Baoji Xu

Baoji Xu, Ph.D.


Department: SR-NEURO-XU LAB
Business Phone: (561) 228-2340
Business Email:

About Baoji Xu

Dr. Xu received his Ph.D. in molecular biology at Stanford University, California and postdoctoral training in neuroscience at the University of California San Francisco, California. He subsequently became Professor at Georgetown University Medical Center in Washington, DC. In 2013, he moved to the Scripps Research Institute Florida.

Additional Positions:
Affiliate Professor
2015 – 2015 · Florida Atlantic University, Charles E Schmidt College of Medicine
2013 – 2013 · The Scripps Research Institute
Adjunct Professor
2013 – 2018 · Georgetown University Medical Center
Ad hoc grant reviewer of NIH Molecular Neuropharmacology and Signaling (MNPS) study section,
2010 – 2010 · NIH Neurological Sciences and Disorders C (NSD-C) study section, and National Science Foundation
Associate Professor with tenure
2009 – 2013 · Georgetown University Medical Center
Ad hoc grant reviewer of NIH Clinical Neuroplasticity and Neurotransmitters (CNNT) study section
2008 – 2008 · National Institutes of Health
Assistant Professor
2003 – 2009 · Georgetown University Medical Center
Research Scientist II
2001 – 2002 · Chiron Corporation
Postdoctoral Fellow
1995 – 2001 · University of California, San Francisco
Related Links:


Annual IPN Junior Faculty Award
2009 · Georgetown University
Scientist Development Grant Award
2004-2007 · American Heart Association
Whitehall Foundation Award
2003-2006 · Whitehall Foundation
Predoctoral Fellowship
1989-1994 · Rockefeller Foundation

Research Profile

The goal of our laboratory is to understand how both healthy and diseased brains work. We focus on the mechanisms by which growth factors such as brain-derived neurotrophic factor (BDNF) regulate the development and function of brain neural circuits that control body weight, learning, mood, and social behaviors. We hope that our research will lead to discovery of novel therapeutics for neurodegenerative diseases, neurodevelopmental disorders, and obesity.

Central control of eating behavior and obesity Obesity has become a leading worldwide health problem because of its high prevalence. Obese children and adults are developing type-2 diabetes at high rates, and are at significant risk for life-threatening cardiovascular disease and cancer. Despite the enormous economic cost of obesity, there is currently no effective and safe treatment available for this health issue. Understanding the central mechanism that controls food intake and energy expenditure will provide opportunities to develop novel interventions for obesity.

Our group has played a leading role in discovering brain-derived neurotrophic factor (BDNF) as a key regulator of body weight by suppressing food intake and promoting energy expenditure. We and others have shown that disruption in BDNF-to-TrkB signaling leads to severe obesity in humans and mice. We are conducting studies to identify neural circuits that control appetite and energy expenditure in mice by using biochemical, behavioral, genetic, physiological and viral approaches. Identification of the circuits will allow us to further investigate what signals are generated upon eating to stimulate BDNF release from neurons in the brain, how the released BDNF alters the activity of the circuits, and how the circuits stop eating and stimulate energy utilization. This research project will help us understand not only how our body controls eating, a fundamental behavior, but also how the brain functions.

Autism spectrum disorders Autism spectrum disorders (ASD) are a heterogeneous group of neurodevelopmental disorders with deficits in two core domains: social interaction and communication, and repetitive behaviors or restrictive behaviors. Prevalence of ASD is 1 in 68 children under 8 years of age in the USA and is higher in males (1 in 42) than in females (1 in 189). There is a strong genetic basis for ASD. Mutations in hundreds of genetic loci, including both germline and de novo mutations, have been implicated in underlying ASD. Because of this high genetic heterogeneity, it is essential to find common pathophysiology pathways in order to develop therapeutic strategies for ASD. One common pathophysiology pathway underlying ASD is likely to be exaggerated protein synthesis, as mutations in several negative regulators of protein synthesis, such as PTEN, TSC1, TSC2 and FMRP, cause ASD. We are interested in identifying groups of cells in which exaggerated translation causes ASD-like behaviors and elucidating molecular mechanisms by which exaggerated translation alters the function of the cells.

