Lindsay M De Biase

Title(s)Assistant Professor, Physiology
ORCID ORCID Icon0000-0003-0177-5601 Additional info
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    Title(s)Assistant Professor, Neurobiology

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    Collapse Education and Training
    Yale University, New Haven, CTB.S.05/2003Molecular Cellular and Developmental Biology
    Johns Hopkins University School of Medicine, Baltimore, MDPh.D.10/2011Neuroscience
    National Institutes on Drug Abuse , Baltimore, MD07/2018Postdoctoral Training
    Collapse Awards and Honors
    Johns Hopkins School of Medicine2009Robert Goodman Scholars Award
    NIH2014Fellows Award for Research Excellence
    Annual Meeting of Greater Baltimore Chapter, Society for Neuroscience2014First Place, Postdoctoral poster
    NIH2015Fellows Award for Research Excellence
    Winter Conference on Brain Research, Breckenridge, CO2016Second Place; Poster awards
    NIH2016Fellows Award for Research Excellence
    NIDA Women’s Science Advisory Committee2017Excellence in Scientific Research Award
    NIDA2017NIDA Postdoctoral Fellow Mentoring Award
    Brain and Behavior Research Foundation2018NARSAD Young Investigator Award
    Glen Foundation and American Foundation for Aging Research2019Grant for Junior Faculty
    Parkinson's Foundation2021Stanley Fahn Junior Faculty Award
    McKnight Brain Research Foundation / AFAR 2021Innovator Award in Cognitive Aging

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    Lindsay M. De Biase, PhD is an Assistant Professor in the Department of Physiology in the David Geffen School of Medicine at UCLA. She received her B.S in Cellular, Molecular, and Developmental Biology at Yale University in 2003. Upon graduation, she worked as a research assistant with Drs. Eric Hoffman and Robert Frieshtat at the Children’s National Medical Center in Washington D.C. investigating gene expression changes associated with amyotrophic lateral sclerosis (Lou Gehrig’s disease) and acute lung injury. Dr. De Biase then entered the Neuroscience Graduate Program at Johns Hopkins School of Medicine where she earned her Ph.D. working with Dr. Dwight Bergles on synaptic signaling from neurons to oligodendrocyte precursor cells (OPCs). During her thesis work, Dr. De Biase developed novel approaches for electrophysiological analysis of neuron-OPC synapses and discovered that OPC synaptic connectivity varies across brain regions and is rapidly lost as the cells mature into oligodendrocytes, consistent with the hypothesis that this signaling acts as a brake on OPC differentiation. Dr. De Biase then completed postdoctoral training at the National Institute on Drug Abuse, where she discovered that microglia in distinct basal ganglia nuclei exhibit regionally-specialized phenotypes, overturning the widespread belief that these cells are equivalent throughout the CNS. Her work also provided evidence that local regulatory cues play a critical role in shaping microglial diversity. She joined UCLA's faculty in the fall of 2018.

    Research in the De Biase Lab focuses on understanding causes and consequences of microglial regional specialization within basal ganglia circuits.

    Microglia are dynamic, macrophage-like cells within the CNS. In disease and injury contexts, they undergo dramatic changes in cell phenotype that result in powerful neuroprotective and/or neurotoxic effects. In the healthy brain, microglia remove cellular debris and pathogens from surrounding tissue and can modulate both neuronal membrane properties and synapses, positioning these cells as key contributors to both physiological and pathological circuit function.

    Microglia are not equivalent throughout the brain and exhibit specialized phenotypes in different nuclei of the basal ganglia (BG), circuits involved in reward and motivation. We know almost nothing about the potential impact of this regional microglial variation on function and resilience of surrounding neurons. Work in the De Biase lab focuses on three overarching questions: 1) How does microglial variation impact synaptic function of BG neurons and associated reinforcement-driven behaviors? 2) How does basal phenotype shape microglial injury responses and influence susceptibility of BG neurons to damage? 3) What regulatory cues instruct basal phenotypes of BG microglia? We pursue these questions using multiple technical approaches including slice electrophysiology, advanced imaging, and molecular biology.

    An overarching goal of this research program is to promote innovative approaches to treating CNS circuit dysfunction and disease. Microglia are ubiquitous, capable of self-renewal, highly plastic, and can be influenced from the periphery, making them highly attractive targets for therapeutic interventions in a broad range of pathological contexts. Information obtained from these research efforts will be particularly relevant for pathological alterations that impact BG circuits, such as addiction and other psychiatric illness, neurodegeneration, toxic poisoning, and focal inflammatory conditions.

