Possible role of 1-methylnicotinamide in the pathogenesis of Parkinson's disease

Fukushima, Tetsuhito; Kaetsu, Akihiko; Lim, Heejin; Moriyama, Masaki

doi:10.1078/0940-2993-00214

Cited by 37 publications

(32 citation statements)

References 19 publications

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“…[48][49][50] NMND has been shown to have N-methylated pyridines-like dopaminergic toxicity. 51 NMND has also been demonstrated to destroy cerebral complex 1 subunits 52 and complex 1 deficiency plays a role in the pathogenesis of Parkinson's disease. [53][54][55] The changes in urinary 2PY, NMNA and NMND observed in the current study suggested possible perturbation of tryptophannicotinic acid metabolism in autistic individuals.…”

Section: Endogenous Biochemical Differences In Autismmentioning

confidence: 99%

Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls

et al. 2010

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Autism is an early-onset developmental disorder with a severe life-long impact on behavior and social functioning that has associated metabolic abnormalities. The urinary metabolic phenotypes of individuals (age range=3-9 years old) diagnosed with autism using the DSM-IV-TR criteria (n=39; male=35; female=4), together with their non-autistic siblings (n=28; male=14; female=14) and age-matched healthy volunteers (n=34, male=17; female=17) have been characterized for the first time using Additionally, metabolic phenotype (metabotype) differences were observed between autistic and control children, which were associated with perturbations in the relative patterns of urinary mammalian-microbial co-metabolites including dimethylamine, hippurate and phenyacetylglutamine. These biochemical changes are consistent with the known abnormalities of gut microbiota found in autistic individuals and the associated gastrointestinal dysfunction and may be of value in monitoring the success of therapeutic interventions.3

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Section: Endogenous Biochemical Differences In Autismmentioning

confidence: 99%

Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls

et al. 2010

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“…PD patients had higher levels of NNMT activity and protein in brain tissue than controls 17) . MNA destroyed several subunits of cerebral complex I, especially 30 kDa protein 18) , and MNA injection in rat substantia nigra pars compacta significantly decreased dopamine content in striatum 19) . Therefore, MNA is suspected as an agent causing idiopathic PD.…”

Section: Discussionmentioning

confidence: 99%

Correlations Among Heavy Metals in Blood and Urine and Their Relations to Depressive Symptoms in Parkinson’s Disease Patients

Fukushima

Tan

Luo

et al. 2014

FJMS

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: Objectives : From our previous results, manganese (Mn) and iron (Fe) in the blood of Parkinson's disease (PD) patients without depression were higher than those of both the PD patients with depression and controls, the hypothesis that "two types of PD exist -PD without depression and affected by Mn and Fe, and PD with depression and unaffected by Mn or Fe" was induced. To investigate the hypothesis, correlations among blood and urine metals were compared in the subjects. Methods : Subjects comprised PD patients with depression, PD patients without depression and controls recruited from an outpatient clinic in China. Morning blood and urine samples were used to measure concentrations of metals. Results : In the controls, Mn, Fe and zinc (Zn) levels in blood strongly correlated with each other. The correlation coefficient between Mn and Zn in blood was significant in the PD patients with depression and the controls, but not in the PD patients without depression. Correlations of Fe between blood and urine in the PD patients without depression were significant, but not in the PD patients with depression and the controls. Conclusions : A common route of simultaneous intake of Mn, Fe and Zn could exist in our subjects, however in PD patients without depression, a large intake of Mn may have been from another route. Some results of the PD patients without depression were different from those of the PD patients with depression and the controls. Thus, two types of PD may exist.

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“…A minor metabolite of nicotinamide is N-methylnicotinamide [31], which interacts with complex 1 in mitochondria to produce oxygen radicals and destroy complex 1 [64]. Injection of N-methylnicotinamide into the rodent midbrain decreases striatal dopamine [64]. The formation of Nmethylnicotinamide from nicotinamide in the brain should be examined.…”

Section: Nicotinamidementioning

confidence: 99%

“…The major metabolic product of nicotinamide is NAD, in the brain and other organs [31]. A minor metabolite of nicotinamide is N-methylnicotinamide [31], which interacts with complex 1 in mitochondria to produce oxygen radicals and destroy complex 1 [64]. Injection of N-methylnicotinamide into the rodent midbrain decreases striatal dopamine [64].…”

Section: Nicotinamidementioning

confidence: 99%

Parkinson’s Disease—Apoptosis and Dopamine Oxidation

Adams¹

2012

OJApo

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Tyrosine hydroxylase, monoamine oxidase and aldehyde dehydrogenase all form oxygen radicals as part of their mechanisms of action. These oxygen radicals damage dopaminergic neurons in the substantianigra of the midbrain and cause them to die by a process of necrosis or apoptosis. Oxygen radicals quickly abstract hydrogen from DNA forming DNA radicals and causing DNA fragmentation, activation of DNA protective mechanisms, NAD depletion and cell death. Tyrosine hydroxylase is present in all dopaminergic neurons, is involved in the synthesis of dopamine and forms oxygen radicals in a redox mechanism involving its cofactor, tetrahydrobiopterin. Levodopa is used therapeutically in Parkinson's disease patients since it is a precursor for dopamine, an inhibitor of tyrosine hydroxylase, and prolongs patient's lives. Monoamine oxidase converts dopamine into 3,4-dihydroxyphenylacetaldehyde and forms oxygen radicals.Aldehyde dehydrogenase oxidizes the aldehyde and forms oxygen radicals and 3,4-dihydroxyphenylacetic acid. The treatment of Parkinson's disease should involveinhibitors of oxygen radical formation in dopaminergic neurons and neuroprotective agents that stimulate DNA repair and prevent cell death.

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Possible role of 1-methylnicotinamide in the pathogenesis of Parkinson's disease

Cited by 37 publications

References 19 publications

Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls

Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls

Correlations Among Heavy Metals in Blood and Urine and Their Relations to Depressive Symptoms in Parkinson’s Disease Patients

Parkinson’s Disease—Apoptosis and Dopamine Oxidation

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