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Gibson Team in the Lab

Featured Clinical Trials

CLINICAL TRIAL: 
Complete
Benfotiamine in Alzheimer's Disease: A Pilot Study (Benfotiamine)
Conditions: 
Neurodegenerative Diseases

Research Projects

Gibson Lab
RESEARCH PROJECT: 
Complete
A Clinical Trial Testing Whether Glucose Metabolism Is an Effective Therapeutic Target in Alzheimer’s Disease
Thiamine (vitamin B1) dependent processes are reduced in Alzheimer’s disease. Thiamine deficiency mimics many aspects of Alzheimer’s disease including the reduced glucose metabolism and exaggeration of the plaque and tangle pathology.
Gibson Lab
RESEARCH PROJECT: 
In Progress
The Molecular Basis for the Alzheimer’s Disease Related Decline in Key Mitochondrial Enzymes Is Unknown
We postulate that critical enzymes are modified post-translationally in Alzheimer’s disease. The focus is on the key mitochondrial enzyme alpha-ketoglutarate dehydrogenase complex (KGDHC).
Gibson Lab
RESEARCH PROJECT: 
In Progress
Mitochondrially Mediated Post-Translational Modification of Thousands of Cellular Proteins May Be Critical in Alzheimer’s Disease
Reducing the enzyme KGHDC has widespread consequences on cell and brain function. We postulate this is because it is responsible for post-translation modification of thousands of proteins by succinylation.
Gibson Lab
RESEARCH PROJECT: 
In Progress
To Test Whether Changes in Metabolism and Calcium Regulation Seen in Animal Models or Peripheral Tissues form Alzheimer’s Disease Patients Occur in Human Neurons Derived from Inducible Pluripotent Stem Cells
Alzheimer’s disease related changes in releasable internal calcium stores as well as in mitochondrial function have been suggested from animal studies and cultured cells from Alzheimer’s disease patients such as fibroblasts, and make good therapeutic targets.
Gibson Lab
RESEARCH PROJECT: 
In Progress
Mitochondrial and Metabolic Dysfunction in Age-Related Neurodegeneration
The investigators on the program project have two mechanisms for resource sharing.
Gibson Lab
RESEARCH PROJECT: 
In Progress
KGDHC and Neurodegenerative Disease

Mitochondrial dysfunction and oxidative stress are consistent features of multiple neurodegenerative diseases including Alzheimer’s disease (AD).

Gibson Lab
RESEARCH PROJECT: 
In Progress
Enzymes of the Tricarboxylic Acid Cycle in Neurodegeneration

Diminished brain metabolism and oxidative stress are characteristic features of Alzheimer's disease (AD). The mechanisms underlying these changes are as yet poorly defined.

Gibson Lab
RESEARCH PROJECT: 
In Progress
Thiamine Deficiency
Thiamine (vitamin B1) deficiency (TD) produces a mild, chronic impairment of oxidative metabolism that models the diminished metabolism and reduced activities of the thiamine-dependent mitochondrial enzymes that occur in brain in several common age-related neurodegenerative disorders.

Technologies

Western Blots

Western blots are used extensively to study post-translational modifications of the α-ketoglutarate dehydrogenase complex (KGDHC). The figure shows the separation of ketoglutarate dehydrogenase complex by blue-native gel.

Associated

Research Labs: 
Gibson Lab

Conditions & Recovery

Cognitive Recovery icon
Cognitive Recovery
Remember and speak clearly.
Neurodegenerative Diseases icon
Neurodegenerative Diseases
Worldwide, 50 million people are living with Alzheimer's and other dementias.

Research Methods

Behavioral Testing, Calcium Imaging of Living Cells, Cell Death, Drug Discovery, Enzyme Activity Measures, Gene Expression, Genetic Encoding of Probes to Monitor Metabolism in Living Cells, High-Resolution Imaging, Histochemistry, Histology, Hypoxia, Immunocytochemistry, Immunoprecipitation, Intracellular Imaging of Living Cells, Mass Spectrometry, Measurements on Human Blood, Metabolism, Molecular Studies, Neural Differentiation, Non-Invasive Neuromodulation, Oxidative Stress, Quantitative Western Blots, Stem Cells, Subcellular Fractionation, Tissue Culture