Corpus ID: 89287063

Glucose-6-phosphate dehydrogenase deficiency: A possible risk factor for neurodegeneration associated with aging and amphetamine use

  title={Glucose-6-phosphate dehydrogenase deficiency: A possible risk factor for neurodegeneration associated with aging and amphetamine use},
  author={Margaret M. Loniewska},
Glucose-6-phosphate dehydrogenase (G6PD) regenerates the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), which is important for reactive oxygen species (ROS) detoxification. ROS have been implicated in the development of neurodegenerative diseases in aging as well as the neurotoxic effects of amphetamine analogs. Using a mutant G6PD-deficient mouse model, we investigated the potential neuroprotective role of G6PD in aging-related and amphetamine-initiated neurotoxicity… Expand


Increased neuronal glucose-6-phosphate dehydrogenase and sulfhydryl levels indicate reductive compensation to oxidative stress in Alzheimer disease.
An upregulation of glucose-6-phosphate dehydrogenase together with increased sulfhydryls in Alzheimer disease is found, indicating that reductive compensation may play an important role in combating oxidative stress in dementia. Expand
Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease.
The limited available data indicate a complex interplay in which adverse effects of G6PD deficiency may outweigh potential protective effects in the face of cardiac stress, and definitive clinical studies in large populations are needed. Expand
Neuroprotection by Transgenic Expression of Glucose-6-Phosphate Dehydrogenase in Dopaminergic Nigrostriatal Neurons of Mice
Analysis of DNS neurons by histological, neurochemical, and functional methods showed that even a moderate increase of G6PD activity rendered transgenic mice more resistant than control littermates to the toxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Expand
Brain glucose-6-phosphate dehydrogenase protects against endogenous oxidative DNA damage and neurodegeneration in aged mice.
G6PD is important in protecting against the neurodegenerative effects of endogenous ROS in aging, and it is suggested that common hereditary G6PD deficiencies may constitute a risk factor for some neurodegenersative diseases. Expand
Glucose 6-Phosphate Dehydrogenase Deficiency Increases Redox Stress and Moderately Accelerates the Development of Heart Failure
Contrary to the hypothesis, G6PD deficiency increased redox stress in response to infarction or pressure overload, and was found only a modest acceleration of left ventricular remodeling, suggesting that the risk for developing heart failure is higher but limited by compensatory mechanisms. Expand
X-linked glucose-6-phosphate dehydrogenase deficiency inMus musculus
A mouse with X-linked glucose-6-phosphate dehydrogenase (G6PD) deficiency has been recovered in offspring of 1-ethyl-1-nitrosourea-treated male mice and is presently the only animal model for X- linked G6PD deficiency in humans. Expand
Reduced DNA oxidation in aged prostaglandin H synthase-1 knockout mice.
Results suggest that PHS-1-dependent accumulation of oxidatively damaged macromolecules including DNA may contribute to the mechanisms and risk factors of aging-related neurodegeneration. Expand
Dehydroepiandrosterone, glucose-6-phosphate dehydrogenase, and longevity
Both in vitro and in vivo experimental studies strongly indicate that DHEA and related steroids inhibit inflammation and associated epithelial hyperplasia, carcinogenesis, and atherosclerosis, at least in part, through the inhibition of G6PDH and oxygen-free radical formation. Expand
Glucose-6-phosphate dehydrogenase deficiency.
The three-dimensional structure of G6PD shows a classical dinucleotide binding domain and a novel beta + alpha domain involved in dimerization, which indicates that single amino acid substitutions are a major cause of deficiency. Expand
Mesencephalic and striatal protein profiles in mice over-expressing glucose-6-phosphate dehydrogenase in dopaminergic neurons.
The changes in the nigrostriatal protein profile could partially explain the protection against MPTP-induced neuronal damage, and could also lead to new potential targets for antioxidant pharmacological intervention. Expand