Multiple sclerosis and vitamin B12 metabolism

Reynolds, E. H.

doi:10.1016/0165-5728(92)90137-a

Cited by 46 publications

(19 citation statements)

References 22 publications

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“…Detailed association studies of SNPs of ABCD4 found a possible correlation of 5 SNPs with the AMN phenotype, which deserves further investigation [164]. Vitamin B12 is known to play a positive role in myelin protection and its deficiency is associated with neurodegenerative diseases such as multiple sclerosis [351,352]. Vitamin B12 is known to play a positive role in myelin protection and its deficiency is associated with neurodegenerative diseases such as multiple sclerosis [351,352].…”

Section: Modifier Genesmentioning

confidence: 99%

X-linked Adrenoleukodystrophy

Trompier¹,

Savary²

2013

Colloquium Series on the Genetic Basis of Human Disease

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Section: Modifier Genesmentioning

confidence: 99%

X-linked Adrenoleukodystrophy

Trompier¹,

Savary²

2013

Colloquium Series on the Genetic Basis of Human Disease

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“…This makes sense given that NAD is perhaps followed by pyridoxyl phosphate in the shear total number of known reactions requiring these co-factors respectively. Furthermore, it is well known that deficiencies of cobalamin lead to demyelination and such deficiencies have on occasion been observed in MS (reviews [60, 220, 221]). Thus, in order to maintain optimal NAD function it seems ideal to include increased administration of pyridoxyl phosphate and cobalamin.…”

Section: Potential Nad-related Pharmacotherapeutic Strategies For mentioning

confidence: 99%

The Importance of NAD in Multiple Sclerosis

Penberthy¹,

Tsunoda²

2009

CPD

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The etiology of multiple sclerosis (MS) is unknown but it manifests as a chronic inflammatory demyelinating disease in the central nervous system (CNS). During chronic CNS inflammation, nicotinamide adenine dinucleotide (NAD) concentrations are altered by (T helper) Th1-derived cytokines through the coordinated induction of both indoleamine 2,3-dioxygenase (IDO) and the ADP cyclase CD38 in pathogenic microglia and lymphocytes. While IDO activation may keep autoreactive T cells in check, hyper-activation of IDO can leave neuronal CNS cells starving for extracellular sources of NAD. Existing data indicate that glia may serve critical functions as an essential supplier of NAD to neurons during times of stress. Administration of pharmacological doses of non-tryptophan NAD precursors ameliorates pathogenesis in animal models of MS. Animal models of MS involve artificially stimulated autoimmune attack of myelin by experimental autoimmune encephalomyelitis (EAE) or by viral-mediated demyelination using Thieler's murine encephalomyelitis virus (TMEV). The Wld S mouse dramatically resists razor axotomy mediated axonal degeneration. This resistance is due to increased efficiency of NAD biosynthesis that delays stress-induced depletion of axonal NAD and ATP. Although the Wld S genotype protects against EAE pathogenesis, TMEV-mediated pathogenesis is exacerbated. In this review, we contrast the role of NAD in EAE versus TMEV demyelinating pathogenesis to increase our understanding of the pharmacotherapeutic potential of NAD signal transduction pathways. We speculate on the importance of increased SIRT1 activity in both PARP-1 inhibition and the potentially integral role of neuronal CD200 interactions through glial CD200R with induction of IDO in MS pathogenesis. A comprehensive review of immunomodulatory control of NAD biosynthesis and degradation in MS pathogenesis is presented. Distinctive pharmacological approaches designed for NADcomplementation or targeting NAD-centric proteins (SIRT1, SIRT2, PARP-1, GPR109a, and CD38) are outlined towards determining which approach may work best in the context of clinical application.

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“…In previous studies, elevated homocysteine levels were observed in MS patients with vitamin B deficiency (28)(29)(30). In a recent study, elevated homocysteine levels were reported in a total group of 72 MS patients compared to 23 controls (31).…”

Section: Serum Homocysteine In a ''New'' Neurodegenerative Disease: Mmentioning

confidence: 90%

Homocysteine in relation to cognitive performance in pathological and non-pathological conditions

Teunissen¹,

Boxtel²,

Jolles³

et al. 2005

Clinical Chemistry and Laboratory Medicine (CCLM)

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Elevated serum homocysteine has been associated with increased risk of Alzheimer's disease. Furthermore, elevated homocysteine levels are related to cognitive dysfunction in the elderly. The aim of the present study was to explore the disease specificity of the relation between serum total homocysteine levels and cognitive function. For this, we summarize data from several studies on homocysteine levels in both normal and pathological conditions performed in our laboratories and evaluate possible mechanisms of effects of elevated homocysteine levels in the central nervous system. Total homocysteine levels were measured in serum of: 1) healthy aging individuals; 2) patients with Alzheimer's and Parkinson's disease and patients with other cognitive disorders; and 3) patients with multiple sclerosis. Increased serum homocysteine concentration was related to worse cognitive performance over a 6-year period in the normal aging population (r=-0.36 to -0.14, p<0.01 for the Word learning tests; r=0.76, p<0.05 for the Stroop Colored Word test). Homocysteine was only increased in patients with Parkinson's disease on L-Dopa therapy (18.9 vs. 16.5 micromol/L in healthy controls), and not in dementia patients. Homocysteine was elevated in patients with progressive multiple sclerosis (15.0 micromol/L, n=39, compared to 12.0 micromol/L in 45 controls) and correlated to both cognitive and motor function (r=-0.33 and -0.33, p<0.05, respectively). The relationship between homocysteine and cognitive function in non-pathological and pathological situations indicates that changes in its levels may play a role in cognitive functioning in a broad spectrum of conditions.

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Multiple sclerosis and vitamin B12 metabolism

Cited by 46 publications

References 22 publications

X-linked Adrenoleukodystrophy

X-linked Adrenoleukodystrophy

The Importance of NAD in Multiple Sclerosis

Homocysteine in relation to cognitive performance in pathological and non-pathological conditions

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