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Book ; Conference proceedings: Mitochondria and oxidative stress in neurodegenerative disorders

Gibson, Gary E.

[result of a Conference Entitled Mitochondria and Oxidative Stress in Neurodegenerative Disorders, held on September 26 - 29, 2007 at the New York Academy of Sciences]

(Annals of the New York Academy of Sciences ; 1147)

2008

Event/congress	Conference Entitled Mitochondria and Oxidative Stress in Neurodegenerative Disorders (2007, NewYorkNY)
Author's details	ed. by Gary E. Gibson
Series title	Annals of the New York Academy of Sciences ; 1147
Collection
Keywords	Neurodegenerative Diseases / physiopathology ; Mitochondria / physiology ; Oxidative Stress / physiology
Language	English
Size	XII, 414 S. : Ill., graph. Darst.
Publisher	Blackwell
Publishing place	Boston, Mass
Publishing country	United States
Document type	Book ; Conference proceedings
HBZ-ID	HT015794638
ISBN	978-1-57331-713-9 ; 1-57331-713-6
Database	Catalogue ZB MED Medicine, Health

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Se 110 -1147-	verfügbar in Königswinter	Königswinter

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Article ; Online: The α-Ketoglutarate Dehydrogenase Complex as a Hub of Plasticity in Neurodegeneration and Regeneration.

Hansen, Grace E / Gibson, Gary E

International journal of molecular sciences

2022 Volume 23, Issue 20

Abstract: Abnormal glucose metabolism is central to neurodegeneration, and considerable evidence suggests that abnormalities in key enzymes of the tricarboxylic acid (TCA) cycle underlie the metabolic deficits. Significant recent advances in the role of metabolism ...

Abstract	Abnormal glucose metabolism is central to neurodegeneration, and considerable evidence suggests that abnormalities in key enzymes of the tricarboxylic acid (TCA) cycle underlie the metabolic deficits. Significant recent advances in the role of metabolism in cancer provide new insight that facilitates our understanding of the role of metabolism in neurodegeneration. Research indicates that the rate-limiting step of the TCA cycle, the α-ketoglutarate dehydrogenase complex (KGDHC) and its substrate alpha ketoglutarate (KG), serve as a signaling hub that regulates multiple cellular processes: (1) is the rate-limiting step of the TCA cycle, (2) is sensitive to reactive oxygen species (ROS) and produces ROS, (3) determines whether KG is used for energy or synthesis of compounds to support growth, (4) regulates the cellular responses to hypoxia, (5) controls the post-translational modification of hundreds of cell proteins in the mitochondria, cytosol, and nucleus through succinylation, (6) controls critical aspects of transcription, (7) modulates protein signaling within cells, and (8) modulates cellular calcium. The primary focus of this review is to understand how reductions in KGDHC are translated to pathologically important changes that underlie both neurodegeneration and cancer. An understanding of each role is necessary to develop new therapeutic strategies to treat neurodegenerative disease.
MeSH term(s)	Humans ; Ketoglutarate Dehydrogenase Complex/metabolism ; Neurodegenerative Diseases/metabolism ; Reactive Oxygen Species/metabolism ; Calcium/metabolism ; Ketoglutaric Acids ; Glucose ; Tricarboxylic Acids
Chemical Substances	Ketoglutarate Dehydrogenase Complex (EC 1.2.4.2) ; Reactive Oxygen Species ; Calcium (SY7Q814VUP) ; Ketoglutaric Acids ; Glucose (IY9XDZ35W2) ; Tricarboxylic Acids
Language	English
Publishing date	2022-10-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232012403
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Article ; Online: The α-Ketoglutarate Dehydrogenase Complex as a Hub of Plasticity in Neurodegeneration and Regeneration

