Our mission is to understand and prevent disorders of the brain
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Our mission is to understand and prevent disorders of the brain
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Dementia is a progressive multifactorial disorder and the only top cause of death that cannot be effectively treated or prevented. It will impact future generations with increasing magnitude and represents one of the biggest health challenges of our time.
We believe that basic and translational science can steer the course toward effective treatment and prevention of dementia and other devastating disorders of the brain. Dementia involves multiple converging pathobiological pathways. Impairments in glial functions and glial-neuronal interactions are emerging as central drivers of dementia and other CNS disorders. Our primary goal is to harness glial-neuronal interactions for treating and preventing disease, including frontotemporal dementia and Alzheimer's disease.
We use multipronged experimental methods to unravel glial pathobiology, glial interactions with other neural cell types, glial roles in cognitive function and behavior, and how changes in glial cells influence disease.
Recent Achievements
Found that astrocytic production of mitochondrial reactive oxygen species (mtROS) is site-specific, regulated by neuroimmune signaling, and causes selective changes in protein oxidation and gene transcription.
Established that astrocytic mtROS produced by complex III amplifies tauopathy associated with FTD and other dementias.
Uncovered that FTD/AD-linked changes in astrocytic TDP-43 disrupt antiviral signaling and cause selective neuronal vulnerability and progressive cognitive decline.
Determined that astrocytic release of chemokines and activation neuronal chemokine receptors regulates presynaptic function and hippocampal transmission.
Discovered that astrocytic G protein-coupled receptor signaling modulates cognitive function in a bidirectional and sex-dimorphic manner.
Identified the astrocytic glutamate receptor mGluR3 as an important regulator of spatial memory and search behavior.
Meet Us
Meet Us
Anna G. Orr, Ph.D.
Principal Investigator, Group Leader and Mentor
Nan and Stephen Swid Assistant Professor of Frontotemporal Dementia Research
Assistant Professor of Neuroscience
Adam L. Orr, Ph.D.
Principal Investigator, Group Leader and co-Mentor
Assistant Professor of Research in Neuroscience
Translational Project Lead, Redox Therapeutics
Dr. Anna Orr received her Ph.D. in Neuroscience from Emory University under the mentorship of Dr. Stephen Traynelis, and focused on the molecular mechanisms regulating microglial motility and neuroinflammation. She completed postdoctoral training with Dr. Lennart Mucke at the Gladstone Institute of Neurological Disease and UCSF, where she investigated the effects of astrocytic receptor signaling on cognitive function and Alzheimer’s disease. Dr. Orr’s research has been supported by the NIA, NINDS, the Association for Frontotemporal Degeneration, Alzheimer’s Drug Discovery Foundation, BrightFocus Foundation, Alzheimer's Association, Leon Levy Foundation, and other organizations. She has been honored with the Neuroscience Teaching and Mentoring Award from the Weill Cornell Graduate School and is currently the Nan and Stephen Swid Assistant Professor of Frontotemporal Dementia Research and Assistant Professor of Neuroscience at Weill Cornell Medicine.
Dr. Adam Orr received his Ph.D. in Neuroscience from Emory University under the guidance of Dr. Xiao-Jiang Li, where he studied mitochondrial transport in Huntington’s disease. He then trained with Dr. Martin Brand at the Buck Institute for Research on Aging where he explored mitochondrial reactive oxygen species production and discovered novel small molecules that selectively block mitochondrial production of reactive oxygen species. He has also worked at the Gladstone Institutes in the labs of Drs. Ken Nakamura and Robert Mahley and collaborated with two start-up companies to therapeutically correct mitochondrial dysfunction in disease. He has been generously supported by the Sanofi iAward, NIA, NINDS, Brightfocus Foundation, the Association for Frontotemporal Degeneration, and the Daedalus Fund for Innovation from the BioPharma Alliances and Research Collaborations at WCM. He is currently Assistant Professor of Neuroscience at Weill Cornell Medicine.
Till Zimmer, Ph.D.
