INSIDE WINTER 2011

Functional ConnectionBetween Brain AreasImpaired in Schizophrenia

1Researchers illuminate howgenetic variant may lead to

schizophrenia.

A Promising Approachfor Pontine Gliomas

1Studying an innovative methodfor delivering therapy to inop-

erative brain tumors in children.

Immunotherapy AgentSlows Rate of Brain CellLoss in Alzheimer’s Disease

3Phase II study shows lowerrates of brain shrinkage in

Alzheimer’s patients receivingIVIG for 18 months.

Gene Vital to Brain’s StemCells Implicated in DeadlyBrain Cancer

4Protein identified that maycause brain cancer in humans.

Diffuse pontine gliomas make up just 10 to 15 per-cent of pediatric brain tumors. But their progress

is swift, and they are uniformly fatal. NewYork-Presbyterian Hospital/Weill Cornell Medical Centerinvestigators are now assessing an innovative means ofdelivering radioimmunotherapy to these difficult-to-treat inoperable brain-stem tumors, which most com-monly strike children between the ages of 6 and 10.

“Among parents and physicians, there is a lot of desper-ation, a lot of anticipation, and a lot of hope with regard tothese tumors,” said Mark M. Souweidane, MD, who is leadingthe research. Dr. Souweidane is Professor of NeurologicalSurgery at Weill Cornell Medical College, Vice Chairmanof the Department of Neurological Surgery, and Directorof Pediatric Neurological Surgery, NewYork-PresbyterianPhyllis and David Komansky Center for Children’s Health. see Pontine Gliomas, page 5

SAVE THE DATEBrain Attack andCerebrovascular DiseaseUpdate 2011March 9, 2011The Rockefeller University New York, New York

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Children with diffuse pontine gliomas may appearotherwise quite healthy except for the symptoms associ-ated with the tumor – including altered eye movementsand facial expressions, headaches, vomiting, and fatigue.“Their hearts are healthy, their kidneys are healthy.There’s nothing short of this one-and-a-half to two-inchtumor in the brain stem that we need to cure, which isvery frustrating,” noted Dr. Souweidane.

The tumor remains localized in the brain stem, even-tually interfering with such vital functions as heart rate,respiration, swallowing, and clearing of the throat.Surgery and chemotherapy are ineffective. The standardof care is temporizing external beam radiation therapy.But even with this approach, all patients recur, and themedian survival time is only 9 to 12 months.

ADVANCES IN NEUROSCIENCE

PSYCHIATRY, NEUROLOGY AND NEUROSURGERY

Functional Connection Between Brain AreasImpaired in Schizophrenia, Study FindsContributing faculty for this article: Joseph A. Gogos, MD, PhD, and Maria Karayiorgou, MD

A Promising Approach for Pontine GliomasContributing faculty for this article: Mark M. Souweidane, MD

Affiliated with Columbia University College of Physicians and Surgeons and Weill Cornell Medical College

Patients with schizophrenia may have any of anarray of symptoms, including delusions, hallucina-

tions, thought disorder, flat affect, poverty of speech(alogia), asociality, and lack of motivation. Patients alsoinvariably have cognitive symptoms, including poorexecutive functioning, an inability to sustain attention,and deficits in workingmemory—and thesecognitive symptoms arebetter predictors of apatient’s functional out-come than the severityof other symptoms,according to ColumbiaUniversity researchersJoseph A. Gogos, MD, PhD, Associate Professor ofPhysiology and Cellular Biophysics, Neuroscience, andMaria Karayiorgou, MD, Professor of Psychiatry inGenetics and Physiology and Acting Chief of theDivision of Medical Genetics in the Department ofPsychiatry. see Brain Areas Impaired in Schizophrenia, page 2

In what may provide the most compelling evidenceto date, the researchers have illuminated how a geneticvariant may lead to schizophrenia by causing a disrup-tion in communication between the hippocampus andprefrontal cortex regions of the brain, areas believed tobe responsible for carrying out working memory.

