Glucose-6-phosphate dehydrogenase deficiency and Alzheimer’s disease: Partners in crime? The hypothesis

Ulusu, Nuriye Nuray

doi:10.1016/j.mehy.2015.05.006

Cited by 34 publications

(26 citation statements)

References 74 publications

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“…The speculated metabolic paradigm shift often occurs in a bid to cater for the excess energy demand in response to neuroinflammation (Missiroli et al, 2020). G6PDH is a rate-limiting enzyme that catalyzes the irreversible conversion of glucose-6-phosphate to 6-phosphogluconolactone in pentose phosphate pathway (Ulusu, 2015;Zhang et al, 2014). Due to the essentiality of the G6PDH in the glycolytic pathway, it's deficiency has been reported to promote oxidative stress, because the reduced nicotinamide adenine dinucleotide phosphate (NADPH) maintained by this enzyme is important in supplying glutathione to cells, for mopping up of excess highly reactive hydroxyl ions (Mejías et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Due to the essentiality of the G6PDH in the glycolytic pathway, it's deficiency has been reported to promote oxidative stress, because the reduced nicotinamide adenine dinucleotide phosphate (NADPH) maintained by this enzyme is important in supplying glutathione to cells, for mopping up of excess highly reactive hydroxyl ions (Mejías et al, 2006). In fact, G6PDH deficiency and AD have colloquially been regarded as "partners in crime" (Ulusu, 2015).…”

Section: Discussionmentioning

confidence: 99%

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Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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Alzheimer's disease is the most common cause of dementia and is hallmarked by β-amyloid plaque and neurofibrillary tangles deposition in the CNS. The complex mechanism that underlies AD pathogenesis has made the development of a definitive cure futile. Exploring the possible therapeutic advantages of combining two neuromodulatory molecules with different mechanisms of neuroprotection is an interesting way of drug discovery. Ascorbic acid (AA), a potent antioxidant molecule, and nicotine (NIC), an allosteric modulator of nAChRs, have both been documented to independently proffer neuroprotection in experimental and clinical neurodegenerative cases. This study elucidated the putative therapeutic advantages of combining ascorbic acid and nicotine as a treatment regimen against the aluminium induced anxiety, corticohippocampal histopathology and perturbed neuroenergetics in rats induced with Alzheimer-like neuropathology Rats treated with 100 mg/kg aluminium chloride for 28 days presented with significantly increased stretch attend posture frequency and centre square entry. Aluminium significantly depleted the activities of G6PDH while increasing lactate levels. Corticohippocampal histomorphology of these animals showed poor histoarchitecture, increased congophilic and argentophilic densities that were coupled with increased anti-NSE immunopositivity. Animals post-treated with NIC (10mg/kg) and AA (100mg/kg) for 28 days presented with reduced anxiety level and improved corticohippocampal histomorphology. AA normalized G6PDH and lactate levels while the congophilic density was reduced by NIC. Corticohippocampal argentophilic density anti-NSE immunopositivity were also normalized by AA+NIC. The findings from this study have shown that a combination of ascorbic acid and nicotine effectively mitigated aluminium-induced corticohippocampal neuropathology and perturbed neuroenergetics.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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“…For instance, glucose-6-phosphate dehydrogenase deficiency is the most common human congenital defect of metabolism. It affects a part of the population, and usually shows no signs or symptoms until exposed to certain medications, foods or infections (21). Deficiency of this enzyme does abide by the above criteria to some extent albeit neonatal screening for this enzyme deficiency has been suggested in few researches (27).…”

Section: Discussionmentioning

confidence: 99%

Comparison of Spectrophotometric and Fluorimetric Methods in Evaluation of Biotinidase Deficiency

İşeri-Erten¹,

Dikmen²,

Ulusu³

2016

Journal of Medical Biochemistry

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SummaryBackgroundBiotin, a water-soluble vitamin, is used as a co-factor by enzymes involved in carboxylation reactions. Biotinidase (BTD) catalyzes the recycling of biotin from endogenous and dietary sources. Biotinidase deficiency (BD) is an autosomal recessively inherited disorder of biotin recycling that is associated with neurologic and cutaneous consequences when untreated. The aim of the study was to compare the results of spectrophotometric and fluorimetric methods, as well as to evaluate the advantages and disadvantages of both methods in current research practices.MethodsStudy group was chosen among the BD suspected newborn, children and parents (n = 52) who applied to Hacettepe University Pediatric Metabolism Unit.ResultsBTD activity is stable for 2 hours at room temperature and at 4 °C, and for 4 months at –20 °C and –80 °C. Genetic and clinical results showed that 25% of the total number of patients had complete BD which was treated with 10 mg/day biotin, while 15.38% of the patients had partial BD, and they were prescribed biotin 5 mg/day. The area under the ROC curve was 0.960±0.25 and 0.927± 0.41 for the fluorimetric and spectrophotometric method, respectively. Fluorimetric method showed 100% sensitivity and 97% specificity, whereas spectrophotometric method showed 90.5% sensitivity and 93.7% specificity.ConclusionsFluorimetric method is superior to the spectrophotometric method due to higher sensitivity and specificity.

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“…Besides COVID-19 deaths in the elderly population and people with chronic diseases, 0.9% of deaths by COVID-19 have had no any confirmed chronic conditions [1]. One health condition that could be increasing mortality risk in the COVID-19 infected people is glucose-6 phosphate dehydrogenase (G6PD) enzyme deficiency, which is the most common enzyme deficiency worldwide affecting more than 400 million people and causes a variety of diseases [2]. Wu et al reported that G6PD deficiency cells were infected with Human coronavirus (HCoV) 229E in a higher rate compared to normal cells.…”

Section: Pathogens and Global Healthmentioning

confidence: 99%

“…Previous studies have confirmed that virus infection induces production of both reactive oxygen species (ROS) and reactive nitrogen species (RNS), both can damage proteins, DNA and cellular components of cells when antioxidant enzyme metabolism is impaired. Since G6PD deficiency results in the redox imbalance in the erythrocytes leading to hemolysis and tissue damage as a result of insufficient oxygen transportation, COVID-19 might increase the mortality risk of patients with G6PD deficiency [2][3][4][5].…”

Section: Pathogens and Global Healthmentioning

confidence: 99%

Is glucose-6-phosphate dehydrogenase enzyme deficiency a factor in Coronavirus-19 (COVID-19) infections and deaths?

Aydemir

Ulusu

2020

Pathogens and Global Health

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Glucose-6-phosphate dehydrogenase deficiency and Alzheimer’s disease: Partners in crime? The hypothesis

Cited by 34 publications

References 74 publications

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Comparison of Spectrophotometric and Fluorimetric Methods in Evaluation of Biotinidase Deficiency

Is glucose-6-phosphate dehydrogenase enzyme deficiency a factor in Coronavirus-19 (COVID-19) infections and deaths?

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