Postdoctoral Associate in Neuroscience, BrightFocus Foundation Fellow and Alzheimer’s Association Fellow
Till Zimmer received his Ph.D. at the University Medical Centers Amsterdam under the supervision of Dr. Eleonora Aronica in Amsterdam, Netherlands. His thesis work focused on the pathogenic triad of neuroinflammation, oxidative stress, and iron metabolism in epilepsy with a focus on astrocytes. He was also a Fellow of the Marie Skłodowska-Curie Actions of the European Commission. Till is interested in reactive oxygen species and oxidative stress, lipid biology, and gliopathy in the pathogenesis of neurological disease. His work in the Orr lab is supported by both the Alzheimer’s Association and the BrightFocus Foundation fellowship programs. Till also serves on several committees, including the Appel Institute Postdoctoral Initiative and the Diversity, Equity and Inclusion committees.
Minwoo Wendy Jang, Ph.D.
Postdoctoral Associate in Neuroscience, National Research Foundation of Korea Fellow
Minwoo Wendy Jang received her Ph.D. in Neuroscience (Nano-Bio-Information-Technology integrated major) at KU-KIST Graduate School of Converging Science and Technology, Korea University, Republic of Korea under the supervision of Dr. C. Justin Lee. Her thesis work mainly focused on characterizing pathophysiological functions of TMEM43 in glial cells of the cochlea and the brain. Minwoo was also engaged in elucidating the molecular mechanisms of astrocytic volume changes in the hippocampus and astrocyte-neuronal interactions during hemodynamic responses in the sensory cortex. In the Orr lab, Minwoo is hoping to expand her research and investigate molecular and physiological roles of astrocytes in neuropsychiatric and neurological disorders.
Daniel Barnett, B.S.
Neuroscience Graduate Student, National Institutes of Health F31 NRSA Fellow
Daniel Barnett received his Bachelor’s degree in Neuroscience from the University of Rochester. During his undergraduate training, Daniel worked in the laboratory of Dr. Houhui Xia studying the role of protein phosphatase-1 in synaptic transmission and plasticity. For this research, he was awarded Rochester’s de Kiewiet Research Fellowship and the Discover Grant. Daniel also conducted research with Dr. Dragony Fu, where he studied the impact of tRNA modification enzymes on the cellular stress response. He has also received Honorable Mention for his NSF Graduate Research Fellowship proposal. In the Orr Lab, Daniel is examining glial biology and glial-neuronal interactions through the lens of oxidative mechanisms in healthy and pathological conditions.
Stephanie Jackvony, B.A.
Neuroscience Graduate Student, National Institutes of Health F31 NRSA Fellow
Stephanie Jackvony received her Bachelor’s degree in Behavioral Neuroscience and Philosophy from Connecticut College. During her undergraduate training, Stephanie conducted clinical fMRI research with Dr. Daniel Dickstein at Bradley Hospital, where they studied cognitive flexibility and examined biomarkers of psychiatric disorders. Her work at Bradley Hospital inspired her Honors thesis in Dr. Joseph Schroeder’s laboratory, where she examined the effects of an altered light/dark cycle and methylphenidate treatment on learning and memory in an animal model of ADHD. Stephanie was awarded the Barry Goldwater Scholarship. She also received Honorable Mention for her NSF Graduate Research Fellowship proposal and developed a new graduate course at Weill Cornell, ‘Introduction to Neuroimmunology’. Stephanie is interested in antiviral pathways in brain aging and disease.
Laraib Ijaz, M.S.
Neuroscience Graduate Student
Laraib Ijaz received her Master’s degree in Neuroscience from Stony Brook University. During her training, Laraib worked in the laboratory of Dr. Christine DeLorenzo analyzing markers of pediatric multiple sclerosis. Her thesis focused on a novel brain development index and other brain imaging parameters in this population. Thereafter, Laraib worked at the New York Stem Cell Foundation with Dr. Valentina Fossati on a project using human iPSC-derived microglia-like cells to investigate the roles of MEF2C, a factor implicated in Alzheimer’s disease. In the Orr lab, Laraib is interested in glial cell pathophysiology associated with dementia, and in antiviral pathway alterations in brain aging and disease. Outside of the Orr lab, Laraib enjoys spending time with her family and creating memories with her sons.
Caroline Booraem, B.S.
Neuroscience Graduate Student
Caroline Booraem received her Bachelor’s degree in Neuroscience, Psychology, and Religion from Amherst College, where she played Varsity women’s ice hockey. After graduation, she worked in Dr. Matthew Bever’s laboratory at Brigham and Women’s Hospital in Boston, where she examined the immune response after ischemic stroke and intracerebral hemorrhage in patient samples and animal models. This work focused on how peripheral immune cells are affected by such injuries and contribute to inflammation in the brain. In the Orr lab, Caroline is interested in the roles of oxidative stress and neuroimmune interactions in physiological states and disease models. Outside of the lab, Caroline enjoys running in Central Park, knitting, and reading.