In a recently published study, Drs. Karayiorgou andGogos and their colleagues, Joshua A. Gordon, MD, PhD,and Torfi Sigurdsson, PhD, demonstrated that a keyphysiological problem underlying cognitive symptomsof schizophrenia, in particular a deficit in working

Though schizophrenia is best known for its delusionsand hallucinations, it is the disease’s impact on suchcognitive abilities like working memory — a keyelement of executive functioning — that best predicthow well a person will function in society.

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ADVANCES IN NEUROSCIENCE: PSYCHIATRY, NEUROLOGY AND NEUROSURGERY

continued from Brain Areas Impaired in Schizophrenia, page 1

models allow us to use higher resolution tech-niques that provide information on the behav-ior of individual neurons.”

Rare structural mutations (microdeletionsor microduplications of DNA) such as the22q11.2 microdeletion are collectively animportant component of the genetic make-upof schizophrenia, “but at present the onlyindividual structural mutation unequivocallyassociated with schizophrenia is the 22q11.2microdeletion,” said Dr. Gogos. “Links to ad-ditional mutations are very likely to be estab-lished in the near future.”

About a third of people with 22q11.2microdeletions will eventually develop schiz-ophrenia. These microdeletions for the mostpart develop de novo and account for up to 2percent of cases with non-familial schizophre-nia (60 to 80 percent of people with schizo-phrenia have no family history of the disease).

“The 22q11.2 microdeletion encompassesabout 25 genes encoding a variety of pro-teins that play a role in important neuronalfunctions, including, for example, a proteinresponsible for the production of a class of mol-ecules (microRNAs) that regulate neuronalgene expression,” said Dr. Karayiorgou.

“While dysconnectivity between the pre-frontal lobe and hippocampus contributes tocognitive deficits in patients with schizophre-nia, it is less clear how this dysconnectivitycan lead to psychosis,” she added. “It’s possi-ble that dysconnectivity resulting from the22q11.2 microdeletion may be more perva-sive and affect connections between the pre-frontal lobe and other cortical and subcorticalareas. So it is very likely that other symptomsresult when abnormal dysconnectivity causes

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memory, results from an abnormal connectionbetween the hippocampus and prefrontal cortex(Nature Vol 464;April 1, 2010; p. 763-768). Theresearchers studied working memory in a pop-ulation of mice genetically engineered to carrythe equivalent of a microdeletion on humanchromosome 22 (22q11.2), one of the mainknown genetic risk factors for schizophrenia,which was discovered by Dr. Karayiorgou 15years ago. The mice (Df(16)A mice) have sever-al abnormalities analogous to those in peoplewith schizophrenia. According to Dr. Gogos,the Columbia team focused their research on thephysiology underlying working memory

normal, wild-type mice and Df(16)A miceperformed a T-maze task in which they werefirst directed to enter one of two arms, thenhad to remember the arm visited during theprevious phase and enter the opposite arm.

Explaining how the hippocampus and thepre-frontal cortex synchronize, Dr. Karayiorgounoted, “The coordinated, rhythmic activity ofneuronal populations in the brain gives rise tooscillations at a broad range of frequencies,which synchronize neural firing of intercon-nected cells in and between brain areas. Forexample, prefrontal cortex neuron firing ismodulated by hippocampus theta-frequency.”

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Reduced hippocampal–prefrontal synchrony correlates with behavioural performance in Df(16)A+/– mice. A, Coherence between the prefrontal cortex and the hippocampusduring habituation sessions before training on the spatial working memory task. B, Days taken to reach criterion performance on the spatial working memory task. C, Daystaken to reach criterion versus theta coherence during habituation sessions for each animal. Animals with lower theta coherence before training take longer to learn the spatialworking memory task. Green line, linear regression of data from Df(16)A+/– mice. D, Development of hippocampal–prefrontal coherence during acquisition of the workingmemory task: theta coherence (top) and choice accuracy (bottom) during early (trials 1–5), middle (trials 26–30) and late (session in which criterion was reached) stages oftraining in wild-type (left) and Df(16)A+/– (right) mice. *P<0.05, **P<0.01. Data shown, mean +/– s.e.m.