Alzheimer’s disease Alzheimer’s disease (AD) is the most common neurodegenerative disease that causes problems with memory, thinking and behavior. Recent human genomic studies have implicated dysfunction of microglial cells, the resident immune cells in the brain, as an important cause for AD. Microglial dysfunction likely leads to deficits in clearance of toxic protein aggregates such as beta-amyloid (Ab) polymers and cell debris. We are interested in the cellular and biochemical process by which microglia sense and remove cell debris and protein aggregates in the brain. In addition, aging is the largest risk factor for AD and is associated with a reduction in uptake and metabolism of glucose, the main fuel source of the brain. We are also interested in elucidating biochemical pathways that regulate glucose metabolism in the brain and investigating how the activity of these pathways is reduced in aging brain.

Drug discovery No disease-modifying treatment is currently available for AD. In light of the failure of recent clinical trials that target Ab, there is an urgent need to develop drugs that target the AD pathophysiology, i.e. dysfunction and loss of synapses followed by neuronal loss. It is well documented that BDNF promotes neuronal survival and stimulates synaptogenesis and synaptic plasticity. Thus, increasing BDNF levels could halt or reverse the progress of AD by enhancing the function of existing synapses, inducing formation of new synapses, and preventing additional neuronal loss. The proof of principle for this concept has been shown in AD animal models. However, BDNF is a poor therapeutic agent due to its pharmacological properties. It is also difficult to find small-molecule compounds (~500 Da) that mimic the action of 56-fold larger BDNF protein (~28 kDa in dimer). We are searching for small-molecule compounds that stimulate production of endogenous BDNF in neurons. Because reduced levels of BDNF are also associated with obesity, anxiety and other brain disorders, these BDNF-boosting compounds could be useful for other diseases.

Open Researcher and Contributor ID (ORCID)