Evelyn Hardin, B.S.
Neuroscience Graduate Student
Evelyn Hardin received her Bachelor's degree in Neuroscience from Duke University with minors in History and Psychology. During her training, she worked in the laboratory of Dr. Richard Mooney studying auditory cortical circuits in hearing and deaf mice, and completed her honors thesis and post-graduate training with Dr. Cagla Eroglu. In the Eroglu lab, Evelyn investigated the roles of astrocyte-secreted protein Hevin/SPARCL1 in developmental synapse sculpting and microglial activity, and how astrocyte-neuron catenin-cadherin interactions govern cortical layer-specific astrocyte morphogenesis. In the Orr lab, Evelyn is interested in investigating mechanisms of ALS/FTD-linked genetic mutations and proteinopathies, and neuroimmune interactions in the context of ALS/FTD pathology. Outside of lab, Evelyn enjoys playing the harp, games and puzzles of all kinds, and taking long walks to explore NYC.
Amr Fatafta, B.A.
Research Technician I
Amr Fatafta received his Bachelor’s degree in Molecular Biology from Skidmore College, with a minor in Management and Business. During undergraduate training, Amr worked in the laboratory of Dr. Bernard Possidente, where he studied the effects of glial tauopathy on circadian rhythms in fruit flies. Amr also examined how deletion of SNORD-116 affects circadian rhythms in a mouse model of Prader-Willi syndrome. Outside the Orr lab, Amr is exploring his new neighborhood in Queens, with all of its locally owned hidden gems.
Alyssa Bodmer, B.S.
Research Technician I
Alyssa Bodmer received her Bachelor’s degree in Neuroscience and Dance from Connecticut College. During undergraduate training, she participated in Dr. Joseph Schroeder’s research, analyzing the effects of cocaine on locomotor activity and stereotypy in rats. She received the Ann Sloan Devlin Award for Excellence in Research Methods for a study she created and conducted, examining the effects of N95 masks on emotion perception and approachability of professors in an academic setting to investigate the impact of mask wearing on student-professor relationships. Outside the Orr lab, Alyssa performs with Mark Bankin Dance Company, as well as in other dance projects.
LAB ALUMNI (One or more years in the Orr lab)
Avital Licht-Murava, Ph.D.
Orr lab position: Senior Postdoctoral Fellow
Current position: Head of preclinical research, Cytora Stem
Fernando Palaguachi, B.S.
Orr lab position: Research Technician I-II
Current position: Master’s program student, NYU
Samantha Meadows-Ortiz, Ph.D.
Orr lab position: Neuroscience Graduate Student, NSF Fellow
Current position: Scientific consultant, UBS
Constance Zhou, Ph.D.
Orr lab position: Neuroscience Graduate Student
Current position: MD-PhD Student, Weill Cornell/Rockefeller/Sloan Kettering Tri-I Program
Join Us
Join Us
We welcome motivated students and postdoctoral fellows who are passionate about neuroscience, unraveling mechanisms of disease, and contributing to a supportive and collaborative research environment.
The Orr lab seeks candidates with interests in behavioral neuroscience, electrophysiology, neural cell signaling, molecular biology, and omic approaches, including transcriptomics/translatomics, proteomics, and lipidomics. We welcome inquiries from graduate students and postdoctoral fellows interested in basic and translational neuroscience, and strongly encourage underrepresented and minority applicants to consider our lab.
We offer the rare advantage of two dedicated mentors that support trainee research and career development. See additional details at WCM Postdoctoral Affairs: Open Postdoctoral Positions in the Orr Lab
Check out the links below to learn more about our research activities, lab news, and core values!
Our laboratory is located in a new state-of-the-art Belfer Research Building in the vibrant upper east side of Manhattan and is part of the bustling biomedical complex of Weill Cornell Medicine, Sloan Kettering, Rockefeller University, and NewYork-Presbyterian Hospital. If you are interested in joining our team, please send your CV and a summary of previous work and current interests to ago2002@med.cornell.edu.
Research Highlights
Research Highlights
Are there differences in glial function between males and females?