A B C D

“It’s possible that imaging approaches such as fMRI couldbe used to examine the pattern of connectivity among brainregions and facilitate diagnosis of specific subtypes ofschizophrenia in patients.”

— Maria Karayiorgou, MD

see Brain Areas Impaired in Schizophrenia, page 5

because it is easier to study in animal modelsthan symptoms such as psychosis and asociality.

“We hypothesized that cognitive deficitsare likely to be mediated by the same abnor-mal physiological processes as other symp-toms,” added Dr. Gogos, “and that by study-ing cognition in mutant models we can offersome more general insights into the patho-physiology of the disease.”

Previous research with animal models hasshown that neural activity in the hippocampusand prefrontal cortex becomes synchronizedduring the performance of a spatial workingmemory task. In this study, the Columbiateam measured the synchronization of neuralactivity between these brain areas while both

In this study, the research team found thatsynchrony between the hippocampus andprefrontal cortex increased during tasksrequiring working memory in wild-typemice, while the mutant mice showed dramat-ically reduced hippocampus-prefrontal cortexsynchrony.

“Similar experiments in individuals withschizophrenia are extremely challenging,”said Dr. Gogos. “Although methods such asfunctional MRI (fMRI) have been used inschizophrenia patients to record neural activi-ty, and abnormal prefrontal cortex–hippocam-pus coupling has been observed, the resultsremain inconclusive since the methods usedtend to be crude and macroscopic. Animal

MRIs of lateral ventricles (fluid-filled spaces at thecenter of the brain). Color codes show differences inrate of ventricular enlargement (a measure of brainvolume loss) over 1 year in patients treated with IVIGcontinuously or after 6 months of placebo. (courtesyof Dana Moore)

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ADVANCES IN NEUROSCIENCE: PSYCHIATRY, NEUROLOGY AND NEUROSURGERY

Slowing the Rate of Brain Volume Loss in Alzheimer’s DiseaseContributing faculty for this article: Norman R. Relkin, MD, PhD, Dana Moore, PhD, and Diamanto Tsakanikas, PhD

Several years ago, building on findings inanimal models that vaccines can generate

anti-amyloid antibodies with a potent effecton the underlying pathology of Alzheimer’sdisease, researchers in the Memory DisordersProgram at NewYork-Presbyterian/WeillCornell began evaluating the effectiveness ofintravenous immune globulin (IVIG). At theApril 2010 meeting of the AmericanAcademy of Neurology, Norman R. Relkin,MD, PhD, Director, reported the results of arecently concluded phase II study showingthat Alzheimer’s patients who received IVIGfor 18 months had significantly lower ratesof brain shrinkage (6.7 percent versus 12.7percent per year) and less whole-brain atro-phy (1.6 percent versus 2.2 percent per year)than subjects in the control arm, who receiveda placebo during the first six months.

IVIG, a plasma protein replacement therapy,is prepared from the plasma of approximately10,000 healthy human donors, and contains allfour subgroups of IgG antibodies. IVIG is FDA-approved for immune deficiency and autoim-mune disorders and some types of cancer.

In the phase II study, Dr. Relkin and col-leagues enrolled 24 patients with mild to mod-erate AD whose symptoms had progressed oncurrently available medications. For the first sixmonths, they compared four different doses ofIVIG, from 0.2 g/kg every 2 weeks to 0.8 g/kgevery 4 weeks, to saline placebo. For the next12 months those in the placebo group wereassigned to receive one of the four IVIG dosesand the rest of the patients continued on theirprevious dose. “On our primary and several sec-ondary outcome measures those who receivedcontinuous IVIG treatment over 18 monthsdid significantly better than those who hadgotten a delayed start,” said Dr. Relkin. Theprotective effect of IVIG was even more clear inthe group that received the dose determined tobe optimal in an earlier phase I study (0.4 g/kgevery 2 weeks).

“There was about a 50 percent reduction inbrain shrinkage in the continuously IVIG-treat-

“The antibodies in IVIG, which are natu-rally produced by humans, recognize the mis-folded, aggregated, pathologic forms of amy-loid, but largely ignore the physiologic mole-cules that we all produce from birth,” accord-ing to Dr. Relkin. “They only respond whenthe molecules start to aggregate to the toxicoligomers and fibrils that we find in the brainof Alzheimer’s disease patients.

