Effects of Dietary Folic Acid on the Expression of Myelin Basic Protein in the Brain and Spinal Cord of Pregnant and Lactating Rats

Lee, Ji Hye; Lee, Yo A.; Oh, Ki-Won; Chang, Namsoo

doi:10.1159/000275945

Cited by 7 publications

(4 citation statements)

References 65 publications

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“…Folate functions, along with vitamin B12, as a one-carbon methyl donor. The lack of these methylation reactions reduces the synthesis of nucleotides and may affect other important regulators of neuronal function such as myelin basic protein [2][3][4]. In cases where there is a high index of suspicion for SCD, folate, copper, and zinc levels should be checked alongside vitamin B12.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin B12 plays an integral role in DNA synthesis and fatty chain metabolism, which are required for neuronal myelin synthesis and maintenance. Decreased levels contribute to the interruption of methylmalonyl-CoA mutase, which is an important enzyme necessary for myelin synthesis [2][3][4]. In rare cases, clinical vitamin B12 deficiency can persist despite normal measured levels.…”

Section: Introductionmentioning

confidence: 99%

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A Rare Case of Folate Deficiency-Induced Subacute Combined Degeneration of the Spinal Cord: A Case Report

Guntupalli,

Lurie,

Stoll

et al. 2023

Cureus

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Folate deficiency is a rare cause of subacute combined degeneration (SCD). SCD is characterized by demyelination of the dorsal and lateral columns of the cervical and thoracic spine most commonly caused by vitamin B12 deficiency. Folate deficiency, which can be clinically indistinguishable from B12 deficiency, leads to a variety of presentations, including absent vibratory sensation and proprioception, sensory ataxia, and progressive motor weakness. Recognizing the clinical sequelae of SCD is essential for timely diagnosis and treatment. We present a case of a 38-year-old male with progressive ascending bilateral lower extremity numbness and motor weakness in the presence of normal vitamin B12 and methylmalonic acid levels. MRI of the entire neuraxis revealed a diagnosis of SCD, which was managed with oral folate replacement. We aim to highlight this rare cause of SCD, which can lead to permanent neurological deficits if not promptly recognized and treated.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Rare Case of Folate Deficiency-Induced Subacute Combined Degeneration of the Spinal Cord: A Case Report

Guntupalli,

Lurie,

Stoll

et al. 2023

Cureus

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“…Recent studies indicate that presenilin-1 mutation increases the vulnerability of oligodendrocytes to folate deficiency in vitro 46 , and that folate deficiency has no effects on MBP expression in the maternal brain and spinal cord 47 . Here our present study provides evidence that folate deficiency by low dietary folate during pregnancy and lactation causes defects in oligodendrocyte development and myelination.…”

Section: Discussionmentioning

confidence: 99%

Folate Metabolism Regulates Oligodendrocyte Survival and Differentiation by Modulating AMPKα Activity

Weng

Wang

et al. 2017

Sci Rep

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Folate, an essential micronutrient, is a critical cofactor in one-carbon metabolism for many cellular pathways including DNA synthesis, metabolism and maintenance. Folate deficiency has been associated with an increased risk of neurological disease, cancer and cognitive dysfunction. Dihydrofolate reductase (DHFR) is a key enzyme to regulate folate metabolism, however folate/DHFR activity in oligodendrocyte development has not been fully understood. Here we show that folate enhances oligodendrocyte maturation both in vitro and in vivo, which is accompanied with upregulation of oligodendrocyte-specific DHFR expression. On the other hand, pharmacological inhibition of DHFR by methotrexate (MTX) causes severe defects in oligodendrocyte survival and differentiation, which could be reversed by folate intake. We further demonstrate that folate activates a metabolic regulator AMPKα to promote oligodendrocyte survival and differentiation. Moreover, activation of AMPKα partially rescues oligodendrocyte defects caused by DHFR-inhibition both in vitro and in vivo. Taken together, these findings identify a previously uncharacterized role of folate/DHFR/AMPKα axis in regulating oligodendrocyte survival and myelination during CNS development.

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“…GGH, a critical enzyme in maintaining folate homeostasis through catalyzing hydrolysis, acts as the most important variable to differentiate MOG patients from HCs. It has been demonstrated that folate intake during pregnancy is important in myelin maintenance [31]. CTSF is also among the top five most important variables listed to discriminate patients.…”

Section: Modulation In the Proteome Pattern In The Csf Of Mogad Patie...mentioning

confidence: 99%

Proteomic profiling of cerebrospinal fluid in pediatric myelin oligodendrocyte glycoprotein antibody-associated disease

et al. 2022

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Background Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an autoimmune demyelinating disorder of the central nervous system. Methods Extracted proteins from 34 cerebrospinal fluid (CSF) samples [patients with MOGAD (MOG group, n = 12); healthy controls (HC group, n = 12); patients with MOG seronegative and metagenomics next-generation sequencing-negative inflammatory neurological diseases (IND group, n = 10)] were processed and subjected to label-free quantitative proteomics. Supervised partial least squares-discriminant analysis (PLS-DA) and orthogonal PLS-DA (O-PLS-DA) models were also performed based on proteomics data. Functional analysis of differentially expressed proteins (DEPs) was performed using Gene Ontology, InterPro, and Kyoto Encyclopedia Genes and Genomes. An enzyme-linked immunosorbent assay was used to determine the complement levels in serum from patients with MOGAD. Results Four hundred and twenty-nine DEPs (149 upregulated and 280 downregulated proteins) were identified in the MOG group compared to the HC group according to the P value and fold change (FC). Using the O-PLS-DA model, 872 differentially abundant proteins were identified with variable importance projection (VIP) scores > 1. Five proteins (gamma-glutamyl hydrolase, cathepsin F, interalpha-trypsin inhibitor heavy chain 5, latent transforming growth factor beta-binding protein 4 and leukocyte-associated immunoglobulin-like receptor 1) overlapping between the top 30 DEPs with top-ranked P value and FC and top 30 proteins in PLS-DA VIP lists were acquired. Functional analysis revealed that the dysregulated proteins in the MOG group were primarily involved in complement and coagulation cascades, cell adhesion, axon guidance, and glycosphingolipid biosynthesis compared to the HC group. Conclusion The proteomic alterations in CSF samples from children with MOGAD identified in the current study might provide opportunities for developing novel biomarker candidates.

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Effects of Dietary Folic Acid on the Expression of Myelin Basic Protein in the Brain and Spinal Cord of Pregnant and Lactating Rats

Cited by 7 publications

References 65 publications

A Rare Case of Folate Deficiency-Induced Subacute Combined Degeneration of the Spinal Cord: A Case Report

A Rare Case of Folate Deficiency-Induced Subacute Combined Degeneration of the Spinal Cord: A Case Report

Folate Metabolism Regulates Oligodendrocyte Survival and Differentiation by Modulating AMPKα Activity

Proteomic profiling of cerebrospinal fluid in pediatric myelin oligodendrocyte glycoprotein antibody-associated disease

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