Astrocytic Receptors Modulate Cognition in a Sex-dimorphic Manner
Our study establishes that hippocampal astrocytes modulate cognition differently in males and females, thereby promoting mechanistic differences in brain function. We found that, in female mice, activation of astrocytic Gi/o receptor pathway enhances memory, whereas activation of astrocytic Gs receptor pathway impairs memory. In contrast, these pathways have the opposite effects in males. Sex differences were also induced by mGluR3, a major glutamate receptor in astrocytes that engages the Gi/o pathway. Thus, normal brain function requires a sex-specific balance in astrocytic receptor signaling. It is likely that aging, disease, environmental and genetic factors, and therapeutics that alter this balance cause sex-specific cognitive changes.
How do astrocytes influence disease?
Astrocytes Have Context-Specific Effects That Can Facilitate Selective Vulnerability
We review the emerging evidence from our lab and many others that astrocytes are highly dynamic and multifaceted, and that astrocytic responses and contributions in neurodegenerative disease are selective and context-dependent. We propose that astrocytes contribute to selective vulnerability in pathogenic conditions through maladaptive transitions to context-divergent phenotypes that impair specific brain regions and functions. Further studies of astrocytes in health and disease may provide new therapeutic approaches to enhance resilience against cognitive decline and neurodegenerative processes.
What promotes cognitive decline in dementia?
Dementia-linked Protein Buildup in Astrocytes Disrupts Antiviral Pathways, Causing Selective Neuronal Vulnerability and Cognitive Decline
Our work reveals that aberrant extranuclear accumulation of TDP-43 in astrocytes occurs in dementia. In mouse models, this buildup was sufficient to disrupt antiviral immune mechanisms in specific brain regions and increase chemokine signaling by astrocytes. These changes promoted selective impairments in presynaptic transmission and cognitive function. Blockers of antiviral pathways and chemokine signaling might alleviate cognitive decline in dementia and related disorders.
Leveraging Existing Therapeutics to Counteract Cognitive Deficits
New results show that short-term treatment with low doses of a selective receptor blocker enhances spatial memory in aging animals with chronic amyloid pathology, suggesting that existing drugs might counteract cognitive dysfunction in people with neurodegenerative disease.
Precise Blockade of Cell Damage Caused by Reactive Oxygen
Mitochondria produce ATP, but also generate reactive oxygen species implicated in disease-related cell damage. Newly discovered tools will help to precisely target reactive oxygen species without affecting the crucial process of ATP production.
Astrocytes Promote Forgetting in Health and Disease
'Star-shaped' glial cells are known to support neuronal health and function. New findings suggest that these cells may also be crucial for information storage and contribute to memory loss in disease. Therapeutically targeting these cells might prevent cognitive dysfunction in diverse disorders.
Find us
Find us
Publications
Publications
The following list contains preprints, peer-reviewed research articles, and invited reviews. Access the articles using the journal links below. Author abbreviations: Anna G. Orr (Orr AG), Adam L. Orr (Orr AL)
2024
Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology
Barnett D, Zimmer TS, Booraem C, Palaguachi F, Meadows SM, Xiao H, Chouchani ET, Orr AG, Orr AL
Hippocampal astrocytes induce sex-dimorphic effects on memory
Meadows SM, Palaguachi F, Jang MW, Licht-Murava A, Barnett D, Zimmer TS, Zhou C, McDonough S, Orr AL, Orr AG
Astrocytes in selective vulnerability to neurodegenerative disease
Zimmer TS, Orr AL, Orr AG
Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production
Bennett NK, Lee M, Orr AL, Nakamura K
2023
Astrocytes as drivers and disruptors of behavior: new advances in basic mechanisms and therapeutic targeting
Barnett D, Bohmbach K, Grelot V, Charlet A, Dallerac G, Ju YH, Nagai J, Orr AG (invited review)
Effects of adenosine A2A receptors on cognitive function in health and disease
International Review of Neurobiology
Garcia CP, Licht-Murava A, Orr AG (invited review)
Astrocytic TDP-43 dysregulation impairs memory by modulating antiviral pathways and interferon-inducible chemokines
Licht-Murava A, Meadows SM, Palaguachi F, Song SC, Jackvony S, Bram Y, Zhou C, Schwartz RE, Froemke RC, Orr AL, Orr AG.
