Barbara Strupp


Barbara Strupp

217 Weill Hall & 102 Savage Hall
Phone: (607) 255-2694
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Curriculum Vitae
Biographical Statement:

 Barbara Strupp received her Bachelor's degree in Ethology from Washington University in 1976, and her Ph.D. degree in Psychology in 1982 from Cornell University.  She conducted postdoctoral research at the National Institutes of Health (Biological Psychiatry Branch, NIMH) from 1981-1983.   She then returned to Cornell University in 1983, funded by a National Institutes of Health New Investigator Research Award.  She currently serves as Professor in the Division of Nutritional Sciences, and Adjunct Professor in the Department of Psychology.  Professor Strupp is a member of the Graduate Fields of Nutrition, Psychology, and Environmental Toxicology and the Program in Neuroscience.   Her research group has been funded by three institutes at the NIH (NICHD, NIDA, and NIMH). These grants have supported research on numerous causes of human cognitive dysfunction (malnutrition, PKU, early lead exposure, prenatal cocaine exposure, Down syndrome, and Fragile X syndrome), as well as the development of novel techniques for detecting and delineating cognitive and affective dysfunction in rodent models.

Strupp’s research primarily deals with causes of human cognitive dysfunction, studies that involve both children and rodent models. The goals of the animal studies are to determine the nature and underlying neural basis of the cognitive dysfunction, with implications for therapeutic intervention and for elucidating basic brain-cognition relationships.  Current projects (described below) focus on (1) the lasting effects of maternal choline supplementation in rodent models (including a murine model of Down syndrome) and humans, and (2) the lasting effects of developmental exposure to manganese. 

Current Professional Activities:

National Institutes of Health, Special Emphasis Panel (SEP), review applications submitted for PAR13-195 – “Preclinical Research on Model Organisms to Predict Treatment Outcomes for Disorders Associated with Intellectual and Developmental Disabilities”, June 2015.

Director of Graduate Studies, Graduate Field of Nutrition, Cornell University

Cornell University Graduate Field Membership: Psychology; Nutrition; Environmental Toxicology

Appointments and Tenure Committee, Division of Nutritional Sciences, Cornell University, 2014-17; Co-Chair, 2014-2015; Chair, 2015-2016;

Life Sciences Advisory Council (LSAC), member, 2014-2017

Neurobehavioral Teratology Society, member

Society for Neuroscience, member

Special Review Committee, RFA on "Centers for Children's Environmental Health and Disease Prevention Research (RFA-ES-14-002)", May 10-12, 2015 (invited).

Current Research Activities:

1. Maternal choline supplementation (research using animal models):  We have found that supplementing the maternal diet during pregnancy and lactation significantly improves attention, spatial cognition, and emotion regulation in a mouse model of Down syndrome.  A more circumscribed improvement in attention was also seen in the Wildtype littermates.  I am currently involved in a collaborative study with investigators at  Rush University Medical Center and NYU to elucidate the underlying neural mechanisms.   We have found that MCS improves spatial cognition in the Ts65Dn mice which is mediated, at least in part, by protection of medial septal cholinergic neurons, which atrophy in these mice with the onset of Alzheimer-like neuropathology.  We have also found that MCS increases adult hippocampal neurogenesis in the Ts65Dn mice, and that this correlates with the improved spatial cognition of these mice. Furthermore we have found evidence for improved neurotrophin function in these trisomic mice, which may contribute to the protection of BFCN neurons in these mice, and subsequently their improved cognitive functioning.  The results of these studies will have implications for minimizing cognitive and affective function in individuals who have Down syndrome as well as provide new information concerning the mechanism by which perinatal choline supplementation exerts lifelong benefits on cognitive functioning in normal rodents.  These findings will have important clinical implications for identifying the choline intake during pregnancy and lactation that is optimal for cognitive functioning throughout the lifespan.  These collaborative studies linking behavioral and neural changes are in progress. 

2. Maternal choline supplementation (research with human subjects): We are currently assessing cognitive and affective functioning in 7 year children whose mothers participated in a randomized controlled trial of maternal choline supplementation during either the last trimester of pregnancy or the first 3 months postnatally.  Maternal choline intake was completely controlled at either 480 mg/day or 930 mg/day during these periods of time. This will be the first randomized trial of the effects of maternal choline supplementation on cognition, affect, and HPA axis stress reactivity in school-aged children, a time when neurobehavioral tests predict later academic outcomes and adult functioning. This study is a collaboration with several DNS colleagues (Drs. Caudill, Canfield and Finkelstein). .    