Grace E. Hansen / Gary E. Gibson

International Journal of Molecular Sciences, Vol 23, Iss 20, p

2022 Volume 12403

Abstract	Abnormal glucose metabolism is central to neurodegeneration, and considerable evidence suggests that abnormalities in key enzymes of the tricarboxylic acid (TCA) cycle underlie the metabolic deficits. Significant recent advances in the role of metabolism in cancer provide new insight that facilitates our understanding of the role of metabolism in neurodegeneration. Research indicates that the rate-limiting step of the TCA cycle, the α-ketoglutarate dehydrogenase complex (KGDHC) and its substrate alpha ketoglutarate (KG), serve as a signaling hub that regulates multiple cellular processes: (1) is the rate-limiting step of the TCA cycle, (2) is sensitive to reactive oxygen species (ROS) and produces ROS, (3) determines whether KG is used for energy or synthesis of compounds to support growth, (4) regulates the cellular responses to hypoxia, (5) controls the post-translational modification of hundreds of cell proteins in the mitochondria, cytosol, and nucleus through succinylation, (6) controls critical aspects of transcription, (7) modulates protein signaling within cells, and (8) modulates cellular calcium. The primary focus of this review is to understand how reductions in KGDHC are translated to pathologically important changes that underlie both neurodegeneration and cancer. An understanding of each role is necessary to develop new therapeutic strategies to treat neurodegenerative disease.
Keywords	α-ketoglutarate dehydrogenase complex ; metabolic plasticity ; mitochondria ; Alzheimer’s disease ; tricarboxylic acid cycle ; cell signaling ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	612
Language	English
Publishing date	2022-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Perspectives of Canadian health leaders on the relationship between medical assistance in dying and palliative and end-of-life care services: a qualitative study.

Shapiro, Gilla K / Tong, Eryn / Nissim, Rinat / Zimmermann, Camilla / Allin, Sara / Gibson, Jennifer L / Lau, Sharlane C L / Li, Madeline / Rodin, Gary

CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne

2024 Volume 196, Issue 7, Page(s) E222–E234

Abstract: ... the relationship between the services across 4 PATH levels: client-centred services (e.g., educate public); health ... operations (e.g., cultivate compassionate and proactive leadership); health systems (e.g., conduct broad and ... inclusive consultation and planning); and intersectoral initiatives (e.g., provide standard ...

Abstract	Background: Medical assistance in dying (MAiD) was legalized in Canada in 2016, but coordination of MAiD and palliative and end-of-life care (PEOLC) services remains underdeveloped. We sought to understand the perspectives of health leaders across Canada on the relationship between MAiD and PEOLC services and to identify opportunities for improved coordination. Methods: In this quantitative study, we purposively sampled health leaders across Canada with expertise in MAiD, PEOLC, or both. We conducted semi-structured interviews between April 2021 and January 2022. Interview transcripts were coded independently by 2 researchers and reconciled to identify key themes using content analysis. We applied the PATH framework for Integrated Health Services to guide data collection and analysis. Results: We conducted 36 interviews. Participants expressed diverse views about the optimal relationship between MAiD and PEOLC, and the desirability of integration, separation, or coordination of these services. We identified 11 themes to improve the relationship between the services across 4 PATH levels: client-centred services (e.g., educate public); health operations (e.g., cultivate compassionate and proactive leadership); health systems (e.g., conduct broad and inclusive consultation and planning); and intersectoral initiatives (e.g., provide standard practice guidelines across health care systems). Interpretation: Health leaders recognized that cooperation between MAiD and PEOLC services is required for appropriate referrals, care coordination, and patient care. They identified the need for public and provider education, standardized practice guidelines, relationship-building, and leadership. Our findings have implications for MAiD and PEOLC policy development and clinical practice in Canada and other jurisdictions.
MeSH term(s)	Humans ; Canada ; Suicide, Assisted ; Terminal Care ; Qualitative Research ; Medical Assistance ; Palliative Care
Language	English
Publishing date	2024-02-25
Publishing country	Canada
Document type	Journal Article
ZDB-ID	215506-0
ISSN	1488-2329 ; 0008-4409 ; 0820-3946
ISSN (online)	1488-2329
ISSN	0008-4409 ; 0820-3946
DOI	10.1503/cmaj.231241
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Article: Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease.

Gibson, Gary E / Feldman, Howard H / Zhang, Sheng / Flowers, Sarah A / Luchsinger, José A

Frontiers in medicine

2022 Volume 9, Page(s) 1033272

Abstract: of the study. ...

Abstract	of the study.
Language	English
Publishing date	2022-10-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2022.1033272
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Article ; Online: Succinylation Links Metabolism to Protein Functions.

Yang, Yun / Gibson, Gary E

Neurochemical research

2019 Volume 44, Issue 10, Page(s) 2346–2359

Abstract: Post-translational modifications (PTMs) are important regulators of protein function, and integrate metabolism with physiological and pathological processes. Phosphorylation and acetylation are particularly well studied PTMs. A relatively recently ... ...