Quantitative proteomic analysis reveals apoE4-dependent phosphorylation of the actin-regulating protein VASP
Molecular and Cellular Proteomics
Cakir Z, Lord SJ, Zhou Y, Jang GM, Polacco BJ, Eckhardt M, Jimenez-Morles D, Newton BW, Orr AL, Johnson JR, da Cruz A, Mullins RD, Krogan NJ, Mahley RW, Swaney DL.
2022
Astrocytes regulate spatial memory in a sex-specific manner
Meadows SM, Palaguachi F, Licht-Murava A, Barnett D, Zimmer TS, Zhou C, McDonough SR, Orr AL, Orr AG.
Astrocytic TDP-43 dysregulation impairs memory by modulating antiviral pathways and interferon-inducible chemokines
Licht-Murava A, Meadows SM, Palaguachi F, Song SC, Bram Y, Zhou C, Jackvony S, Schwartz RE, Froemke RC, Orr AL, Orr AG.
Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
Xia D, Lianoglou S, Sandmann T, Calvert M, Suh JH, Thomsen E, Dugas J, Pizzo ME, DeVos SL, Earr TK, Lin CC, Davis S, Ha C, Leung AW, Nguyen H, Chau R, Yulyaningsih E, Lopez I, Solanoy H, Masoud ST, Liang CC, Lin K, Astarita G, Khoury N, Zuchero JY, Thorne RG, Shen K, Miller S, Palop JJ, Garceau D, Sasner M, Whitesell JD, Harris JA, Hummel S, Gnörich J, Wind K, Kunze L, Zatcepin A, Brendel M, Willem M, Haass C, Barnett D, Zimmer TS, Orr AG, Scearce-Levie K, Lewcock JW, Di Paolo G, Sanchez PE.
2020
The use of site-specific suppressors to measure the relative contributions of different mitochondrial sites to skeletal muscle superoxide and hydrogen peroxide production
Goncalves RLS, Watson MA, Wong HS, Orr AL, Brand MD.
Branched photoswitchable tethered ligands enable ultra-efficient optical control and detection of class C G protein-coupled receptors
Acosta-Ruiz A, Gutzeit VA, Skelly MJ, Meadows S, Lee S, Parekh P, Orr AG, Liston C, Pleil K, Broichhagen J, Levitz J.
2019
To be or not to be pink(1): contradictory findings in an animal model for Parkinson's disease
de Haas R, Heltzel LCMW, Tax D, van den Broek P, Steenbreker H, Verheij MMM, Russel FGM, Orr AL, Nakamura K, Smeitink JAM.
Neuronal apolipoprotein E4 expression results in proteome-wide alterations and
compromises bioenergetic capacity by disrupting mitochondrial function
Journal of Alzheimer’s Disease
Orr AL, Kim C, Jimenez-Morales D, Newton BW, Johnson JR, Krogan NJ, Swaney DL, Mahley RW.
2018
Plate-based measurement of superoxide and hydrogen peroxide production by isolated mitochondria
Wong HS, Monternier PA, Orr AL, Brand MD.
Istradefylline reduces memory deficits in aging mice with plaque pathology
Neurobiology of Disease *Featured on the journal cover.
Orr AG, Lo I, Schumacher H, Ho K, Gill M, Guo W, Kim DH, Knox A, Saito T, Saido TC, Simms J, Toddes C, Wang X, Yu GQ, Mucke L.
2017
Loss of α-synuclein does not affect mitochondrial bioenergetics in rodent neurons
Pathak D, Berthet A, Bendor J, Yu K, Sellnow R, Orr AL, Nguyen M, Edwards R, Manfredsson F, Nakamura K.
Long-term oral kinetin does not protect against α-synuclein-induced neurodegeneration in rodent models of Parkinson’s disease
Orr AL, Rutaganira FU, De Roulet D, Huang EJ, Hertz NT, Shokat KM, Nakamura K.
2016
Suppressors of superoxide-H2O2 production at site Iq of mitochondrial complex I protect against stem cell hyperplasia and ischemia-reperfusion injury
Brand MD, Goncalves RLS, Orr AL, Vargas L, Gerencser AA, Jensen MB, Wang YT, Melov S, Turk CN, Matzen JT, Dardov VJ, Petrassi HM, Meeusen SL, Perevoshchikova IV, Jasper H, Brookes PS, Ainscow EK.