3.  Dr Paul Soloway and I are planning to investigate whether the lasting cognitive benefits of maternal choline supplementation in the Ts65Dn mouse model of Down syndrome and normal littermates are mediated by epigenetics effects due to choline's role as a methyl donor.  These studies will also help ascertain possible adverse effects of MCS on other systems (e.g., cancer).

4.  I am collaborating on a project with collaborators at UC Santa Cruz and the University of Illinois to investigate the lasting cognitive and neural effects of early developmental exposure to Manganese.  We have found evidence for attentional and fine motor dysfunction in the rats exposed early in life, and have found evidence for catecholaminergic alterations in these same animals.  Importantly treatment with methylphenidate (Ritalin) completely normalized the fine motor dysfunction in the manganese exposed animals.  We are planning future studies to further explore the mechanisms underlying these areas of dysfunction and test potential therapies.  

Current Public Engagement Activities:

 Special Review Committee, RFA on "Centers for Children's Environmental Health and Disease Prevention Research (RFA-ES-14-002)", May 10-12, 2015 (invited).

ZRG1 BBBP-T (57), Special Emphasis Panel (SEP), review applications submitted for PAR13-195 – “Preclinical Research on Model Organisms to Predict Treatment Outcomes for Disorders Associated with Intellectual and Developmental Disabilities”, June 2015.


Washington University, B.A. (Ethology), 1976

Cornell University, Ph.D. (Biopsychology), 1982

National Institutes of Health (National Institute of Mental Health) Postdoctoral Fellow, 1981-1983

Courses Taught:

NS 7030         Graduate Seminar in Nutrition

Tox 6110:        Molecular Toxicology

NS 4010         Empirical Research in Nutrition

NS 4990         Honors Research in Nutrition

sych 4700    Undergraduate Research in Psychology

Bio 2990         Undergraduate Research in Biology

Bio 4990         Undergraduate Research in Biology


Related Websites:

Psychology Web Page

Program in Neuroscience

Graduate Field of Environmental Toxicology

Administrative Responsibilities:

Member, Curriculum Committee, Division of Nutritional Sciences, Cornell University, 2011-present

Appointments and Tenure Committee, Division of Nutritional Sciences, Cornell University, 2014-17; Co-Chair, 2014-2015; Chair: 2015-2016

Life Sciences Advisory Council (LSAC), Cornell University, member, 2014-2017

Interim Director of Undergraduate Studies, Division of Nutritional Sciences, Cornell University, January –June, 2015.

Director of Graduate Studies, Field of Nutrition, Cornell University, January 2016-August 2018.

Experiential Learning Committee, Division of Nutritional Sciences, Cornell University, January-June 2015


Selected Publications:

Strupp BJ & Beaudin S.  Assessing the neurobehavioral effects of early toxicant exposure: A perspective from animal research. In: Bellinger D (ed.), Human Developmental Neurotoxicology, New York, NY: Taylor & Francis Group, 2006: 415-445. 

Grantham-McGregor S, Cheung YB, Cueto S, Glewwe P, Richter L, Strupp B; International Child Development Steering Group. Developmental potential in the first 5 years for children in developing countries. Lancet. 2007 Jan; 369(9555):60-70.

Stangle DE, Smith D, Beaudin SA, Strawderman MS, Levitsky DA, and Strupp BJ. Succimer chelation improves cognition and arousal regulation in lead-exposed rats but produces lasting cognitive impairment in the absence of lead exposure.  Environ Health Perspect. 2007 Feb;115(2):201-9. Epub 2006 Oct 30.

McNaughton, C. H.,  Moon, J., Strawderman, M. S., Maclean K. N., Evans, J., Strupp, B. J. (2008). Evidence for social anxiety and impaired social cognition in a mouse model of Fragile X syndrome. Behav. Neurosci, 2008 Apr;122(2):293-300. 

Moon J, Ota KT, Driscoll LL, Levitsky DA, Strupp BJ (2008).  A mouse model of Fragile X syndrome exhibits heightened arousal and/or emotion following errors or reversal of contingencies.  Developmental Psychobiology, 2008 Jul;50(5):473-85. 

