The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Ulusu N.n. - One of the best experts on this subject based on the ideXlab platform.
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Glucose-6-phosphate dehydrogenase a novel hope on a blood-based diagnosis of Alzheimer’s disease
2017Co-Authors: Evlice A., Ulusu N.n.Abstract:PubMedID: 27378307Alzheimer’s disease (AD) is a multi-factorial neurodegenerative disorder that numerous factors have key properties in the development of this Proteopathy. Glucose-6-phosphate dehydrogenase (G6PD) is the most common form of enzymopathy. We have examined G6PD enzyme activity levels in the serum of newly diagnosed AD patients compared with control subjects without dementia from the both sexes. Serum G6PD levels were found to be significantly higher (approximately two times) in AD patients compared to control geriatric subjects in both sexes. We have concluded that G6PD seems to play an integral role in the progress and/or prevention of AD. © 2016, Belgian Neurological Society
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Evaluation of Renal Function in Alzheimer's Disease and Geriatric Patients: Results from a Turkish Two-Center Study
2017Co-Authors: Erbayraktar Z., Evlice A.t., Yilmaz G., Yazici C., Yener G., Ulusu N.n.Abstract:Background: Alzheimer's disease (AD) is a severe multifactorial neurodegenerative Proteopathy associated with advanced age. Discrepancies in the renal function of these patients compared to geriatric patients with dementia have rarely been reported. In this study, we aimed to disclose the importance of associated renal changes for the pathogenesis of AD. Methods: Patients with AD (n=107) and geriatric patients with dementia and without dementia (n=124) (231 patients in total) from Dokuz Eylul and Cukurova University Hospitals were enrolled in the study. We measured serum Na, K, Cl, Ca, BUN, creatinine, total protein levels and MDRD [eGFR] in all groups. Results: From Izmir Center, the first study arm consisted of patients with AD dementia (n=74), and the second arm included geriatric patients with dementia (n=79). From Adana, 78 patients were recruited to the study, of which 33 were with AD and 45 were geriatric patients without dementia. When we analyzed comparatively the AD and geriatric dementia patients study arms, a statistically significant difference was observed both in the median age (p
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A Turkish 3-center study evaluation of serum folic acid and vitamin B12 levels in Alzheimer disease
2015Co-Authors: Ulusu N.n., Erbayraktar Z., Evlice A.t., Yilmaz G., Yener G., Aras S., Avci A.Abstract:PubMedID: 26738362Background/aim: Alzheimer disease, a common Proteopathy of advanced age, is characterized by cortical atrophy, neuron degeneration, neuronal loss, and accumulation of extracellular amyloid ß plaques. We aimed to investigate serum vitamin B12 and folic acid levels in Alzheimer disease and other dementia patients, as a potential screening test to detect presymptomatic Alzheimer disease in Turkish patients. Materials and methods: We evaluated folic acid and vitamin B12 levels in Alzheimer disease patients as well as in other dementia and geriatric patients from Ankara, Dokuz Eylül, and Çukurova university hospitals; 290 female and male geriatric subjects were enrolled. Vitamin B12 and folic acid levels were measured using Roche E170 and Beckman Coulter DXI 800 immunoassays (chemiluminescence) according to the manufacturers’ guideline in all centers. Results: We evaluated the results of folic acid and vitamin B12 in Alzheimer disease, other dementias and geriatric patients. No significant difference between the groups regarding the routine control of biochemical parameters was observed. Conclusion: Currently, serum folic and vitamin B12 levels are not diagnostically reliable tests for screening presymptomatic Alzheimer disease. However, the results may statistically be significant if we increase the sample size. © TÜBİTAK
Souvik Bhattacharjee - One of the best experts on this subject based on the ideXlab platform.