2015
Astrocytic adenosine receptor A2A and Gs-coupled signaling regulate memory
Orr AG, Hsiao EC, Wang MM, Ho K, Kim DH, Wang X, Guo W, Kang J, Yu GQ, Adame A, Devidze N, Dubal DB, Masliah E, Conklin BR, Mucke L.
Suppressors of superoxide production from mitochondrial complex III.
Orr AL, Vargas L, Turk CN, Baaten JE, Matzen JT, Dardov VJ, Attle SJ, Li J,Quackenbush DC, Goncalves RLS, Perevoshchikova IV, Petrassi HM, Meeusen SL, Ainscow EK, Brand MD.
2014
Novel inhibitors of mitochondrial sn-glycerol 3-phosphate dehydrogenase
PLoS ONE
Orr AL, Ashok D, Sarantos MR, Ng R, Shi T, Gerencser AA, Hughes RE, Brand MD.
Production of superoxide/H2O2 by dihydroorotate dehydrogenase in rat skeletal muscle mitochondria
Hey-Mogensen M, Goncalves RL, Orr AL, Brand MD.
2013
Inhibitors of ROS production by the ubiquinone-binding site of mitochondrial complex I identified by chemical screening
Orr AL, Ashok D, Sarantos MR, Shi T, Hughes RE, Brand MD.
Sites of superoxide and hydrogen peroxide production during fatty acid oxidation in rat skeletal muscle mitochondria
Perevoshchikova IV, Quinlan CL, Orr AL, Gerencser AA, Brand M.
Sites of reactive oxygen species generation by mitochondria oxidizing different substrates
Quinlan CL, Perevoshchikova IV, Orr AL, Hey-Mogensen, M, Brand MD.
NF-kB activity is inversely correlated to RNF11 expression in Parkinson's disease
Pranski EL, Van Sanford CD, Dalal NV, Orr AL, Karmali D, Cooper DS, Gearing M, Lah JJ, Levey AI, Betarbet RS.
The role of mitochondrial function and cellular bioenergetics in aging and disease
British Journal of Dermatology
Brand MD, Orr AL, Perevoshchikova IV, Quinlan CL.
2012
Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model
Sanchez PE, Zhu L, Verret L, Vossel KA, Orr AG, Cirrito JR, Devidze N, Ho K, Yu GQ, Palop JJ, Mucke L.
A refined analysis of superoxide production from mitochondrial sn-glycerol 3-phosphate dehydrogenase
Journal of Biological Chemistry
Orr AL, Quinlan CL, Perevoshchikova IV, Brand MD.
Mitochondrial complex II can generate reactive oxygen species at high rates in both the forward and reverse reactions
Journal of Biological Chemistry
Quinlan CL, Orr AL, Perevoshchikova IV, Treberg JT, Brand MD.
Neuronal RING finger protein 11 (RNF11) regulates canonical NF-κB signaling
Pranski EL, Dalal NV, Herskowitz JH, Orr AL, Roesch LA, Fritz JJ, Heilman C, Lah JJ, Levey AI, Betarbet RS.
Comparative distribution of protein components of the A20 ubiquitin-editing complex in normal human brain
Pranski EL, Van Sanford CD, Dalal NV, Orr AL, Karmali D, Cooper DS, Costa N, Heilman CJ, Gearing M, Lah JJ, Levey AI, Betarbet RS.
Native rates of superoxide production from multiple sites in isolated mitochondria measured using endogenous reporters
Quinlan CL, Treberg JT, Perevoshchikova IV, Orr AL, Brand MD.
2011
Reversing EphB2 depletion rescues cognitive functions in Alzheimer model
Cisse M, Halabisky B, Harris J, Devidze N, Dubal DB, Sun B, Orr AG, Lotz G, Kim DH, Hamto P, Ho K, Yu GQ, Mucke L.
A reduction in ATP demand and mitochondrial activity with neural differentiation of human embryonic stem cells
Birket MJ, Orr AL, Gerencser AA, Madden DT, Vitelli C, Swistowski A, Brand MD, Zeng X.