Abstract	Post-translational modifications (PTMs) are important regulators of protein function, and integrate metabolism with physiological and pathological processes. Phosphorylation and acetylation are particularly well studied PTMs. A relatively recently discovered novel PTM is succinylation in which metabolically derived succinyl CoA modifies protein lysine groups. Succinylation causes a protein charge flip from positive to negative and a relatively large increase in mass compared to other PTMs. Hundreds of protein succinylation sites are present in proteins of multiple tissues and species, and the significance is being actively investigated. The few completed studies demonstrate that succinylation alters rates of enzymes and pathways, especially mitochondrial metabolic pathways. Thus, succinylation provides an elegant and efficient mechanism to coordinate metabolism and signaling by utilizing metabolic intermediates as sensors to regulate metabolism. Even though the brain is one of the most metabolically active organs, an understanding of the role succinylation in the nervous system is largely unknown. Data from other tissues and other PTMs suggest that succinylation provides a coupling between metabolism and protein function in the nervous system and in neurological diseases. This review provides a new insight into metabolism in neurological diseases and suggests that the drug development for these diseases requires a better understanding of succinylation and de-succinylation in the brain and other tissues.
MeSH term(s)	Acyl Coenzyme A/metabolism ; Animals ; Humans ; Lysine/metabolism ; Metabolic Networks and Pathways/physiology ; Mitochondria/metabolism ; Protein Processing, Post-Translational/physiology ; Proteome/metabolism
Chemical Substances	Acyl Coenzyme A ; Proteome ; succinyl-coenzyme A (BSI27HW5EQ) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2019-03-22
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-019-02780-x
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Article ; Online: Interactions of Mitochondria/Metabolism and Calcium Regulation in Alzheimer's Disease: A Calcinist Point of View.

Gibson, Gary E / Thakkar, Ankita

Neurochemical research

2017 Volume 42, Issue 6, Page(s) 1636–1648

Abstract: Decades of research suggest that alterations in calcium are central to the pathophysiology of Alzheimer's Disease (AD). Highly reproducible changes in calcium dynamics occur in cells from patients with both genetic and non-genetic forms of AD relative to ...

Abstract	Decades of research suggest that alterations in calcium are central to the pathophysiology of Alzheimer's Disease (AD). Highly reproducible changes in calcium dynamics occur in cells from patients with both genetic and non-genetic forms of AD relative to controls. The most robust change is an exaggerated release of calcium from internal stores. Detailed analysis of these changes in animal and cell models of the AD-causing presenilin mutations reveal robust changes in ryanodine receptors, inositol tris-phosphate receptors, calcium leak channels and store activated calcium entry. Similar anomalies in calcium result when AD-like changes in mitochondrial enzymes or oxidative stress are induced experimentally. The calcium abnormalities can be directly linked to the altered tau phosphorylation, amyloid precursor protein processing and synaptic dysfunction that are defining features of AD. A better understanding of these changes is required before using calcium abnormalities as therapeutic targets.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Calcium/physiology ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Oxidative Stress/physiology
Chemical Substances	Calcium Channels ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-02-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-017-2182-3
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Article ; Online: Mitochondria/metabolic reprogramming in the formation of neurons from peripheral cells: Cause or consequence and the implications to their utility.

Gibson, Gary E / Thakkar, Ankita

Neurochemistry international

2017 Volume 117, Page(s) 65–76

Abstract: The induction of pluripotent stem cells (iPSC) from differentiated cells such as fibroblasts and their subsequent conversion to neural progenitor cells (NPC) and finally to neurons is intriguing scientifically, and its potential to medicine is nearly ... ...

Abstract	The induction of pluripotent stem cells (iPSC) from differentiated cells such as fibroblasts and their subsequent conversion to neural progenitor cells (NPC) and finally to neurons is intriguing scientifically, and its potential to medicine is nearly infinite, but unrealized. A better understanding of the changes at each step of the transformation will enable investigators to better model neurological disease. Each step of conversion from a differentiated cell to an iPSC to a NPC to neurons requires large changes in glycolysis including aerobic glycolysis, the pentose shunt, the tricarboxylic acid cycle, the electron transport chain and in the production of reactive oxygen species (ROS). These mitochondrial/metabolic changes are required and their manipulation modifies conversions. These same mitochondrial/metabolic processes are altered in common neurological diseases so that factors related to the disease may alter the cellular transformation at each step including the final phenotype. A lack of understanding of these interactions could compromise the validity of the disease comparisons in iPSC derived neurons. Both the complexity and potential of iPSC derived cells for understanding and treating disease remain great.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Cellular Reprogramming/physiology ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mitochondria/metabolism ; Neural Stem Cells/metabolism ; Neurons/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2017-06-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2017.06.007
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Article ; Online: Serum Metabolomic and Lipidomic Profiling Reveals Novel Biomarkers of Efficacy for Benfotiamine in Alzheimer's Disease.

