My major focus is the role of mitochondrial dysfunction and altered energy metabolism in the context of neurodegenerative diseases and aging. Mitochondrial abnormalities are implicated to play a major role in aging and age-related neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease (PD). Further, HIV appears to increase the risk for several age-associated diseases, including cognitive impairment and antiretroviral drugs are associated with neurotoxic side effects, including mitochondrial toxicity, which likely contribute to the development of HIV-associated neurocognitive disorders (HAND). The goal of my work in the laboratory is to elucidate the mechanisms leading to alterations in mitochondrial energy metabolism in order to develop therapeutic strategies to treat or prevent neurodegeneration.
Currently recruiting graduate students. Please contact if you are interested.
Techniques Used in the Lab
- Bioenergetic analysis
- Quantitative mass spectrometry (Super-SILAC and SWATH-MS)
- Percoll gradient preparation of synaptosomes and brain mitochondria
- Flow cytometry
- Immunohistochemistry
- Immunofluorescence microscopy
- Cell culture (primary cells and cell lines)
- Western blots
- Traditional PCRs and Real-Time PCR
Funding
Immunometabolism in Parkinson’s Disease: Peripheral Markers and Correlation with Neuroimaging.
UNMC CoNDA Pilot Project awarded under NIH/NIGMS 1P20GM130447 (PI: Wilson)
This project investigates if peripheral immunometabolism changes correlate with neuroimaging findings and can be used to evaluate Parkinson’s Disease onset and progression.
Role: PI
Impact of Traumatic Brain Injury on Tauopathy-Induced Synaptotoxicity: Implication for Alzheimer’s Disease and Related Dementias
DOD CDMRP PRARP New Investigator Research Award AZ180035
This research project examines the hypothesis that with traumatic brain injury, deposition of pathologic human tau leads to synaptic dysfunction, resulting in functional impairment.
Role: PI
Mechanisms of Presynaptic Energetic Failure Due to Age-Related Pathologic Tau Accumulation
NIH/NIA 1R01AG059785-01
This project will investigate the mechanisms underlying age-associated mitochondrial impairment within nerve terminals in the context of tau pathology. These studies are designed to identify new targets for Alzheimer’s disease based on overlapping and unique changes that we observe with normal brain aging and in the context of tau pathology, specifically, alterations in presynaptic mitochondrial function.
Role: PI
Mechanisms of Synaptic Energetic Failure Due to Pink1/Parkin Deficiency
Michael J. Fox Foundation 15288
The application proposes studies that will test the hypothesis that combined Pink1/Parkin deficiency leads to a reproducible rat model of Parkinson's disease due to the accumulation of damaged/dysfunctional mitochondria at striatal synapses resulting in energetic failure and deficient neurotransmitter release. Determining mechanisms of region-specificity of mitochondrial dysfunction and selective vulnerability of striatal nerve terminals in this novel rat model will significantly advance the understanding of neurodegeneration linked to Pink1/Parkin mutations and potentially idiopathic PD.
Role: PI
Signatures of Cannabis Abuse in NeuroHIV (SCAN): An Integrated Molecular and Imaging Approach
DHHS/NIH/NIDA 1R01DA047828-01 (PI: Wilson)
The award investigates the impact of chronic cannabis abuse on neuroimaging and molecular markers of brain and cognitive function. Our multi-pronged approach will evaluate neural circuitry and dynamics, mitochondrial function, and other molecular and systems-level metrics, with a focus on integration across levels of study.
Role: Co-I
Parkin as a Protective Strategy Against Mitochondrial DNA Stress
Michael J. Fox Foundation 11845.01 (PI: Fox)
This study examines the hypothesis that enhancing Parkin function mediates increased quality control in conditions of mitochondrial stress.
Role: Co-PI
Personnel
Currently recruiting graduate students. Please contact if you are interested.