Genetic Dissection of BDNF and TrkB Expression in Glial Cells.
Biomolecules. 14(1) [DOI] 10.3390/biom14010091. [PMID] 38254691.
Neurotrophin-3 from the dentate gyrus supports postsynaptic sites of mossy fiber-CA3 synapses and hippocampus-dependent cognitive functions
Molecular Psychiatry. [DOI] 10.1038/s41380-023-02404-5.
Genetic Val66Met BDNF Variant Increases Hyperphagia on Fat-rich Diets in Mice
Endocrinology. 164(3) [DOI] 10.1210/endocr/bqad008. [PMID] 36631165.
High throughput assay for compounds that boost BDNF expression in neurons
SLAS Discovery. 28(3):88-94 [DOI] 10.1016/j.slasd.2023.02.005. [PMID] 36842668.
Rapid and Lasting Effects of Activating BDNF-Expressing PVH Neurons on Energy Balance.
eNeuro. 9(2):ENEURO.0009-22.2022 [DOI] 10.1523/ENEURO.0009-22.2022.
Discrete TrkB-expressing neurons of the dorsomedial hypothalamus regulate feeding and thermogenesis
Proceedings of the National Academy of Sciences. 118(4) [DOI] 10.1073/pnas.2017218118. [PMID] 33468645.
3’UTRs Regulate Mouse Ntrk2 mRNA Distribution in Cortical Neurons.
Journal of molecular neuroscience : MN. 70(11):1858-1870 [DOI] 10.1007/s12031-020-01579-8. [PMID] 32430868.
Elevated protein synthesis in microglia causes autism-like synaptic and behavioral aberrations
Nature Communications. 11(1) [DOI] 10.1038/s41467-020-15530-3. [PMID] 32286273.
TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits
Nature Communications. 11(1) [DOI] 10.1038/s41467-020-15537-w. [PMID] 32265438.
TrkB-expressing paraventricular hypothalamic neurons suppress appetite through multiple neurocircuits.
Nature communications. 11(1) [DOI] 10.1038/s41467-020-15537-w. [PMID] 32265438.
Activation of Anxiogenic Circuits Instigates Resistance to Diet-Induced Obesity via Increased Energy Expenditure.
Cell metabolism. 29(4):917-931.e4 [DOI] 10.1016/j.cmet.2018.12.018. [PMID] 30661931.
Caspase-2 promotes AMPA receptor internalization and cognitive flexibility via mTORC2-AKT-GSK3β signaling.
Nature communications. 10(1) [DOI] 10.1038/s41467-019-11575-1. [PMID] 31399584.
TrkB-expressing neurons in the dorsomedial hypothalamus are necessary and sufficient to suppress homeostatic feeding
Proceedings of the National Academy of Sciences. 116(8):3256-3261 [DOI] 10.1073/pnas.1815744116. [PMID] 30718415.
Orphan receptor GPR158 controls stress-induced depression.
eLife. 7 [DOI] 10.7554/eLife.33273. [PMID] 29419376.
Distinct cellular toxicity of two mutant huntingtin mRNA variants due to translation regulation.
PloS one. 12(5) [DOI] 10.1371/journal.pone.0177610. [PMID] 28494017.
Wnt5a is essential for hippocampal dendritic maintenance and spatial learning and memory in adult mice
Proceedings of the National Academy of Sciences. 114(4):E619-E628 [DOI] 10.1073/pnas.1615792114. [PMID] 28069946.
Control of spine maturation and pruning through proBDNF synthesized and released in dendrites.
Molecular and cellular neurosciences. 71:66-79 [DOI] 10.1016/j.mcn.2015.12.010. [PMID] 26705735.
Neurotrophic factor control of satiety and body weight
Nature Reviews Neuroscience. 17(5):282-292 [DOI] 10.1038/nrn.2016.24. [PMID] 27052383.
Neurotrophic factor control of satiety and body weight.
Nature reviews. Neuroscience. 17(5):282-92 [DOI] 10.1038/nrn.2016.24. [PMID] 27052383.
NF1 Is a Direct G Protein Effector Essential for Opioid Signaling to Ras in the Striatum.
Current biology : CB. 26(22):2992-3003 [DOI] 10.1016/j.cub.2016.09.010. [PMID] 27773571.
Regulation of Energy Balance via BDNF Expressed in Nonparaventricular Hypothalamic Neurons.
Molecular endocrinology (Baltimore, Md.). 30(5):494-503 [DOI] 10.1210/me.2015-1329. [PMID] 27003443.
TNP [N2-(m-Trifluorobenzyl), N6-(p-nitrobenzyl)purine] ameliorates diet induced obesity and insulin resistance via inhibition of the IP6K1 pathway.
Molecular metabolism. 5(10):903-917 [DOI] 10.1016/j.molmet.2016.08.008. [PMID] 27689003.
Ventromedial hypothalamic expression of Bdnf is required to establish normal patterns of afferent GABAergic connectivity and responses to hypoglycemia.
Molecular metabolism. 5(2):91-101 [DOI] 10.1016/j.molmet.2015.11.007. [PMID] 26909317.
Brain-derived neurotrophic factor is required for axonal growth of selective groups of neurons in the arcuate nucleus.
Molecular metabolism. 4(6):471-82 [DOI] 10.1016/j.molmet.2015.03.003. [PMID] 26042201.
Discrete BDNF Neurons in the Paraventricular Hypothalamus Control Feeding and Energy Expenditure.
Cell metabolism. 22(1):175-88 [DOI] 10.1016/j.cmet.2015.05.008. [PMID] 26073495.
HuD interacts with Bdnf mRNA and is essential for activity-induced BDNF synthesis in dendrites.
PloS one. 10(2) [DOI] 10.1371/journal.pone.0117264. [PMID] 25692578.
