Damon T Page

Damon T Page, Ph.D.

Associate Professor

Department: SR-NEURO-PAGE LAB
Business Phone: (561) 228-2899
Business Email: damonpage@ufl.edu

About Damon T Page

Damon, Associate Professor in the Department of Neuroscience, received his bachelor’s degree in biology from Eastern Oregon University and his PhD from the University of Cambridge. He was a postdoctoral fellow at the MRC Laboratory of Molecular Biology and the Massachusetts Institute of Technology (MIT).

Additional Positions:
Associate Professor, Neuroscience
2016 – 2022 · Scripps Research
Assistant Professor, Neuroscience
2011 – 2016 · Scripps Research
Senior Analyst
2010 – 2011 · Allen Institute for Brain Science
Postdoctoral Fellow
2004 – 2010 · Massachusetts Institute of Technology
Postdoctoral Fellow
2002 – 2004 · Massachusetts Institute of Technology

Research Profile

My laboratory is focused on understanding how the components that make up the cellular architecture of the brain (neuronal and glial cell types) are generated and assemble into functional circuits that underlie behavior and cognition. The mechanisms by which these processes occur are largely unknown, and yet, disruptions can have enormous societal and personal consequences in the form of neurodevelopmental and psychiatric disorders. Such disorders provide a window into the basic genetic, molecular and cellular mechanisms involved in building the brain. This insight may be used in turn to benefit those affected by mental illness, pointing to molecular targets for improved diagnostics and therapeutics.

Autism spectrum disorder (ASD) is one such disorder. ASD is characterized by a range of phenotypes, including deficits in social behavior, as well as an altered trajectory of brain growth in some cases. Clues to mechanisms come from reports that PTEN-PI3K-mTOR, monoamine, neuropeptide and synaptic signaling pathways have been implicated in ASD pathogenesis. Understanding how these risk factors influence brain and behavior will give us basic insight into how the brain develops and how this process is altered in ASD.

Along these lines, my laboratory makes use of transgenic and knockout mice to understand the biology of how risk factors for autism and related neurodevelopmental disorders influence the development of cell types and circuits underlying behavior and cognition, and to test efficacy of potential therapeutics. The development of structural and functional connectivity in the cerebral cortex, the seat of our highest cognitive capabilities and a structure that is highly relevant for autism, is a major area of focus for our work.

We use a variety of techniques, including mouse genetics, histology, molecular cell biology, cell culture, genomics, informatics, pharmacology, imaging and behavioral phenotyping.