“Our multi-center phase III study of IVIGin AD, co-sponsored by the NIH and Baxter,is currently underway,” says Dr. Relkin.Participating researchers at 38 sites in NorthAmerican are enrolling a total of 360 patientsto examine the effects of two different doses ofIVIG compared to placebo over an 18-monthperiod. “It’s been seven years since a new med-ication was approved for treating Alzheimer’sdisease,” Dr Relkin pointed out, “and it willbe at least another two years before the phaseIII IVIG study is completed. But if the resultsof the phase III study are at all similar to thoseof phase I and II, it will well be worth thewait.”

Around age 30 our brains begin to shrink at a well-defined rate of about .5 percent per year, and the changes

become conspicuous after age 60. In patients with Alzheimer’s disease (AD) these changes occur at two to four

times the normal rate, providing neurologists with a concrete measure of brain degeneration, which correlates

with declines in areas such as cognition, global outcome, behavior, and daily function.

ed group as a whole,” noted Dr. Relkin, “but wefound that the effect was dose dependent and inthe dose group that had the best clinical out-come. The rate of brain volume loss as measuredby ventricular enlargement was just 3 percent,the same as is reported in normal adults.”

Diamanto Tsakanikas, PhD, a neuropsy-chologist in the Weill Cornell MemoryDisorders Program, performed cognitive andbehavioral testing on the study subjects. Shefound that brain volume changes closely paral-leled positive outcomes on the Clinical GlobalImpressions of Change scale, the Alzheimer’sDisease Assessment Scale-Cognitive Subscale(ADAS-cog), and the Neuropsychiatric

“There was about a 50 percent reduction in brain shrinkagein the continuously IVIG-treated group as a whole...”

— Norman R. Relkin, MD, PhD

Ventricular Surface Atrophy MapsPlacebo

None Mild Moderate Severe

IVIG

Inventory. Patients in the uninterruptedIVIG-treatment group scored better thanthose in the delayed start of treatment or sub-optimal dosing groups, she reported.

The hallmark of AD is an accumulation ofamyloid in the brain, which begins longbefore symptoms become evident. Many ADresearchers now believe that these deposits area kind of “tombstone” of amyloid pathologyrather than the culprits behind the disease.Instead, Dr. Relkin, says, “It is the aggregat-ed soluble forms of amyloid – amyloidoligomers and higher order aggregates gener-ated in the process of misfolding – that arehighly toxic to brain cells and ultimately leadto neurodegeneration.”

“Aggregated forms of amyloid bind toreceptors involved in neurotransmission andgenerate abnormal currents that disrupt neuronalintegrity, thereby initiating a series of otherevents that actually mediate the cell death. Theseinclude inflammation, disordering of the neu-ronal cytoskeleton, reactive oxygen speciesattacking cell membranes, and a host of otherthings,” explained Dr. Relkin.

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ADVANCES IN NEUROSCIENCE: PSYCHIATRY, NEUROLOGY AND NEUROSURGERY

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Gene Vital to Brain’s Stem CellsImplicated in Deadly Brain CancerContributing faculty for this article: Antonio Iavarone, MD, and Anna Lasorella, MD

Astudy co-led by Antonio Iavarone, MD, Associate Professor of Neurology andPathology and Cell Biology, and Anna Lasorella, MD, Assistant Professor of

Pediatrics and Pathology and Cell Biology, both of Columbia’s Institute for CancerGenetics at the Herbert Irving Comprehensive Cancer Center, has identified aprotein that activates brain stem cells to make new neurons during braindevelopment, but that may be hijacked later in life to cause brain cancer inhumans. The protein called Huwe1 normally functions to eliminate other unnec-essary proteins and was found to act as a potential tumor suppressor in braincancer. The findings were published in the August 18, 2009 issue of DevelopmentalCell and the paper was selected as the feature cover story.