Stable G protein-effector complexes in striatal neurons: mechanism of assembly and role in neurotransmitter signaling.
eLife. 4 [DOI] 10.7554/eLife.10451. [PMID] 26613416.
BDNF signaling and survival of striatal neurons.
Frontiers in cellular neuroscience. 8 [DOI] 10.3389/fncel.2014.00254. [PMID] 25221473.
Loss of Ntrk2/Kiss1r signaling in oocytes causes premature ovarian failure.
Endocrinology. 155(8):3098-111 [DOI] 10.1210/en.2014-1111. [PMID] 24877631.
Ablation of TrkB expression in RGS9-2 cells leads to hyperphagic obesity.
Molecular metabolism. 2(4):491-7 [DOI] 10.1016/j.molmet.2013.08.002. [PMID] 24327964.
BDNF (I)rising from exercise.
Cell metabolism. 18(5):612-4 [DOI] 10.1016/j.cmet.2013.10.008. [PMID] 24206660.
Behavioral and transcriptome alterations in male and female mice with postnatal deletion of TrkB in dorsal striatal medium spiny neurons.
Molecular neurodegeneration. 8 [DOI] 10.1186/1750-1326-8-47. [PMID] 24369067.
Distinct roles for somatically and dendritically synthesized brain-derived neurotrophic factor in morphogenesis of dendritic spines.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 33(28):11618-32 [DOI] 10.1523/JNEUROSCI.0012-13.2013. [PMID] 23843530.
Midbrain-derived neurotrophins support survival of immature striatal projection neurons.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 33(8):3363-9 [DOI] 10.1523/JNEUROSCI.3687-12.2013. [PMID] 23426664.
Molecular and neural bases underlying roles of BDNF in the control of body weight.
Frontiers in neuroscience. 7 [DOI] 10.3389/fnins.2013.00037. [PMID] 23519010.
The skinny on brain-derived neurotrophic factor: evidence from animal models to GWAS.
Journal of molecular medicine (Berlin, Germany). 91(11):1241-7 [DOI] 10.1007/s00109-013-1071-8. [PMID] 23828555.
BDNF promotes differentiation and maturation of adult-born neurons through GABAergic transmission.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 32(41):14318-30 [DOI] 10.1523/JNEUROSCI.0709-12.2012. [PMID] 23055503.
Dendritic BDNF synthesis is required for late-phase spine maturation and recovery of cortical responses following sensory deprivation.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 32(14):4790-802 [DOI] 10.1523/JNEUROSCI.4462-11.2012. [PMID] 22492034.
Dendritically targeted Bdnf mRNA is essential for energy balance and response to leptin.
Nature medicine. 18(4):564-71 [DOI] 10.1038/nm.2687. [PMID] 22426422.
Sustained expression of brain-derived neurotrophic factor is required for maintenance of dendritic spines and normal behavior.
Neuroscience. 212:1-18 [DOI] 10.1016/j.neuroscience.2012.03.031. [PMID] 22542678.
Chronic deprivation of TrkB signaling leads to selective late-onset nigrostriatal dopaminergic degeneration.
Experimental neurology. 228(1):118-25 [DOI] 10.1016/j.expneurol.2010.12.018. [PMID] 21192928.
TrkB receptor controls striatal formation by regulating the number of newborn striatal neurons.
Proceedings of the National Academy of Sciences of the United States of America. 108(4):1669-74 [DOI] 10.1073/pnas.1004744108. [PMID] 21205893.
TrkB signaling in parvalbumin-positive interneurons is critical for gamma-band network synchronization in hippocampus.
Proceedings of the National Academy of Sciences of the United States of America. 108(41):17201-6 [DOI] 10.1073/pnas.1114241108. [PMID] 21949401.
BDNF overexpression in the forebrain rescues Huntington’s disease phenotypes in YAC128 mice.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 30(44):14708-18 [DOI] 10.1523/JNEUROSCI.1637-10.2010. [PMID] 21048129.
Distinct 3′UTRs differentially regulate activity-dependent translation of brain-derived neurotrophic factor (BDNF)
Proceedings of the National Academy of Sciences. 107(36):15945-15950 [DOI] 10.1073/pnas.1002929107. [PMID] 20733072.
Retrograde neurotrophic signaling requires a protein interacting with receptor tyrosine kinases via C2H2 zinc fingers.
Molecular biology of the cell. 21(1):36-49 [DOI] 10.1091/mbc.E09-04-0321. [PMID] 19864463.
ApoE4 decreases spine density and dendritic complexity in cortical neurons in vivo.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 29(48):15317-22 [DOI] 10.1523/JNEUROSCI.4026-09.2009. [PMID] 19955384.
New insights in the biology of BDNF synthesis and release: implications in CNS function.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 29(41):12764-7 [DOI] 10.1523/JNEUROSCI.3566-09.2009. [PMID] 19828787.
New insights into the role of brain-derived neurotrophic factor in synaptic plasticity.
Molecular and cellular neurosciences. 42(2):81-9 [DOI] 10.1016/j.mcn.2009.06.009. [PMID] 19577647.