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remodeling of the malaria parasite and host human red cell by vesicle amplification that induces artemisinin resistance
2018Co-Authors: Alassane Mbengue, Souvik Bhattacharjee, Isabelle Coppens, Niraja Suresh, Mehdi Ghorbal, Zdenek Slouka, Innocent Safeukui, Hsin Yao Tang, David W SpeicherAbstract:Artemisinin resistance threatens world-wide malaria control and elimination. Elevation of phosphatidylinositol-3-phosphate (PI3P) can induce resistance in blood-stages of Plasmodium falciparum. The parasite unfolded protein response (UPR) has also been implicated, as a proteostatic mechanism that may diminish artemisinin-induced toxic Proteopathy. How PI3P acts and its connection to the UPR remain unknown, although both are conferred by mutation in P. falciparum Kelch13 (K13), the marker of artemisinin resistance. Here we used cryo-immunoelectron microscopy to show that K13 concentrates at PI3P-tubules/vesicles of the parasite’s endoplasmic reticulum (ER) in infected red cells. K13 co-localizes and co-purifies with the major virulence adhesin PfEMP1. The PfEMP1-K13 proteome is comprehensively enriched in multiple proteostasis systems of protein export, quality-control and folding in the ER and cytoplasm and UPR. Synthetic elevation of PI3P that induces resistance in absence of K13 mutation also yields signatures of proteostasis and clinical resistance. These findings imply a key role for PI3P-vesicle amplification as a mechanism of resistance of infected red cells. As validation, the major resistance mutation K13C580Y quantitatively increased PI3P-tubules/vesicles, exporting them throughout the parasite and the red cell. Chemical inhibitors and fluorescence microscopy showed that alterations in PfEMP1 export to the red cell and cytoadherence of infected cells to a host endothelial receptor, are features of multiple K13 mutants. Together these data suggest that amplified PI3P-vesicles disseminate widespread proteostatic capacity that may neutralize artemisinins toxic Proteopathy and implicate a role for the host red cell in artemisinin resistance. The mechanistic insights generated will have impact on malaria drug development.
David W Speicher - One of the best experts on this subject based on the ideXlab platform.
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remodeling of the malaria parasite and host human red cell by vesicle amplification that induces artemisinin resistance
2018Co-Authors: Alassane Mbengue, Souvik Bhattacharjee, Isabelle Coppens, Niraja Suresh, Mehdi Ghorbal, Zdenek Slouka, Innocent Safeukui, Hsin Yao Tang, David W SpeicherAbstract:Artemisinin resistance threatens world-wide malaria control and elimination. Elevation of phosphatidylinositol-3-phosphate (PI3P) can induce resistance in blood-stages of Plasmodium falciparum. The parasite unfolded protein response (UPR) has also been implicated, as a proteostatic mechanism that may diminish artemisinin-induced toxic Proteopathy. How PI3P acts and its connection to the UPR remain unknown, although both are conferred by mutation in P. falciparum Kelch13 (K13), the marker of artemisinin resistance. Here we used cryo-immunoelectron microscopy to show that K13 concentrates at PI3P-tubules/vesicles of the parasite’s endoplasmic reticulum (ER) in infected red cells. K13 co-localizes and co-purifies with the major virulence adhesin PfEMP1. The PfEMP1-K13 proteome is comprehensively enriched in multiple proteostasis systems of protein export, quality-control and folding in the ER and cytoplasm and UPR. Synthetic elevation of PI3P that induces resistance in absence of K13 mutation also yields signatures of proteostasis and clinical resistance. These findings imply a key role for PI3P-vesicle amplification as a mechanism of resistance of infected red cells. As validation, the major resistance mutation K13C580Y quantitatively increased PI3P-tubules/vesicles, exporting them throughout the parasite and the red cell. Chemical inhibitors and fluorescence microscopy showed that alterations in PfEMP1 export to the red cell and cytoadherence of infected cells to a host endothelial receptor, are features of multiple K13 mutants. Together these data suggest that amplified PI3P-vesicles disseminate widespread proteostatic capacity that may neutralize artemisinins toxic Proteopathy and implicate a role for the host red cell in artemisinin resistance. The mechanistic insights generated will have impact on malaria drug development.
Jorg Hanrieder - One of the best experts on this subject based on the ideXlab platform.