Bhawal, Ruchika / Fu, Qin / Anderson, Elizabeth T / Gibson, Gary E / Zhang, Sheng

International journal of molecular sciences

2021 Volume 22, Issue 24

Abstract: Serum metabolomics and lipidomics are powerful approaches for discovering unique biomarkers in various diseases and associated therapeutics and for revealing metabolic mechanisms of both. Treatment with Benfotiamine (BFT), a thiamine prodrug, for one ... ...

Abstract	Serum metabolomics and lipidomics are powerful approaches for discovering unique biomarkers in various diseases and associated therapeutics and for revealing metabolic mechanisms of both. Treatment with Benfotiamine (BFT), a thiamine prodrug, for one year produced encouraging results for patients with mild cognitive impairment and mild Alzheimer's disease (AD). In this study, a parallel metabolomics and lipidomics approach was applied for the first exploratory investigation on the serum metabolome and lipidome of patients treated with BFT. A total of 315 unique metabolites and 417 lipids species were confidently identified and relatively quantified. Rigorous statistical analyses revealed significant differences between the placebo and BFT treatment groups in 25 metabolites, including thiamine, tyrosine, tryptophan, lysine, and 22 lipid species, mostly belonging to phosphatidylcholines. Additionally, 10 of 11 metabolites and 14 of 15 lipid species reported in previous literature to follow AD progression changed in the opposite direction to those reported to reflect AD progression. Enrichment and pathway analyses show that significantly altered metabolites by BFT are involved in glucose metabolism and biosynthesis of aromatic amino acids. Our study discovered that multiple novel biomarkers and multiple mechanisms that may underlie the benefit of BFT are potential therapeutic targets in AD and should be validated in studies with larger sample sizes.
MeSH term(s)	Alzheimer Disease/blood ; Alzheimer Disease/drug therapy ; Biomarkers/blood ; Case-Control Studies ; Chromatography, Liquid ; Humans ; Lipids/blood ; Mass Spectrometry ; Metabolic Networks and Pathways ; Metabolomics/methods ; Pilot Projects ; Thiamine/administration & dosage ; Thiamine/analogs & derivatives ; Thiamine/pharmacology
Chemical Substances	Biomarkers ; Lipids ; Thiamine (X66NSO3N35) ; benphothiamine (Y92OUS2H9B)
Language	English
Publishing date	2021-12-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222413188
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Article ; Online: Serum Metabolomic and Lipidomic Profiling Reveals Novel Biomarkers of Efficacy for Benfotiamine in Alzheimer’s Disease

Ruchika Bhawal / Qin Fu / Elizabeth T. Anderson / Gary E. Gibson / Sheng Zhang

International Journal of Molecular Sciences, Vol 22, Iss 13188, p

2021 Volume 13188

Abstract	Serum metabolomics and lipidomics are powerful approaches for discovering unique biomarkers in various diseases and associated therapeutics and for revealing metabolic mechanisms of both. Treatment with Benfotiamine (BFT), a thiamine prodrug, for one year produced encouraging results for patients with mild cognitive impairment and mild Alzheimer’s disease (AD). In this study, a parallel metabolomics and lipidomics approach was applied for the first exploratory investigation on the serum metabolome and lipidome of patients treated with BFT. A total of 315 unique metabolites and 417 lipids species were confidently identified and relatively quantified. Rigorous statistical analyses revealed significant differences between the placebo and BFT treatment groups in 25 metabolites, including thiamine, tyrosine, tryptophan, lysine, and 22 lipid species, mostly belonging to phosphatidylcholines. Additionally, 10 of 11 metabolites and 14 of 15 lipid species reported in previous literature to follow AD progression changed in the opposite direction to those reported to reflect AD progression. Enrichment and pathway analyses show that significantly altered metabolites by BFT are involved in glucose metabolism and biosynthesis of aromatic amino acids. Our study discovered that multiple novel biomarkers and multiple mechanisms that may underlie the benefit of BFT are potential therapeutic targets in AD and should be validated in studies with larger sample sizes.
Keywords	metabolomics ; lipidomics ; Alzheimer’s disease ; serum ; thiamine ; benfotiamine ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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