Brain-derived neurotrophic factor over-expression in the forebrain ameliorates Huntington’s disease phenotypes in mice.
Journal of neurochemistry. 105(2):369-79 [PMID] 18086127.
Cre recombinase-mediated gene deletion in layer 4 of murine sensory cortical areas.
Genesis (New York, N.Y. : 2000). 46(6):289-93 [DOI] 10.1002/dvg.20393. [PMID] 18543315.
Distinct role of long 3′ UTR BDNF mRNA in spine morphology and synaptic plasticity in hippocampal neurons.
Cell. 134(1):175-87 [DOI] 10.1016/j.cell.2008.05.045. [PMID] 18614020.
Retinal TrkB receptors regulate neural development in the inner, but not outer, retina.
Molecular and cellular neurosciences. 38(3):431-43 [DOI] 10.1016/j.mcn.2008.04.004. [PMID] 18511296.
Brain-derived neurotrophic factor and TrkB modulate visual experience-dependent refinement of neuronal pathways in retina.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 27(27):7256-67 [PMID] 17611278.
Relationship of brain-derived neurotrophic factor and its receptor TrkB to altered inhibitory prefrontal circuitry in schizophrenia.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 25(2):372-83 [PMID] 15647480.
TrkB receptors are required for follicular growth and oocyte survival in the mammalian ovary.
Developmental biology. 267(2):430-49 [PMID] 15013804.
Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor.
Nature neuroscience. 6(7):736-42 [PMID] 12796784.
Requirement of the orphan nuclear receptor SF-1 in terminal differentiation of ventromedial hypothalamic neurons.
Molecular and cellular neurosciences. 22(4):441-53 [PMID] 12727442.
TrkB receptor signaling is required for establishment of GABAergic synapses in the cerebellum.
Nature neuroscience. 5(3):225-33 [PMID] 11836532.
Late-onset corticohippocampal neurodepletion attributable to catastrophic failure of oxidative phosphorylation in MILON mice.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 21(20):8082-90 [PMID] 11588181.
Cortical degeneration in the absence of neurotrophin signaling: dendritic retraction and neuronal loss after removal of the receptor TrkB.
Neuron. 26(1):233-45 [PMID] 10798407.
The Role of Brain-Derived Neurotrophic Factor Receptors in the Mature Hippocampus: Modulation of Long-Term Potentiation through a Presynaptic Mechanism involving TrkB
The Journal of Neuroscience. 20(18):6888-6897 [DOI] 10.1523/jneurosci.20-18-06888.2000.
Role of neurotrophin receptor TrkB in the maturation of rod photoreceptors and establishment of synaptic transmission to the inner retina.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 19(20):8919-30 [PMID] 10516311.
RNA-DNA hybrid formation at the human mitochondrial heavy-strand origin ceases at replication start sites: an implication for RNA-DNA hybrids serving as primers.
The EMBO journal. 15(12):3135-43 [PMID] 8670814.
A persistent RNA-DNA hybrid is formed during transcription at a phylogenetically conserved mitochondrial DNA sequence
Molecular and Cellular Biology. 15(1):580-589 [DOI] 10.1128/mcb.15.1.580. [PMID] 7528331.
Efficient incorporation of anti-HIV deoxynucleotides by recombinant yeast mitochondrial DNA polymerase.
The Journal of biological chemistry. 270(32):18929-34 [PMID] 7642550.
Properties of Mitochondrial DNA Metabolising Enzymes; Implications for Chemotherapy
Purine and Pyrimidine Metabolism in Man VIII. 465-469 [DOI] 10.1007/978-1-4615-2584-4_99.
A human mitochondrial transcriptional activator can functionally replace a yeast mitochondrial HMG-box protein both in vivo and in vitro.
Molecular and cellular biology. 13(3):1951-61 [PMID] 8441424.
Assignment of a yeast protein necessary for mitochondrial transcription initiation.
Nucleic acids research. 20(5):1053-9 [PMID] 1549466.


Aug 2023 ACTIVE
Astrocytic regulation of energy balance on high-fat diet
Role: Principal Investigator
Sep 2022 ACTIVE
Novel role of mitotic kinesin KIF11 in structural plasticity and memory
Role: Other
Apr 2022 ACTIVE
Molecular and cellular basis for autism spectrum disorders caused by exacerbated translation
Role: Principal Investigator
Apr 2022 – Mar 2024
TrkB neurons in the control of body weight
Role: Principal Investigator
Apr 2022 – Mar 2024
Unraveling the role of PVH BDNF neurons in energy balance
Role: Principal Investigator
Apr 2022 – Jun 2022
Molecular and Functional Identification of Neurocircuits Governing Energy Homeostasis (Post Doc Fellowship: Houtz)
Role: Other


Ph.D. in Molecular Biology
1995 · Stanford University
Master's of Science in Plant Physiology
1986 · Shanghai Institute of Plant Physiology, Chinese Academy of Sciences
Bachelor's of Science in Biology
1983 · Xiamen University, China

Contact Details

(561) 228-2340
Business Mailing:
Location C321