SelectedWorks - Brad E. Morrison

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Selected Works of Brad E. Morrison

Assistant Professor, Department of Biological Sciences

With a Ph.D. in molecular and cell biology from the University of Texas at Dallas, and research experience at The University of Texas Southwestern Medical Center in Dallas, The Scripps Research Institute, and the University of California at San Diego, Dr. Brad Morrison joined the faculty of the Department of Biological Sciences at Boise State University in 2013. His current research is focused on elucidating neuroinflammatory contributions and autophagy dysfunction underlying Parkinson's disease pathogenesis.

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About Brad E. Morrison

With a Ph.D. in molecular and cell biology from the University of Texas at Dallas, and research experience at The University of Texas Southwestern Medical Center in Dallas, The Scripps Research Institute, and the University of California at San Diego, Dr. Brad Morrison joined the faculty of the Department of Biological Sciences at Boise State University in 2013. His current research is focused on elucidating neuroinflammatory contributions and autophagy dysfunction underlying Parkinson's disease pathogenesis.

2013 - Present	Assistant Professor, Boise State University ‐ Department of Biological Sciences
Institution Organization Position Type Position Title Time Period to Options Current Position Affiliate my profile with this Institution

Biology, Cell Biology, and Molecular and Cellular Neuroscience

Neurodegenerative Disease, Molecular and Cell Biology, and Genetics

2009-2011 - Helen Dorris Fellow, The Scripps Research Institute
2006 - Best Oral Research Presentation, Biology and Chemistry Graduate Student Symposium, The University of Texas at Dallas
2006 - Annual Award for Best Research Presentation, Department of Cell and Molecular Biology, The University of Texas at Dallas

BIOL 497/597: The Pathophysiology of Neurodegenerative Disease

E-mail: BradMorrison@boisestate.edu

http://orcid.org/0000-0002-6356-7149

Articles (26)

The Role of NAD+ and NAD+-Boosting Therapies in Inflammatory Response by IL-13 (Anton D. Pugel, Alyssa M. Schoenfeld, Sara Z. Alsaifi, et al.) Pharmaceuticals (2024)

The essential role of nicotinamide adenine dinucleotide+ (NAD+) in redox reactions during oxidative respiration is well known, yet the coenzyme and regulator functions of NAD+ in diverse and important processes are still being discovered. Maintaining ...

Nonhistone Lysine Methylation as a Protein Degradation Signal (Nicholas A. Lehning and Brad E. Morrison) Journal of Chemistry (2022)

Protein degradation is a fundamental feature of cellular life, and malfunction of this process is implicated in human disease. Ubiquitin tagging is the best characterized mechanism of targeting a protein for degradation; however, there are ...

Repurposing Drugs to Treat Heart and Brain Illness (Maranda S. Cantrell, Alejandro Soto-Avellaneda, Jackson D. Wall, et al.) Pharmaceuticals (2021)

Drug development is a complicated, slow and expensive process with high failure rates. One strategy to mitigate these factors is to recycle existing drugs with viable safety profiles and have gained Food and Drug Administration ...

Endothelial Cell Contributions to COVID-19 (Alexandra E. Oxford, Fabio Halla, Evan B. Robertson, et al.) Pathogens (2020)

Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation ...

Signaling and Other Functions of Lipids in Autophagy: A Review (Alejandro Soto-Avellaneda and Brad E. Morrison) Lipids in Health and Disease (2020)

The process of autophagy is integral to cellular function. In this process, proteins, organelles, and metabolites are engulfed in a lipid vesicle and trafficked to a lysosome for degradation. Its central role in protein and ...

Enhanced Hyaluronan Signaling and Autophagy Dysfunction by VPS35 D620N (Abir A. Rahman, Alejandro Soto-Avellaneda, Iva Stojkovska, et al.) Neuroscience (2020)

The motor features of Parkinson’s disease (PD) result from the loss of dopaminergic (DA) neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. A PD-causing familial mutation in VPS35 (D620N) ...

Center of Biomedical Research Excellence in Matrix Biology: Building Research Infrastructure, Supporting Young Researchers, and Fostering Collaboration (Julia Thom Oxford, Ken A. Cornell, Jared J. Romero, et al.) International Journal of Molecular Sciences (2020)

The Center of Biomedical Research Excellence in Matrix Biology strives to improve our understanding of extracellular matrix at molecular, cellular, tissue, and organismal levels to generate new knowledge about pathophysiology, normal development, and regenerative medicine. ...

Contributions of VPS35 Mutations to Parkinson’s Disease (Abir A. Rahman and Brad E. Morrison) Neuroscience (2019)

Parkinson’s Disease (PD) is a multi-system neurodegenerative disease where approximately 90% of cases are idiopathic. The remaining 10% of the cases can be traced to a genetic origin and research has largely focused on these ...

