham mice. Chronic hypoperfusion resulted in increased cortical MMP-9 protein levels of FADD hypoperfused mice regardless of genotypes. These results suggest that elevated levels of homocysteine only, as a result of dietary folic acid deficiency, don't lead to memory impairments and neurobiochemical changes. Rather a combination of either chronic hypoperfusion o...

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Section: Discussionsupporting

confidence: 61%

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Jadavji

Farr

Lips

et al. 2015

Behavioural Brain Research

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“…More than 15 mmol/l of Hcy in blood is clinically hyperhomocysteinemia (Maron and Loscalzo, 2009). This condition, arising mostly due to deficiency in the cofactor vitamins along with genotype of the individual, is considered as a risk factor in various disease conditions, such as neural tube defects, cardio-vascular disorders and neuronal disorders (Refsum et al, 2004;Reynolds, 2006;Harshman and Aldoori, 2008;Selhub, 2008;Li et al, 2009;Greene et al, 2009). A better regime of B12 and folic acid is often helpful to counter the levels of hyperhomocysteinemia (hypHcy) (Bronstrup et al, 1998;Kluijtmans et al, 2003;Konstantinova et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Association of MTHFR and RFC1 gene polymorphism with hyperhomocysteinemia and its modulation by vitamin B12 and folic acid in an Indian population

Sukla

Raman

2011

Eur J Clin Nutr

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Background/Objectives: Unlike most Western populations, MTHFR 677T is a rare allele and a risk factor for a variety of disorders in India. What kind of nutritional (environmental) and/or genetic factors could contribute to the genetic risk is not known. To assess the incidence of hyperhomocysteinemia and its correlation with the polymorphism in homocysteine (Hcy)-pathway genes and associated cofactors in the native populations of eastern India. Subjects/Methods: Healthy population from four eastern states of India. Genotyping of SNPs, HPLC and chemiluminescencebased assay for homocysteine, vitamin B12 and folic acid.Results: Approximately 30% of the population has hyperhomocysteinemia (415 mmol/lit; hypHcy) with varying frequencies in the four states from where samples were collected (n ¼ 1426). Polymorphisms of MTR and CBS do not affect hypHcy. 677T and 1298C alleles of MTHFR and G80 RFC-1 show association with hypHcy. In contrast, RFC-1 80AA is protective even in presence of 677T MTHFR. Addition of each mutant allele has an additive effect on Hcy level. Vitamin B12 (cofactor in methionine synthesis) clearly modulates the genotypic effect on Hcy level. Although frequency of individuals with low folic acid is B11, 49% of the population is vitamin B12 deficient (o220 pg/lit) and has a significant negative correlation with Hcy. Individuals with optimum vitamin B12 and folic acid generally have low Hcy, even in risk genotypes. Conclusions: One of the plausible reasons for susceptibility of individuals with MTHFR C677T in the studied population to various disorders is the high frequency of hyperhomocysteinemia and vitamin B12 deficiency in the 'healthy population'. Apparently, supplementation of vitamin B 12 to this health-impoverished community may help lessen the risk of several multifactorial disorders.

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“…B12D can cause nerve damage, spinal cord degeneration as well as serious anemia [21]. In terms of B12DN, B12D induces the damage of the myelin sheath surrounding and protecting nerves.…”

Section: Vitamin B12 Deficiency Neuropathymentioning

confidence: 99%

“…First of all, careful neurological exam is essential to check if the patients have B12DN and other neurological manifestations [21]. To clarify nerve damage due to B12D, nerve conduction velocity test and electromyography must follow.…”

Section: Vitamin B12 Deficiency Neuropathymentioning

confidence: 99%

Overview of symptoms, pathogenesis, diagnosis, treatment, and prognosis of various acquired polyneuropathies

Koh

2017

Hanyang Med Rev

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Vitamin B12, folic acid, and the nervous system

Cited by 687 publications

References 125 publications

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Association of MTHFR and RFC1 gene polymorphism with hyperhomocysteinemia and its modulation by vitamin B12 and folic acid in an Indian population

Overview of symptoms, pathogenesis, diagnosis, treatment, and prognosis of various acquired polyneuropathies

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