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maldi imaging delineates hippocampal glycosphingolipid changes associated with neurotoxin induced Proteopathy following neonatal bmaa exposure
2017Co-Authors: Oskar Karlsson, Wojciech Michno, Yusuf Ransome, Jorg HanriederAbstract:The environmental toxin S-N-methylamino-L-alanine (BMAA) has been proposed to contribute to neurodegenerative diseases. We have previously shown that neonatal exposure to BMAA results in dose-dependent cognitive impairments, proteomic alterations and progressive neurodegeneration in the hippocampus of adult rats. A high BMAA dose (460 mg/kg) also induced intracellular fibril formation, increased protein ubiquitination and enrichment of proteins important for lipid transport and metabolism. The aim of this study was therefore to elucidate the role of neuronal lipids in BMAA-induced neurodegeneration. By using matrix assisted laser desorption/ionization imaging mass spectrometry (MALDI IMS), we characterized the spatial lipid profile in the hippocampus of six month-old rats that were treated neonatally (postnatal days 9-10) with 460 mg/kg BMAA. Multivariate statistical analysis revealed long-term changes in distinct ganglioside species (GM, GD, GT) in the dentate gyrus. These changes could be a consequence of direct effects on ganglioside biosynthesis through the b-series (GM3-GD3-GD2-GD1b-GT1b) and may be linked to astrogliosis. Complementary immunohistochemistry experiments towards GFAP and sloop further verified the role of increased astrocyte activity in BMAA-induced brain damage. This highlights the potential of imaging MS for probing chemical changes associated with neuropathological mechanisms in situ. This article is part of a Special Issue entitled: MALDI Imaging, edited by Dr. Corinna Henkel and Prof. Peter Hoffmann. (
Ulusu Nuriye Nuray - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of Renal Function in Alzheimer’s Disease and Geriatric Patients: Results from a Turkish Two-Center Study
2017Co-Authors: Erbayraktar Zubeyde, Evlice Ahmet Turan, Yilmaz Gokhan, Yazici Canan, Yener Gorsev, Ulusu Nuriye NurayAbstract:Background: Alzheimer’s disease (AD) is a severe multifactorial neurodegenerative Proteopathy associated with advanced age. Discrepancies in the renal function of these patients compared to geriatric patients with dementia have rarely been reported. In this study, we aimed to disclose the importance of associated renal changes for the pathogenesis of AD
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Glucose-6-phosphate dehydrogenase a novel hope on a blood-based diagnosis of Alzheimer's disease
2017Co-Authors: Evlice Ahmet, Ulusu Nuriye NurayAbstract:WOS: 000394999100030PubMed ID: 27378307Alzheimer's disease (AD) is a multi-factorial neurodegenerative disorder that numerous factors have key properties in the development of this Proteopathy. Glucose-6-phosphate dehydrogenase (G6PD) is the most common form of enzymopathy. We have examined G6PD enzyme activity levels in the serum of newly diagnosed AD patients compared with control subjects without dementia from the both sexes. Serum G6PD levels were found to be significantly higher (approximately two times) in AD patients compared to control geriatric subjects in both sexes. We have concluded that G6PD seems to play an integral role in the progress and/or prevention of AD
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EVALUATION OF RENAL FUNCTION IN ALZHEIMER'S DISEASE AND GERIATRIC PATIENTS: RESULTS FROM A TURKISH TWO- CENTER STUDY
2017Co-Authors: Erbayraktar Zubeyde, Evlice Ahmet Turan, Yilmaz Gokhan, Yazici Canan, Yener Gorsev, Ulusu Nuriye NurayAbstract:WOS: 000393585400008PubMed ID: 28680350Background: Alzheimer's disease (AD) is a severe multifactorial neurodegenerative Proteopathy associated with advanced age. Discrepancies in the renal function of these patients compared to geriatric patients with dementia have rarely been reported. In this study, we aimed to disclose the importance of associated renal changes for the patho genesis of AD. Methods: Patients with AD (n = 107) and geriatric patients with dementia and without dementia (n = 124) (231 patients in total) from Dokuz Eylul and Cukurova University Hospitals were enrolled in the study. We measured serum Na, K, Cl, Ca, BUN, creatinine, total protein levels and MDRD [eGFR] in all groups. Results: From Izmir Center, the first study arm consisted of patients with AD dementia (n = 74), and the second arm included geriatric patients with dementia (n = 79). From Adana, 78 patients were recruited to the study, of which 33 were with AD and 45 were geriatric patients without dementia. When we analyzed comparatively the AD and geriatric dementia patients study arms, a statistically significant difference was observed both in the median age (p < 0.001), as well as in the biochemical parameters from Izmir Center: Na (p < 0.001), K (p < 0.001), Cl (p < 0.05), Ca (p < 0.001), BUN (p < 0.05), creatinine (p < 0.001), total protein (p < 0.001) and MDRD [eGFR] (p < 0.001). How ever, these were not significantly different between AD and geriatric patients without dementia in the Adana group. Conclusions: Our results indicate that renal function is prone to alterations in different age groups of patients with AD. However, there is no conclusive evidence that renal function is one of the risk factors in AD