A Fragment of Apolipoprotein E4 Leads to the Downregulation of a CXorf56 Homologue, a Novel ER-Associated Protein, and Activation of BV2 Microglial Cells (Tanner B. Pollock, Jacob M. Mack, Noail F. Isho, et al.) Oxidative Medicine and Cellular Longevity (2019)

Despite the fact that harboring the apolipoprotein E4 (APOE4) allele represents the single greatest risk factor for late-onset Alzheimer’s disease (AD), the exact mechanism by which apoE4 contributes to disease progression remains unknown. Recently, we ...

Nestin-Positive/SOX2−Negative Cells Mediate Adult Neurogenesis of Nigral Dopaminergic Neurons in Mice (Joshua E. Albright, Iva Stojkovska, Abir A. Rahman, et al.) Neuroscience Letters (2016)

The primary clinical motor symptoms of Parkinson’s disease (PD) result from loss of dopaminergic (DA) neurons in the substantia nigra (SN). Consequently, neurogenesis of this group of neurons in the adult brain has drawn considerable ...

IL-13Rα1 Expression in Dopaminergic Neurons Contributes to Their Oxidative Stress–Mediated Loss following Chronic Peripheral Treatment with Lipopolysaccharide The Journal of Immunology (2012)

Inflammation and its mediators, including cytokines and reactive oxygen species, are thought to contribute to neurodegeneration. In the mouse brain, we found that IL-13Rα1 was expressed in the dopaminergic (DA) neurons of the substantia nigra ...

PGC-1α Rescues Huntington’s Disease Proteotoxicity by Preventing Oxidative Stress and Promoting TFEB Function Science Translational Medicine (2012)

Huntington’s disease (HD) is caused by CAG repeat expansions in the (huntingtin htt) gene, yielding proteins containing polyglutamine repeats that become misfolded and resist degradation. Previous studies demonstrated that mutant htt interferes with transcriptional programs ...

AdipoR1 and 2 are Expressed on Warm Sensitive Neurons of the Hypothalamic Preoptic Area and Contribute to Central Hyperthermic Effects of Adiponectin Brain Research (2011)

Adiponectin can act in the brain to increase energy expenditure and reduce body weight by mechanisms not entirely understood. We found that adiponectin type 1 and type 2 receptors (AdipoR1 and AdipoR2) are expressed in ...

Endocannabinoid Hydrolysis Generates Brain Prostaglandins That Promote Neuroinflammation Science (2011)

Phospholipase A2(PLA2) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)–mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol ...

Ccl22/MDC, is a Prostaglandin Dependent Pyrogen, Acting in the Anterior Hypothalamus to Induce Hyperthermia via Activation of Brown Adipose Tissue Cytokine (2011)

CC Chemokine ligand 22 (Ccl22) is a selective, high affinity ligand at the CC chemokine receptor 4 (Ccr4). We have identified cDNAs encoding both ligand and receptor of the Ccl22–Ccr4 pair in cDNA libraries of ...

Hypothalamic and dietary control of temperature-mediated longevity Ageing Research Reviews (2010)

Polydactyly in Mice Lacking HDAC9/HDRP Experimental Biology and Medicine (2008)

Mice lacking histone deacetylase 9 (HDAC9) and its truncated variant, HDRP, exhibit post-axial polydactyly that manifests as an extra big toe on the right hind foot. Polydactyly in HDAC9/ HDRP knockout mice occurs with incomplete ...

Class IIA HDACs in the regulation of neurodegeneration Frontiers in Bioscience (2008)

HDAC4 inhibits cell-cycle progression and protects neurons from cell death Developmental Neurobiology (2008)

Opposing Effects of Sirtuins on Neuronal Survival: SIRT1- Mediated Neuroprotection Is Independent of Its Deacetylase Activity PLOS ONE (2008)

Background Growing evidence suggests that sirtuins, a family of seven distinct NAD-dependent enzymes, are involved in the regulation of neuronal survival. Indeed, SIRT1 has been reported to protect against neuronal death, while SIRT2 promotes neurodegeneration. ...

Histone deacetylases: focus on the nervous system Cellular and Molecular Life Sciences (2007)

Neuroprotection by histone deacetylase-related protein Molecular and Cellular Biology (2006)

Inhibition of neuronal apoptosis by the cyclin-dependent kinase inhibitor GW8510: identification of 3' substituted indolones as a scaffold for the development of neuroprotective drugs Journal of Neurochemistry (2005)

The c-Raf inhibitor GW5074 provides neuroprotection in vitro and in an animal model of neurodegeneration through a MEK-ERK and Akt-independent mechanism Journal of Neurochemistry (2004)

Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis The Journal of Clinical Investigation (2003)