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    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. to make corrections and additions.
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    Altmetrics Details PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. Synapse-specific roles for microglia in development: New horizons in the prefrontal cortex. Front Mol Neurosci. 2022; 15:965756. Blagburn-Blanco SV, Chappell MS, De Biase LM, DeNardo LA. PMID: 36003220; PMCID: PMC9394540.
      View in: PubMed   Mentions: 3  
    2. Microglia Drive Pockets of Neuroinflammation in Middle Age. J Neurosci. 2022 05 11; 42(19):3896-3918. Moca EN, Lecca D, Hope KT, Etienne F, Schaler AW, Espinoza K, Chappell MS, Gray DT, Tweedie D, Sidhu S, Masukawa L, Sitoy H, Mathew R, Saban DR, Greig NH, De Biase LM. PMID: 35396327; PMCID: PMC9097782.
      View in: PubMed   Mentions: 9     Fields:    Translation:AnimalsCells
    3. AMPA Receptors Exist in Tunable Mobile and Immobile Synaptic Fractions In Vivo. eNeuro. 2021 Jul-Aug; 8(4). Gray DT, De Biase LM. PMID: 34301746; PMCID: PMC8313140.
      View in: PubMed   Mentions:    Fields:    Translation:Cells
    4. Maturation of the microglial population varies across mesolimbic nuclei. Eur J Neurosci. 2020 10; 52(7):3689-3709. Hope KT, Hawes IA, Moca EN, Bonci A, De Biase LM. PMID: 32281691.
      View in: PubMed   Mentions: 4     Fields:    Translation:AnimalsCells
    5. Genetic deletion of vesicular glutamate transporter in dopamine neurons increases vulnerability to MPTP-induced neurotoxicity in mice. Proc Natl Acad Sci U S A. 2018 12 04; 115(49):E11532-E11541. Shen H, Marino RAM, McDevitt RA, Bi GH, Chen K, Madeo G, Lee PT, Liang Y, De Biase LM, Su TP, Xi ZX, Bonci A. PMID: 30442663; PMCID: PMC6298109.
      View in: PubMed   Mentions: 23     Fields:    Translation:AnimalsCells
    6. Region-Specific Phenotypes of Microglia: The Role of Local Regulatory Cues. Neuroscientist. 2019 08; 25(4):314-333. De Biase LM, Bonci A. PMID: 30280638.
      View in: PubMed   Mentions: 23     Fields:    Translation:HumansAnimalsCells
    7. Ventral midbrain astrocytes display unique physiological features and sensitivity to dopamine D2 receptor signaling. Neuropsychopharmacology. 2019 01; 44(2):344-355. Xin W, Schuebel KE, Jair KW, Cimbro R, De Biase LM, Goldman D, Bonci A. PMID: 30054584; PMCID: PMC6300565.
      View in: PubMed   Mentions: 38     Fields:    Translation:AnimalsCells
    8. Local Cues Establish and Maintain Region-Specific Phenotypes of Basal Ganglia Microglia. Neuron. 2017 Jul 19; 95(2):341-356.e6. De Biase LM, Schuebel KE, Fusfeld ZH, Jair K, Hawes IA, Cimbro R, Zhang HY, Liu QR, Shen H, Xi ZX, Goldman D, Bonci A. PMID: 28689984; PMCID: PMC5754189.
      View in: PubMed   Mentions: 196     Fields:    Translation:AnimalsCells
    9. Neurons Internalize Functionalized Micron-Sized Silicon Dioxide Microspheres. Cell Mol Neurobiol. 2017 Nov; 37(8):1487-1499. Wallace VJ, Cimbro R, Rubio FJ, Fortuno LV, Necarsulmer JC, Koivula PP, Henderson MJ, DeBiase LM, Warren BL, Harvey BK, Hope BT. PMID: 28260198; PMCID: PMC5583033.
      View in: PubMed   Mentions: 1     Fields:    Translation:HumansAnimalsCells
    10. Same players, different game: AMPA receptor regulation in oligodendrocyte progenitors. Nat Neurosci. 2011 Oct 26; 14(11):1358-60. De Biase LM, Bergles DE. PMID: 22030543.
      View in: PubMed   Mentions: 4     Fields:    Translation:AnimalsCells
    11. NMDA receptor signaling in oligodendrocyte progenitors is not required for oligodendrogenesis and myelination. J Neurosci. 2011 Aug 31; 31(35):12650-62. De Biase LM, Kang SH, Baxi EG, Fukaya M, Pucak ML, Mishina M, Calabresi PA, Bergles DE. PMID: 21880926; PMCID: PMC3179911.
      View in: PubMed   Mentions: 74     Fields:    Translation:AnimalsCells
    12. A requirement for nuclear factor-kappaB in developmental and plasticity-associated synaptogenesis. J Neurosci. 2011 Apr 06; 31(14):5414-25. Boersma MC, Dresselhaus EC, De Biase LM, Mihalas AB, Bergles DE, Meffert MK. PMID: 21471377; PMCID: PMC3113725.
      View in: PubMed   Mentions: 97     Fields:    Translation:HumansAnimalsCells
    13. Excitability and synaptic communication within the oligodendrocyte lineage. J Neurosci. 2010 Mar 10; 30(10):3600-11. De Biase LM, Nishiyama A, Bergles DE. PMID: 20219994; PMCID: PMC2838193.
      View in: PubMed   Mentions: 133     Fields:    Translation:AnimalsCells
    14. Sepsis alters the megakaryocyte-platelet transcriptional axis resulting in granzyme B-mediated lymphotoxicity. Am J Respir Crit Care Med. 2009 Mar 15; 179(6):467-73. Freishtat RJ, Natale J, Benton AS, Cohen J, Sharron M, Wiles AA, Ngor WM, Mojgani B, Bradbury M, Degnan A, Sachdeva R, Debiase LM, Ghimbovschi S, Chow M, Bunag C, Kristosturyan E, Hoffman EP. PMID: 19136373; PMCID: PMC2654976.
      View in: PubMed   Mentions: 31     Fields:    Translation:HumansAnimalsCells
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