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    Conrad Alano, PhD

    TitleAssociate Professor
    SchoolUCSF School of Medicine
    DepartmentNeurology
    Address4150 Clement St
    San Francisco CA 94121
    Phone415-750-2011
    vCardDownload vCard

      Collapse Overview 
      Collapse Overview
      Conrad C. Alano, Ph.D. is a graduate of UC Berkeley (B.A.) and University of Rochester School of Medicine (Ph.D.). He further received training as a REAP fellow in the Neurology Department with Raymond A. Swanson, M.D. at the San Francisco VA Medical Center. Dr. Alano's research has advanced our understanding of the role of mitochondria in various CNS and cardiovascular injury models. Dr. Alano is an active member of the Society for Neuroscience, American Heart Association, American Stroke Association, Mitochondrial Research Society, and the United Mitochondrial Disease Foundation. He has served as an ad hoc reviewer for various journals including Journal of Neuroscience, Journal of Neurochemistry, Journal of Cell Biology, Journal of Neuroscience Research, and the Journal of Cardiovascular Pharmacology. Dr. Alano has received numerous awards and honors for his work, including the Kelsey Wright Award for Scientific Excellence in 2003, the Laverna Titus Award in 2004, and a VA Merit Award in 2007.

      Research Focus.

      Various acute and chronic injuries lead to cell death and brain injury. In neurodegenrative diseases, cells die as a result of a complex cascade of events, such as an increase in free radical generation or activation of cell death pathways. In stroke, cells die because they are deprived of oxygen and nutrients. Mitochondria in cells use oxygen and glucose products to produce energy for the cell, which is why they are nicknamed the “powerhouse” of cells. In addition, mitochondria play a central role in numerous fundamental cellular processes ranging from ATP generation and calcium (Ca2+) homeostasis. However, mitochondria also serve as a signal for cells to die. When mitochondria are failing, they send out molecules that signal the initiation of cell death cascades. For example, dysfunction of the mitochondrial Ca2+ homeostasis and an increase in free radical production has been implicated in the development of neurodegenerative diseases, aging, and cardiac injury. These studies should allow us to identify potential therapeutic intervention targeted towards the treatment of brain injury after an acute stroke episode.

      To better understand the mechanism of stroke leading to brain injury, the goals of our group are the following:

      - Identifying the role of mitochondria in the life and death of brain cells.
      - Determining the signals to mitochondrial that switches its role from life to death.
      - Characterizing the effects of mitochondrial failure leading to cell death.
      - Translating the findings from cell culture models to animal models of stroke, with the overall goal of identifying potential therapeutic intervention for stroke.