Publications

2022
Pten haploinsufficiency causes desynchronized growth of brain areas involved in sensory processing.
iScience. 25(2) [DOI] 10.1016/j.isci.2022.103796. [PMID] 35198865.
2021
Dyrk1a Mutations Cause Undergrowth of Cortical Pyramidal Neurons via Dysregulated Growth Factor Signaling.
Biological psychiatry. 90(5):295-306 [DOI] 10.1016/j.biopsych.2021.01.012. [PMID] 33840455.
2021
Environmental Enrichment Rescues Social Behavioral Deficits and Synaptic Abnormalities in Pten Haploinsufficient Mice.
Genes. 12(9) [DOI] 10.3390/genes12091366. [PMID] 34573348.
2021
Molecular motor KIF3B in the prelimbic cortex constrains the consolidation of contextual fear memory.
Molecular brain. 14(1) [DOI] 10.1186/s13041-021-00873-9. [PMID] 34749771.
2021
Molecular motor protein KIF5C mediates structural plasticity and long-term memory by constraining local translation.
Cell reports. 36(2) [DOI] 10.1016/j.celrep.2021.109369. [PMID] 34260917.
2020
Connecting Genotype with Behavioral Phenotype in Mouse Models of Autism Associated with PTEN Mutations.
Cold Spring Harbor perspectives in medicine. 10(9) [DOI] 10.1101/cshperspect.a037010. [PMID] 31871231.
2020
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.
2020
Social Behavior Is Modulated by Valence-Encoding mPFC-Amygdala Sub-circuitry.
Cell reports. 32(2) [DOI] 10.1016/j.celrep.2020.107899. [PMID] 32668253.
2019
Genetic Suppression of mTOR Rescues Synaptic and Social Behavioral Abnormalities in a Mouse Model of Pten Haploinsufficiency.
Autism research : official journal of the International Society for Autism Research. 12(10):1463-1471 [DOI] 10.1002/aur.2186. [PMID] 31441226.
2019
Pten haploinsufficiency disrupts scaling across brain areas during development in mice.
Translational psychiatry. 9(1) [DOI] 10.1038/s41398-019-0656-6. [PMID] 31804455.
2018
Improved Scalability of Neuron-Based Phenotypic Screening Assays for Therapeutic Discovery in Neuropsychiatric Disorders.
Molecular neuropsychiatry. 3(3):141-150 [DOI] 10.1159/000481731. [PMID] 29594133.
2017
Forebrain depletion of Rheb GTPase elicits spatial memory deficits in mice.
Neurobiology of aging. 50:134-143 [DOI] 10.1016/j.neurobiolaging.2016.11.006. [PMID] 27960107.
2016
Autism-relevant behaviors are minimally impacted by conditional deletion of Pten in oxytocinergic neurons.
Autism research : official journal of the International Society for Autism Research. 9(12):1248-1262 [DOI] 10.1002/aur.1641. [PMID] 27220363.
2016
Hyperconnectivity of prefrontal cortex to amygdala projections in a mouse model of macrocephaly/autism syndrome.
Nature communications. 7 [DOI] 10.1038/ncomms13421. [PMID] 27845329.
2016
Zika virus infection during the period of maximal brain growth causes microcephaly and corticospinal neuron apoptosis in wild type mice.
Scientific reports. 6 [DOI] 10.1038/srep34793. [PMID] 27713505.
2015
Decreased aggression and increased repetitive behavior in Pten haploinsufficient mice.
Genes, brain, and behavior. 14(2):145-57 [DOI] 10.1111/gbb.12192. [PMID] 25561290.
2015
Ectopic expression of the striatal-enriched GTPase Rhes elicits cerebellar degeneration and an ataxia phenotype in Huntington’s disease.
Neurobiology of disease. 82:66-77 [DOI] 10.1016/j.nbd.2015.05.011. [PMID] 26048156.
2015
Pten Mutations Alter Brain Growth Trajectory and Allocation of Cell Types through Elevated β-Catenin Signaling.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 35(28):10252-67 [DOI] 10.1523/JNEUROSCI.5272-14.2015. [PMID] 26180201.
2015
Social Behavioral Deficits Coincide with the Onset of Seizure Susceptibility in Mice Lacking Serotonin Receptor 2c.
PloS one. 10(8) [DOI] 10.1371/journal.pone.0136494. [PMID] 26308619.
2015
Syngap1 haploinsufficiency damages a postnatal critical period of pyramidal cell structural maturation linked to cortical circuit assembly.
Biological psychiatry. 77(9):805-15 [DOI] 10.1016/j.biopsych.2014.08.001. [PMID] 25444158.
2014
A high-resolution spatiotemporal atlas of gene expression of the developing mouse brain.
Neuron. 83(2):309-323 [DOI] 10.1016/j.neuron.2014.05.033. [PMID] 24952961.
2014
Huntingtin promotes mTORC1 signaling in the pathogenesis of Huntington’s disease.
Science signaling. 7(349) [DOI] 10.1126/scisignal.2005633. [PMID] 25351248.
2014
Pten haploinsufficient mice show broad brain overgrowth but selective impairments in autism-relevant behavioral tests.
Human molecular genetics. 23(13):3490-505 [DOI] 10.1093/hmg/ddu057. [PMID] 24497577.
2012
Large-scale cellular-resolution gene profiling in human neocortex reveals species-specific molecular signatures.
Cell. 149(2):483-96 [DOI] 10.1016/j.cell.2012.02.052. [PMID] 22500809.
2011
A candidate circuit approach to investigating autism.
Anatomical record (Hoboken, N.J. : 2007). 294(10):1671-84 [PMID] 22026018.
2011
Multi-scale correlation structure of gene expression in the brain.
Neural networks : the official journal of the International Neural Network Society. 24(9):933-42 [DOI] 10.1016/j.neunet.2011.06.012. [PMID] 21764550.
2009
Computerized assessment of social approach behavior in mouse.
Frontiers in behavioral neuroscience. 3 [DOI] 10.3389/neuro.08.048.2009. [PMID] 20198104.
2009
Differential gene expression in the developing lateral geniculate nucleus and medial geniculate nucleus reveals novel roles for Zic4 and Foxp2 in visual and auditory pathway development.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 29(43):13672-83 [DOI] 10.1523/JNEUROSCI.2127-09.2009. [PMID] 19864579.
2009
Haploinsufficiency for Pten and Serotonin transporter cooperatively influences brain size and social behavior.
Proceedings of the National Academy of Sciences of the United States of America. 106(6):1989-94 [DOI] 10.1073/pnas.0804428106. [PMID] 19208814.
2009
Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons.
Journal of neurodevelopmental disorders. 1(3):224-36 [DOI] 10.1007/s11689-009-9025-8. [PMID] 19816534.
2008
Association between microdeletion and microduplication at 16p11.2 and autism.
The New England journal of medicine. 358(7):667-75 [DOI] 10.1056/NEJMoa075974. [PMID] 18184952.
2008
Multiple roles for apoptosis facilitating condensation of the Drosophila ventral nerve cord.
Genesis (New York, N.Y. : 2000). 46(2):61-8 [DOI] 10.1002/dvg.20365. [PMID] 18257102.
2005
Condensation of the central nervous system in embryonic Drosophila is inhibited by blocking hemocyte migration or neural activity.
Developmental biology. 279(1):233-43 [PMID] 15708571.
2004
A mode of arthropod brain evolution suggested by Drosophila commissure development.
Evolution & development. 6(1):25-31 [PMID] 15108815.
2003
A function for Egf receptor signaling in expanding the developing brain in Drosophila.
Current biology : CB. 13(6):474-82 [PMID] 12646129.
2002
Inductive patterning of the embryonic brain in Drosophila.
Development (Cambridge, England). 129(9):2121-8 [PMID] 11959822.
2000
labial acts to initiate neuronal fate specification, but not axon pathfinding, in the embryonic brain of Drosophila.
Development genes and evolution. 210(11):559-63 [PMID] 11180806.

Grants

Apr 2022 ACTIVE
Regulation of mTOR signaling in the developing cerebral cortex as a point of convergence for multiple autism risk factors
Role: Principal Investigator
Funding: NATL INST OF HLTH NIMH
Apr 2022 ACTIVE
Delineating contributions of PI3K signaling to neurodevelopmental consequences of Pten haploinsufficiency
Role: Principal Investigator
Funding: NATL INST OF HLTH NINDS

Education

Ph.D. in Molecular Biology
2002 · University of Cambridge
Bachelor's of Science in Biology
1999 · Eastern Oregon University

Contact Details

Phones:
Business:
(561) 228-2899
Emails:
Business:
damonpage@ufl.edu
Addresses:
Business Mailing:
120 SCRIPPS WAY
JUPITER FL 33458