“By identifying the normal function of Huwe1, we were able to learn thatderegulation of Huwe1 function is involved in tumor development,” says Dr. Iavarone.

Adds Dr. Lasorella, “This demonstrates that a gene’s basic function must be understoodbefore we can learn how it also plays a role in the development of cancer.”

To understand how brain tumors develop,Drs. Iavarone’s and Lasorella’s teams decidedthat they needed to understand the develop-ment of normal neural stem cells. During nor-mal brain development, neural stem cellsgrow and divide rapidly before developinginto neurons. To successfully change into neu-rons, proteins that keep the cells in an imma-ture, stem cell state must be eliminated. Byconditionally deleting the Huwe1 gene in themouse brain, the researchers demonstratedthat this enzyme is essential for the transitionfrom self-renewing and proliferating neuralstem/progenitor cells to differentiated neu-rons. Drs. Iavarone’s and Lasorella’s researchdemonstrated that Huwe1 is responsible for“crowd control,” for the mechanism that reg-ulates the stem cell mass in the developingbrain – effectively weeding out the unnecessarystem cell-specific proteins and protooncogeneN-Myc and promoting neurogenesis. WithoutHuwe1, Dr. Lasorella discovered that in mice,the N-Myc protein remains elevated and too fewmature neurons form in the brain, resulting inthe brain failing to properly develop.

Because stem cells and cancer cells share thecapacity for rapid proliferation, but cancer cells

The alterations of neural cells in the mouse braincarrying inactivation of Huwe1 are shown with thesuperimposed molecular network responsible for thosealterations. The network was assembled by the lab ofresearch team member Andrea Califano, PhD, acomputational biologist at Columbia University MedicalCenter’s Herbert Irving Comprehensive Cancer Center.

have lost crowd control, Dr. Iavarone thenlooked for Huwe1 alterations in human braintumors. Compared to normal brain tissue, hefound that Huwe1 activity in tumors was sig-nificantly lower than in normal brain tissue.

According to the researchers, human high-grade gliomas carry focal hemizygous dele-tions of the X-linked Huwe1 gene in associa-tion with amplification of the N-Myc locus.Their results indicate that Huwe1 balancesproliferation and neurogenesis in the develop-ing brain and that this pathway is subvertedin malignant brain tumors.

“The loss of Huwe1 may be an importantfactor in the development of brain cancer, sug-gesting that Huwe1 protein function may beused for new therapeutic targets to fight dead-ly brain cancer,” says Dr. Lasorella.

“Our next step will be to analyze the struc-tural changes in Huwe1 and research ways torestore this gene in brain tumor patients,”says Dr. Iavarone. “In mice, giving Huwe1back blocks the ability of normal stem cells toproliferate and develop tumors. We are hope-ful that if we can restore Huwe1 activity inbrain tumor cells resulting from Huwe1 dele-tion, then we can stop the tumor growth.”

BrdU labeling at E15.5 indicate that the ability togenerate neurons that migrate to the most superficiallayers was markedly reduced in the absence of Huwe1.

The research demonstrated that Huwe1 is responsible for“crowd control” for the mechanism that regulates the stemcell mass in the developing brain – effectively weeding outunnecessary stem cell-specific proteins ... and promotingneurogenesis.

Huwe1F/Y Huwe1F/YNes

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ADVANCES IN NEUROSCIENCE: PSYCHIATRY, NEUROLOGY AND NEUROSURGERY

In collaboration with investigators at otherinstitutions, Dr. Souweidane and his colleaguessampled pontine glioma tissue from patients toidentify receptors for a monoclonal antibodycalled 8H9, which is very adept at distinguish-ing between tumor cells and normal brain cells.The researchers attached the antibody to radioac-tive iodine (124I) and validated its safety andtissue perfusion in animal studies.