2010
Interleukin-1 mediates long-term hippocampal dentate granule cell loss following postnatal viral infection
Orr AG, Sharma A, Binder NB, Miller AH, Pearce BD (2010) Journal of Molecular Neuroscience http://www.ncbi.nlm.nih.gov/pubmed/19774496
A subunit-selective potentiator of NR2C- and NR2D-containing NMDA receptors
Mullasseril P, Hansen KB, Vance KM, Ogden KK, Yuan H, Kurtkaya NL, Santangelo R, Orr AG, Le P, Vellano KM, Liotta DC, Traynelis SF. Nature Communications http://www.ncbi.nlm.nih.gov/pubmed/20981015
Implementation of a fluorescence-based screening assay identifies histamine H3 receptor antagonists clobenpropit and iodophenpropit as subunit-selective N-methyl-D-aspartate receptor antagonists
Hansen KB, Mullasseril P, Dawit S, Kurtkaya NL, Yuan H, Vance KM, Orr AG, Kvist T, Ogden KK, Le P, Vellano KM, Lewis I, Kurtkaya S, Du Y, Qui M, Murphy TJ, Snyder JP, Bräuner-Osborne H, Traynelis SF. J Pharmacol Exp Ther http://www.ncbi.nlm.nih.gov/pubmed/20197375
Impaired mitochondrial trafficking in Huntington’s disease
Li XJ, Orr AL, Li S. Biochim Biophys Acta http://www.ncbi.nlm.nih.gov/pubmed/19591925
2009
Adenosine A2A receptor mediates microglial process retraction
Orr AG, Orr AL, Li XJ, Gross RE, Traynelis SF. Nature Neuroscience http://www.ncbi.nlm.nih.gov/pubmed/19525944
Differential regulation of microglial motility by ATP/ADP and adenosine
Gyoneva S, Orr AG, Traynelis SF. Parkinsonism Relat Disorders http://www.ncbi.nlm.nih.gov/pubmed/20082989
2008
N-terminal mutant htt associates with mitochondria directly and disrupts the interaction of mitochondria with trafficking proteins
Orr AL, Li SH, Wang CE, Li H, Wang J, Rong J, Xu X, Mastroberardino PG, Greenamyre JT, Li XJ. Journal of Neuroscience http://www.ncbi.nlm.nih.gov/pubmed/18337408
Sex-dependent effect of BAG-1 in ameliorating motor deficits of Huntington’s disease transgenic mice
Orr AL, Huang S, Roberts MA, Fang ZH, Reed JC, Li SH, Li XJ. Journal of Biological Chemistry http://www.ncbi.nlm.nih.gov/pubmed/18400759
Plasmin potentiates synaptic N-methyl-D-aspartate receptor function in hippocampal neurons through activation of protease-activated receptor-1
Mannaioni G, Orr AG, Hamill CE, Yuan H, Pedone KH, McCoy KL, Berlinguer Palmini R, Junge CE, Lee CJ, Yepes M, Hepler JR, Traynelis SF. Journal of Biological Chemistry http://www.ncbi.nlm.nih.gov/pubmed/18474593
A FRET-based method to study protein thiol oxidation in histological preparations
Mastroberardino PG, Orr AL, Hu X, Na HM, Greenamyre JT. Free Rad Biol Med http://www.ncbi.nlm.nih.gov/pubmed/18620047
Accumulation of N-terminal mutant huntingtin in mouse and monkey models implicated as a pathogenic mechanism in Huntington’s disease
Wang CE, Tydlacka S, Orr A, Yang SH, Graham R, Hayden M, Li SH, Chan A, Li XJ. Human Molecular Genetics http://www.ncbi.nlm.nih.gov/pubmed/18558632
Impaired ubiquitin-proteasome system activity in the synapses of Huntington’s disease mice
Wang J, Wang CE, Orr A, Tydlacka S, Li SH, Li XJ. Journal of Cell Biology http://www.ncbi.nlm.nih.gov/pubmed/18362179
2005
Activation of protease-activated receptor-1 triggers astrogliosis after brain injury
Nicole O, Goldshmidt A, Hamill CE, Sorensen SD, Sastre A, Lyuboslavsky P, Hepler JR, McKeon RJ, Traynelis SF. Journal of Neuroscience http://www.ncbi.nlm.nih.gov/pubmed/15858058
Glial reactivity after damage: implications for scar formation and neuronal recovery
Hamill CE*, Goldshmidt A*, Nicole O, McKeon RJ, Brat DJ, Traynelis SF. Clinical Neurosurgery *Equal contributions. http://www.ncbi.nlm.nih.gov/pubmed/16626052