      Collapse Bibliographic 
      Collapse Publications
      Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help.
      List All   |   Timeline
      1. Vuong B, Hogan-Cann AD, Alano CC, Stevenson M, Chan WY, Anderson CM, Swanson RA, Kauppinen TM. NF-?B transcriptional activation by TNFa requires phospholipase C, extracellular signal-regulated kinase 2 and poly(ADP-ribose) polymerase-1. J Neuroinflammation. 2015; 12:229. PMID: 26637332; PMCID: PMC4670503.
      2. Kim SH, Lu HF, Alano CC. Neuronal Sirt3 protects against excitotoxic injury in mouse cortical neuron culture. PLoS One. 2011; 6(3):e14731. PMID: 21390294; PMCID: PMC3046953.
      3. Tao R, Kim SH, Honbo N, Karliner JS, Alano CC. Minocycline protects cardiac myocytes against simulated ischemia–reperfusion injury by inhibiting poly(ADP-ribose) polymerase-1. J Cardiovasc Pharmacol. 2010 Dec; 56(6):659-68. PMID: 20881608; PMCID: PMC3064957.
      4. Tang KS, Suh SW, Alano CC, Shao Z, Hunt WT, Swanson RA, Anderson CM. Astrocytic poly(ADP-ribose) polymerase-1 activation leads to bioenergetic depletion and inhibition of glutamate uptake capacity. Glia. 2010 Mar; 58(4):446-57. PMID: 19795500.
        View in: PubMed
      5. Zhang J, Chatterjee K, Alano CC, Kalinowski MA, Honbo N, Karliner JS. Vincristine attenuates N-methyl-N'-nitro-N-nitrosoguanidine-induced poly-(ADP) ribose polymerase activity in cardiomyocytes. J Cardiovasc Pharmacol. 2010 Mar; 55(3):219-26. PMID: 20375713; PMCID: PMC2865187.
      6. Alano CC, Garnier P, Ying W, Higashi Y, Kauppinen TM, Swanson RA. NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death. J Neurosci. 2010 Feb 24; 30(8):2967-78. PMID: 20181594; PMCID: PMC2864043.
      7. Tao R, Hoover HE, Honbo N, Kalinowski M, Alano CC, Karliner JS, Raffai R. High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate. Am J Physiol Heart Circ Physiol. 2010 Mar; 298(3):H1022-8. PMID: 20061542; PMCID: PMC2838562.
      8. Tao R, Hoover HE, Zhang J, Honbo N, Alano CC, Karliner JS. Cardiomyocyte S1P1 receptor-mediated extracellular signal-related kinase signaling and desensitization. J Cardiovasc Pharmacol. 2009 Jun; 53(6):486-94. PMID: 19433984; PMCID: PMC2835551.
      9. Alano CC, Tran A, Tao R, Ying W, Karliner JS, Swanson RA. Differences among cell types in NAD(+) compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes. J Neurosci Res. 2007 Nov 15; 85(15):3378-85. PMID: 17853438.
        View in: PubMed
      10. Tao R, Karliner JS, Simonis U, Zheng J, Zhang J, Honbo N, Alano CC. Pyrroloquinoline quinone preserves mitochondrial function and prevents oxidative injury in adult rat cardiac myocytes. Biochem Biophys Res Commun. 2007 Nov 16; 363(2):257-62. PMID: 17880922; PMCID: PMC2844438.
      11. Suh SW, Aoyama K, Alano CC, Anderson CM, Hamby AM, Swanson RA. Zinc inhibits astrocyte glutamate uptake by activation of poly(ADP-ribose) polymerase-1. Mol Med. 2007 Jul-Aug; 13(7-8):344-9. PMID: 17728843; PMCID: PMC1952665.
      12. Alano CC, Kauppinen TM, Valls AV, Swanson RA. Minocycline inhibits poly(ADP-ribose) polymerase-1 at nanomolar concentrations. Proc Natl Acad Sci U S A. 2006 Jun 20; 103(25):9685-90. PMID: 16769901; PMCID: PMC1480467.
      13. Alano CC, Swanson RA. Players in the PARP-1 cell-death pathway: JNK1 joins the cast. Trends Biochem Sci. 2006 Jun; 31(6):309-11. PMID: 16679020.
        View in: PubMed
      14. Ying W, Alano CC, Garnier P, Swanson RA. NAD+ as a metabolic link between DNA damage and cell death. J Neurosci Res. 2005 Jan 1-15; 79(1-2):216-23. PMID: 15562437.
        View in: PubMed
      15. Alano CC, Ying W, Swanson RA. Poly(ADP-ribose) polymerase-1-mediated cell death in astrocytes requires NAD+ depletion and mitochondrial permeability transition. J Biol Chem. 2004 Apr 30; 279(18):18895-902. PMID: 14960594.
        View in: PubMed
      16. Gum ET, Swanson RA, Alano C, Liu J, Hong S, Weinstein PR, Panter SS. Human serum albumin and its N-terminal tetrapeptide (DAHK) block oxidant-induced neuronal death. Stroke. 2004 Feb; 35(2):590-5. PMID: 14726550.
        View in: PubMed
      17. Sevigny MB, Silva JM, Lan WC, Alano CC, Swanson RA. Expression and activity of poly(ADP-ribose) glycohydrolase in cultured astrocytes, neurons, and C6 glioma cells. Brain Res Mol Brain Res. 2003 Oct 7; 117(2):213-20. PMID: 14559156.
        View in: PubMed
      18. Ying W, Chen Y, Alano CC, Swanson RA. Tricarboxylic acid cycle substrates prevent PARP-mediated death of neurons and astrocytes. J Cereb Blood Flow Metab. 2002 Jul; 22(7):774-9. PMID: 12142562.
        View in: PubMed
      19. Alano CC, Beutner G, Dirksen RT, Gross RA, Sheu SS. Mitochondrial permeability transition and calcium dynamics in striatal neurons upon intense NMDA receptor activation. J Neurochem. 2002 Feb; 80(3):531-8. PMID: 11905998.
        View in: PubMed
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