Using convection-enhanced delivery (CED),the therapy is administered via a catheter to thetumor. The catheter is connected to a low-flowpump that administers just a few drops of thechemotherapy agent each hour. This approachpushes the drug through the space between thetumor cells, thereby avoiding toxicity, bypassingthe blood-brain barrier, and delivering high con-centrations of the drug directly to the tumor.

the safety parameters of 124I-8H9 using CED.Another key feature of the 124I -labeled 8H9

therapy is its ability to be tracked using positronemission tomography. Until now, surrogate trac-ers such as MRI contrast agents were the onlyway to track where a molecule travelled once itwas infused into the body. But this methodolo-gy is unable to track where the molecule resideshours, days, or weeks following infusion.Dr. Souweidane and his colleagues plan to usePET imaging to track the presence of 124I -labeled 8H9 therapy once infused into a patient.

“For the first time, we’ll have proof-of-prin-ciple that we can image with accuracy wherethese molecules are going,” he said. “It’s sense-less to think we can provide patients with ade-quate therapy if we can’t get the agent into thetumor bed.”

continued from Pontine Gliomas, page 1

Convection-enhanced delivery… pushes the drug throughthe space between the tumor cells, thereby avoidingtoxicity, bypassing the blood-brain barrier, and deliveringhigh concentrations of the drug directly to the tumor.

Saggital (above) and axial (below) MRI images of achild with a diffuse pontine glioma. The characteristicinfiltrative nature of the tumor is apparent.

abnormal information flow and an inability toaccurately interpret incoming sensory input.”

Drs. Gogos and Karayiorgou plan to con-tinue their exploration of the physiologic con-sequences of the 22q11.2 microdeletion. “Wewant to find out which molecular and synap-tic deficits underlie the impaired functionalconnectivity between the hippocampus andprefrontal cortex, and whether similar alter-ations in communication are present amongother brain areas and in other disease-associat-ed mutations,” noted Dr. Gogos.

“Whether this research will inform thedevelopment of new diagnostic tools and

continued from Brain Areas Impaired in Schizophrenia, page 2

treatments for schizophrenia across the board(i.e. beyond the genetic subtype associatedwith the 22q11.2 microdeletion) is still notclear,” said Dr. Karayiorgou. “It’s possiblethat imaging approaches such as fMRI couldbe used to examine the pattern of connectiv-ity among brain regions and facilitate diag-nosis of specific subtypes of schizophrenia inpatients. It might also be possible to use ourunderstanding of the causes of the impairedfunctional connectivity studies in animalmodels and then humans to identify drugsthat can restore impaired connectivity tophysiological levels.”

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Selectivity of hippocampal–prefrontal synchronydeficits in Df(16)A+/– mice. a, Comparison of phase-locking to theta oscillations in prefrontal cortex andhippocampus across the two genotypes. Phase-locking to prefrontal theta oscillations is intact.

With diffuse pontine glioma remaining sucha formidable clinical challenge, Dr. Souweidanenoted, “This approach is the most excitingthing in pediatric neuro-oncology right now.I’m convinced we can learn how to cure thiscancer if we can find the right agent and theright delivery scheme.”

For more information about this research,visit The Cure Starts Now Foundation Web siteat www.thecurestartsnow.org/research/grants/.

Diffuse pontine gliomas are ideally suited forthis delivery system because they are small andlocalized. “The clinical features of this tumormake it very appealing for this form of localdelivery,” explained Dr. Souweidane. Theresearchers are now planning a phase I study inchildren with diffuse pontine glioma, in collab-oration with Memorial Sloan-Kettering CancerCenter. The research, which is funded by TheCure Starts Now Foundation, seeks to establish

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Important news from the Neuroscience Centers and the Departments of Psychiatry of NewYork-Presbyterian Hospital. Currentresearch projects, clinical trials, and advances in the diagnosis and treatment of patients with neurological and psychiatric diseases.

