Michelle Gray

ORCID: 0000-0003-0808-108X
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About
Contact & Profiles
Research Areas
  • Genetic Neurodegenerative Diseases
  • Mitochondrial Function and Pathology
  • Neurological disorders and treatments
  • Neuroscience and Neuropharmacology Research
  • Peptidase Inhibition and Analysis
  • Treatment of Major Depression
  • Muscle Physiology and Disorders
  • Ubiquitin and proteasome pathways
  • Older Adults Driving Studies
  • Adipose Tissue and Metabolism
  • Urban Transport and Accessibility
  • Schizophrenia research and treatment
  • Parkinson's Disease Mechanisms and Treatments
  • Studies on Chitinases and Chitosanases
  • Sleep and Wakefulness Research
  • Health disparities and outcomes
  • Pharmaceutical studies and practices
  • Plant biochemistry and biosynthesis
  • Transportation and Mobility Innovations
  • Bioinformatics and Genomic Networks
  • Alzheimer's disease research and treatments
  • Attention Deficit Hyperactivity Disorder
  • Cardiovascular Effects of Exercise
  • 14-3-3 protein interactions
  • Cardiac electrophysiology and arrhythmias

University of Alabama at Birmingham
2013-2025

University of California, Los Angeles
2006-2014

Neurobehavioral Systems
2006

Neuronal and non-neuronal cells express the huntingtin (HTT) protein, yet neurodegeneration in Huntington's disease (HD) is largely selective, affecting most prominently striatal medium spiny neurons cortical pyramidal neurons. Selective toxicity of full-length human mutant HTT (fl-mHTT) may be due part to its expression cells. While studies suggest neuronal-glial interactions are important HD fl-mHTT expressed astrocytes, it has not been determined whether astrocytes necessary for...

10.1093/hmg/ddy363 article EN Human Molecular Genetics 2018-10-10

In Huntington's disease (HD), the uninterrupted CAG repeat length, but not polyglutamine predicts onset. However, underlying pathobiology remains unclear. Here, we developed bacterial artificial chromosome (BAC) transgenic mice expressing human mutant huntingtin (mHTT) with uninterrupted, and somatically unstable, repeats that exhibit progressive disease-related phenotypes. Unlike prior mHTT models stable, CAA-interrupted, polyglutamine-encoding repeats, BAC-CAG show robust...

10.1016/j.neuron.2022.01.006 article EN cc-by Neuron 2022-02-02

Caspase cleavage of huntingtin (htt) and nuclear htt accumulation represent early neuropathological changes in brains patients with Huntington's disease (HD). However, the relationship between caspase activation patterns pathogenesis HD remains poorly understood. The lack a phenotype YAC mice expressing caspase-6-resistant (C6R) mutant (mhtt) highlights proteolysis at 586 aa caspase-6 (casp6) site as key mechanism pathology HD. goal this study was to investigate how residue plays role...

10.1523/jneurosci.2071-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-11-10

Mitochondrial dysfunction, transcriptional dysregulation, and protein aggregation are hallmarks of multiple neurodegenerative disorders, including Huntington's disease (HD). Strategies needed to counteract these processes restore neuronal health function in HD. Recent evidence indicates that the transcription factor estrogen-related receptor gamma (ERRγ/Esrrg) is required for normal expression mitochondrial, synaptic, autophagy genes neurons. Further, overexpression Esrrg dopaminergic...

10.1016/j.nbd.2025.106818 article EN cc-by-nc Neurobiology of Disease 2025-01-01

Accumulation of neurotoxic hyperphosphorylated TAU protein is a major pathological hallmark Alzheimer disease and other neurodegenerative dementias collectively called tauopathies. Puromycin-sensitive aminopeptidase (PSA/NPEPPS) novel modifier TAU-induced neurodegeneration with neuroprotective effects via direct proteolysis protein. Here, to examine the PSA/NPEPPS overexpression in vivo mammalian system, we generated crossed BAC-PSA/NPEPPS transgenic mice TAUP301L mouse model...

10.1093/hmg/ddr065 article EN Human Molecular Genetics 2011-02-14

Huntington's disease (HD) is a dominantly inherited neurodegenerative disease. There accumulating evidence that HD patients have increased prevalence of conduction abnormalities and compromised sinoatrial node function which could lead to risk for arrhythmia. We used mutant Huntingtin (mHTT) expressing bacterial artificial chromosome mice determine if they exhibit electrocardiogram (ECG) involving cardiac are known increase sudden arrhythmic death in humans. obtained surface ECGs analyzed...

10.1093/hmg/ddz295 article EN Human Molecular Genetics 2019-12-05

Huntington’s disease (HD) is a dominantly inherited, adult-onset neurodegenerative characterized by motor, psychiatric, and cognitive abnormalities. Neurodegeneration prominently observed in the striatum where GABAergic medium spiny neurons (MSN) are most affected neuronal population. Interestingly, recent reports of pathological changes HD patient striatal tissue have identified significant reduction number parvalbumin-expressing interneurons which becomes more robust tissues higher grade....

10.3389/fnana.2021.673177 article EN cc-by Frontiers in Neuroanatomy 2021-05-24

The objective of this study is to analyze older adults' familiarity with new transportation options and their perception towards autonomous vehicles, as well the impact factors associated barriers on these aspects, in Arkansas, a predominantly rural state. Data from 775 adults aged 60 years or were collected between October 2021 2022. To fulfill objective, used Latent Class Cluster Analysis segment into classes based both perceptions vehicles. By incorporating covariates model, effects class...

10.2139/ssrn.4847623 preprint EN 2024-01-01

ABSTRACT Huntington's disease (HD) is a fatal, progressive neurodegenerative disorder. Prior studies revealed an increase in extracellular glutamate levels after evoking astrocytic SNARE-dependent exocytosis from cultured primary astrocytes mutant huntingtin (mHTT)-expressing BACHD mice compared to control astrocytes, suggesting alterations HD. We used and dominant-negative (dn)SNARE decrease determine whether reducing could rescue neuropathological changes vivo. observed significant...

10.1242/dmm.052002 article EN cc-by Disease Models & Mechanisms 2024-11-01
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