Positions

Overview

  • Dr. Arrant graduated with a B.S. in Toxicology from the University of Louisiana at Monroe in 2007. He then entered the Integrated Toxicology and Environmental Health Program at Duke University, and in 2012 earned a PhD in Pharmacology in the laboratory of Dr. Cynthia Kuhn. In 2013, Dr. Arrant joined the laboratory of Dr. Erik Roberson at the University of Alabama at Birmingham for postdoctoral training with mouse models of frontotemporal dementia. Dr. Arrant was promoted to a Scientist position in 2017, and in 2019 joined the Center for Neurodegeneration and Experimental Therapeutics in UAB’s Department of Neurology as an Assistant Professor.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2019 Reduction of microglial progranulin does not exacerbate pathology or behavioral deficits in neuronal progranulin-insufficient miceNeurobiology of Disease.  124:152-162. 2019
    2018 Partial Tmem106b reduction does not correct abnormalities due to progranulin haploinsufficiencyMolecular Neurodegeneration.  13. 2018
    2018 Progranulin gene therapy improves lysosomal dysfunction and microglial pathology associated with frontotemporal dementia and neuronal ceroid lipofuscinosisJournal of Neuroscience.  38:2341-2358. 2018
    2017 Restoring neuronal progranulin reverses deficits in a mouse model of frontotemporal dementiaBrain.  140:1447-1465. 2017
    2016 Progranulin haploinsufficiency causes biphasic social dominance abnormalities in the tube testGenes, Brain and Behavior.  15:588-603. 2016
    2016 Rho kinase inhibition as a therapeutic for progressive supranuclear palsy and corticobasal degenerationJournal of Neuroscience.  36:1316-1323. 2016
    2015 Simplified dietary acute tryptophan depletion: Effects of a novel amino acid mixture on the neurochemistry of C57BL/6J miceFood & Nutrition Research.  59. 2015
    2015 Effects of exercise on progranulin levels and gliosis in progranulin-insufficient miceeNeuro.  2. 2015
    2014 Exposure to mitochondrial genotoxins and dopaminergic neurodegeneration in Caenorhabditis elegansPLoS ONE.  9. 2014
    2014 Dietary manipulation of serotonergic and dopaminergic function in C57BL/6J mice with amino acid depletion mixturesJournal of Neural Transmission.  121:153-162. 2014
    2014 Early retinal neurodegeneration and impaired Ran-mediated nuclear import of TDP-43 in progranulin-deficient FTLDJournal of Experimental Medicine.  211:1937-1945. 2014
    2013 Use of the light/dark test for anxiety in adult and adolescent male ratsBehavioural Brain Research.  256:119-127. 2013
    2013 Adolescent male rats are less sensitive than adults to the anxiogenic and serotonin-releasing effects of fenfluramineNeuropharmacology.  65:213-222. 2013
    2013 Lower anxiogenic effects of serotonin agonists are associated with lower activation of amygdala and lateral orbital cortex in adolescent male ratsNeuropharmacology.  73:359-367. 2013
    2012 Effects of acute tryptophan depletion on brain serotonin function and concentrations of dopamine and norepinephrine in C57BL/6J and BALB/cJ micePLoS ONE.  7. 2012
    2012 Individual differences in psychostimulant responses of female rats are associated with ovarian hormones and dopamine neuroanatomyNeuropharmacology.  62:2267-2277. 2012
    2010 Dopamine uptake inhibitors but not dopamine releasers induce greater increases in motor behavior and extracellular dopamine in adolescent rats than in adult male ratsJournal of Pharmacology and Experimental Therapeutics.  335:124-132. 2010

    Chapter

    Year Title Altmetric
    2016 Frontotemporal Dementia.  141-175. 2016

    Research Overview

  • My lab investigates the cellular mechanisms underlying functional deficits in dementia and aging. We seek to integrate data from cellular and animal models with data from patients to gain insight into mechanisms of disease and discover new therapeutic targets. We use a variety of approaches, including: rodent behavioral assays, biochemical analysis of genetic mouse models of disease, gene expression with viral vectors, and primary neuronal culture.

    Current projects focus on Frontotemporal Dementia (FTD), a devastating neurodegenerative disorder that is a leading cause of dementia before the age of 60. Loss of function mutations in the progranulin gene are one of the most common genetic causes of FTD. We are investigating the cellular function of progranulin, and how progranulin mutations may cause FTD. We are also investigating the role of endolysosomal dysfunction in FTD.
  • Full Name

  • Andrew Arrant