Advances in Neuroscience: Psychiatry, Neurology and Neurosurgery

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RESOURCES FORPROFESSIONALS• Webcasts • CME Activities • Medical Presentations • Specialty Briefings • Newsletters

Visit nyp.org/pro

Weill CornellMedical CollegeMatthew E. Fink, MDActing Chairman, Neurology and

NeuroscienceChief, Division of Stroke and

Critical Care NeurologyProfessor, Clinical Neurology and

NeuroscienceE-mail: mfink@med.cornell.edu

Philip E. Stieg, PhD, MDNeurosurgeon-in-ChiefProfessor and ChairmanDepartment of Neurological SurgeryE-mail: pes2008@med.cornell.edu

Jack D. Barchas, MDPsychiatrist-in-ChiefChairman, Department of PsychiatryBarklie McKee Henry Professor of

PsychiatryE-mail: jbarchas@med.cornell.edu

Philip J. Wilner, MD, MBAVice President and Medical Director,Behavioral HealthExecutive Vice ChairDepartment of PsychiatryE-mail: pwilner@med.cornell.edu

Editorial Board

Columbia University Collegeof Physicians and SurgeonsTimothy A. Pedley, MDNeurologist-in-ChiefHenry and Lucy Moses Professor and

ChairmanDepartment of NeurologyE-mail: tap2@columbia.edu

Robert A. Solomon, MDDirector of ServiceDepartment of Neurological SurgeryByron Stookey Professor and ChairmanDepartment of Neurological SurgeryE-mail: ras5@columbia.edu

Jeffrey A. Lieberman, MDPsychiatrist-in-ChiefDirector, New York State

Psychiatric InstituteDirector, Lieber Center for

Schizophrenia ResearchLawrence E. Kolb Professor and

Chairman of Psychiatry, Lieber ChairE-mail: jl2616@columbia.edu

Ellen M. Stevenson, MDAssociate Clinical ProfessorDepartment of PsychiatryE-mail: ems8@columbia.edu

Weill CornellMedical CollegeDana W. Moore, PhDInstructor of Neuropsychology

in NeurologyE-mail: dwm2003@med.cornell.edu

Norman R. Relkin, MD, PhDDirector,Memory Disorders ProgramAssociate Professor of Clinical

Neurology and NeuroscienceE-mail: nrelkin@med.cornell.edu

Mark M. Souweidane, MDVice Chair, Neurological SurgeryDirector,Pediatric Neurological Surgery,NewYork-Presbyterian Phyllis andDavid Komansky Center forChildren’s HealthProfessor of Neurological SurgeryE-mail: mmsouwei@med.cornell.edu

Diamanto Tsakanikas, PhDNeuropsychologist,Memory Disorders ProgramInstructor of Neuropsychology

in NeurologyDirector, Clinical Training

in NeuropsychologyE-mail: dit2003@med.cornell.edu

Contributing Faculty

Columbia University Collegeof Physicians and SurgeonsJoseph A. Gogos, MD, PhD Associate Professor of Physiology and

Cellular Biophysics and NeuroscienceE-mail: jag90@columbia.edu

Antonio Iavarone, MDAssociate Professor of Neurology and

Pathology and Cell Biology Institute for Cancer GeneticsHerbert Irving Comprehensive

Cancer CenterE-mail: ai2101@columbia.edu

Maria Karayiorgou, MDActing Chief, Division of Medical

Genetics Professor of Psychiatry in Genetics

and Physiology Department of PsychiatryE-mail: mk2758@columbia.edu

Anna Lasorella, MDAssistant Professor of Pediatrics and

Pathology and Cell BiologyInstitute for Cancer Genetics Herbert Irving Comprehensive

Cancer CenterE-mail: al2179@columbia.edu

Advances in Neuroscience: Psychiatry, Neurology and Neurosurgery is a publication of the Neuroscience Centers and the Departments of Psychiatry of NewYork-Presbyterian Hospital. The Neuroscience Centers are at the forefront of research and practice in the diagnosis, treatment, and rehabilitation of neurologic disease. TheNeuroscience Centers include the Neurological Institute of New York at NewYork-Presbyterian Hospital/Columbia University Medical Center and the Weill CornellNeuroscience Institute at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. The Departments of Psychiatry pursue groundbreaking research and providecomprehensive care of children, adolescents, and adults with psychiatric diseases. The Neuroscience Centers and the Departments of Psychiatry are affiliated withColumbia University College of Physicians and Surgeons and Weill Cornell Medical College. The Department of Psychiatry at NewYork-Presbyterian/Columbia is alsoaffiliated with the New York State Psychiatric Institute.

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