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Succinylation Links Metabolism to Protein Functions

Neurochemical research, 2019-10, Vol.44 (10), p.2346-2359

2019

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The α-Ketoglutarate Dehydrogenase Complex as a Hub of Plasticity in Neurodegeneration and Regeneration

International journal of molecular sciences, 2022-10, Vol.23 (20), p.12403

2022

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Vitamin B1 (thiamine) and dementia

Annals of the New York Academy of Sciences, 2016-03, Vol.1367 (1), p.21-30

2016

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Altered succinylation of mitochondrial proteins, APP and tau in Alzheimer’s disease

Nature communications, 2022-01, Vol.13 (1), p.159-19, Article 159

2022

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Up‐regulation of the mitochondrial malate dehydrogenase by oxidative stress is mediated by miR‐743a

Journal of neurochemistry, 2011-08, Vol.118 (3), p.440-448

2011

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Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy

Human molecular genetics, 2018-08, Vol.27 (16), p.2874-2892

2018

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Cause and consequence: Mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases

Biochimica et biophysica acta, 2010-01, Vol.1802 (1), p.122-134

2010

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Benfotiamine and Cognitive Decline in Alzheimer's Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial

Journal of Alzheimer's disease, 2020-01, Vol.78 (3), p.989-1010

2020

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Serum Metabolomic and Lipidomic Profiling Reveals Novel Biomarkers of Efficacy for Benfotiamine in Alzheimer's Disease

International journal of molecular sciences, 2021-12, Vol.22 (24), p.13188

2021

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Oxidative Stress and Transcriptional Regulation in Alzheimer Disease

Alzheimer disease and associated disorders, 2007-10, Vol.21 (4), p.276-291

2007

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Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications

Annals of neurology, 2005-05, Vol.57 (5), p.695-703

2005

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Novel Metabolic Abnormalities in the Tricarboxylic Acid Cycle in Peripheral Cells From Huntington's Disease Patients

PloS one, 2016-09, Vol.11 (9), p.e0160384

2016

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Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease

Frontiers in medicine, 2022-10, Vol.9, p.1033272-1033272

2022

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Obituary: In Memory of Myron Flint Beal, MD, November 6, 1950–June 12, 2021

Movement disorders, 2021-09, Vol.36 (9), p.2003-2004

2021

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Interactions of Mitochondria/Metabolism and Calcium Regulation in Alzheimer’s Disease: A Calcinist Point of View

Neurochemical research, 2017-06, Vol.42 (6), p.1636-1648

2017

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Thiamine and Oxidants Interact to Modify Cellular Calcium Stores

Neurochemical research, 2010-12, Vol.35 (12), p.2107-2116

2010

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Changes in inflammatory processes associated with selective vulnerability following mild impairment of oxidative metabolism

Neurobiology of disease, 2007-05, Vol.26 (2), p.353-362

2007

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A mitocentric view of Alzheimer's disease suggests multi-faceted treatments

Journal of Alzheimer's disease, 2010-01, Vol.20 Suppl 2 (s2), p.S591-S607

2010

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Mitochondria/metabolic reprogramming in the formation of neurons from peripheral cells: Cause or consequence and the implications to their utility

Neurochemistry international, 2018-07, Vol.117, p.65-76

2018

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Alpha‐ketoglutarate dehydrogenase complex‐dependent succinylation of proteins in neurons and neuronal cell lines

Journal of neurochemistry, 2015-07, Vol.134 (1), p.86-96

2015

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Dopaminergic cell death induced by MPP+, oxidant and specific neurotoxicants shares the common molecular mechanism

Journal of neurochemistry, 2001-02, Vol.76 (4), p.1010-1021

2001

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Selective NADH communication from α-ketoglutarate dehydrogenase to mitochondrial transhydrogenase prevents reactive oxygen species formation under reducing conditions in the heart

Basic research in cardiology, 2020-09, Vol.115 (5), p.53, Article 53

2020

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The RNA-binding protein HuR is essential for the B cell antibody response

Nature immunology, 2015-04, Vol.16 (4), p.415-425

2015

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Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

Neurochemical research, 2015-12, Vol.40 (12), p.2557-2569

2015

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Succinylation Links Metabolism to Protein Functions

The α-Ketoglutarate Dehydrogenase Complex as a Hub of Plasticity in Neurodegeneration and Regeneration

Vitamin B1 (thiamine) and dementia

Altered succinylation of mitochondrial proteins, APP and tau in Alzheimer’s disease

Up‐regulation of the mitochondrial malate dehydrogenase by oxidative stress is mediated by miR‐743a

Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy

Cause and consequence: Mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases

Benfotiamine and Cognitive Decline in Alzheimer's Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial

Serum Metabolomic and Lipidomic Profiling Reveals Novel Biomarkers of Efficacy for Benfotiamine in Alzheimer's Disease

Oxidative Stress and Transcriptional Regulation in Alzheimer Disease

Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications

Protocol for a seamless phase 2A-phase 2B randomized double-blind placebo-controlled trial to evaluate the safety and efficacy of benfotiamine in patients with early Alzheimer's disease (BenfoTeam)

Novel Metabolic Abnormalities in the Tricarboxylic Acid Cycle in Peripheral Cells From Huntington's Disease Patients

Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease

Obituary: In Memory of Myron Flint Beal, MD, November 6, 1950–June 12, 2021

Interactions of Mitochondria/Metabolism and Calcium Regulation in Alzheimer’s Disease: A Calcinist Point of View

Thiamine and Oxidants Interact to Modify Cellular Calcium Stores

Changes in inflammatory processes associated with selective vulnerability following mild impairment of oxidative metabolism

A mitocentric view of Alzheimer's disease suggests multi-faceted treatments

Mitochondria/metabolic reprogramming in the formation of neurons from peripheral cells: Cause or consequence and the implications to their utility

Alpha‐ketoglutarate dehydrogenase complex‐dependent succinylation of proteins in neurons and neuronal cell lines

Dopaminergic cell death induced by MPP+, oxidant and specific neurotoxicants shares the common molecular mechanism

Selective NADH communication from α-ketoglutarate dehydrogenase to mitochondrial transhydrogenase prevents reactive oxygen species formation under reducing conditions in the heart

The RNA-binding protein HuR is essential for the B cell antibody response

Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

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