Moon J., Chen M, Gandhy SU, Strawderman M, Levitsky DA, Maclean KN, and Strupp BJ. Perinatal choline supplementation improves cognitive functioning and emotion regulation in the Ts65Dn mouse model of Down syndrome.  Behavioral Neuroscience, 2010, 124 (3):346–361.

Field MS, Shields KS, Abarinov EV,  Malysheva OV, Allen RH, Stabler SP, Ash JA, Strupp BJ, Stover PJ, and Caudill MA.  Reduced MTHFD1 activity in mice perturbs folate and choline dependent one-carbon metabolism as well as transsulfuration. J. Nutrition, 2013 Jan;143(1):41-5. doi: 10.3945/jn.112.169821. Epub 2012 Nov 28.

Ash JA, Jiang X, Malysheva OV, Fiorenza CG, Bisogni AJ, Levitsky DA, Strawderman MS,  Caudill MA, Stover PJ, Strupp BJ.  Dietary and genetic manipulations of folate metabolism differentially affect neocortical functions in mice.  Neurotoxicol Teratol. 2013 Jul-Aug; 38:79-91. doi: 10.1016/ Epub 2013 May 15.  

Velazquez, R., Kelley, C.M., Powers, B.E., Ash, J.A., Ginsberg, S.D., Mufson, E.J., and Strupp, B.J: B.J: Maternal choline supplementation improves spatial learning and adult hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome, Neurobiol. Dis. 58 (2013) 92–101.

CM. Kelley, BE Powers, R Velazquez, J A Ash, SD Ginsberg, BJ Strupp, EJ Mufson (2013).  Sex differences in cholinergic basal forebrain in the Ts65Dn mouse model of Down syndrome and Alzheimer’s disease, Brain Pathology doi:10.1111/bpa.12073. 

Smith D, Strupp BJ. The Scientific Basis for Chelation: Animal Studies and Lead Chelation (2013).  J Med Toxicol. 2013 Dec;9(4):326-38. doi: 10.1007/s13181-013-0339-2.  PMCID: 3846979

Kelley CM, Powers BE, Velazquez R, Ash JA, Ginsberg SD, Strupp BJ, Mufson EJ (2013). Perinatal choline supplementation differentially alters the basal forebrain cholinergic system of young-adult Ts65Dn and disomic miceJ Comp Neurol. 2014 Apr 15;522(6):1390-410.  PMCID: 3959592

Yan, J., Ginsberg, S.D., Powers, B., Alldred, M.J., Saltzman, A., Strupp, B.J., and Caudill, M.A.: Maternal choline supplementation programs greater activity of the phosphatidylethanolamine N-methyltransferase (PEMT) pathway in adult Ts65Dn trisomic mice. FASEB J., 28: 4312-423, 2014. PMID: 24963152.

Ash A, Velazquez R, Kelley CM, Powers BE, Strawderman M, Ginsberg SD, Mufson EJ, Strupp BJ. Maternal choline supplementation improves spatial mapping and increases number and size of basal forebrain cholinergic neurons in aged Ts65Dn mice; Neurobiology of Disease, 2014 Oct;70:32-42. doi: 10.1016/j.nbd.2014.06.001. Epub 2014 Jun 14.

Driscoll LL & Strupp BJ. Assessment of attention and inhibitory control in rodent developmental neurotoxicity studies.  Neurotoxicology and Teratology, 2014 Sep 16. pii: S0892-0362(14)00162-7. doi: 10.1016/ [Epub ahead of print].

Beaudin SA, Strupp BJ, Lasley SM, Fornal CA, Mandal S, Smith DR.  Oral methylphenidate alleviates the fine motor dysfunction caused by chronic postnatal manganese exposure. Toxicological Sciences, 2015 Apr;144(2):318-27. doi: 10.1093/toxsci/kfv007. Epub 2015 Jan 19. PMID: 25601986

Kelley, C.M., Ash, J.A., Powers, B.E., Velazquez, R., Alldred, M.J., Ikonomovic, M.D., Ginsberg, S.D., Strupp, B.J., and Mufson, E.J.: Effects of maternal choline supplementation on the septohippocampal cholinergic system in the Ts65Dn mouse model of Down syndrome. Curr Alzheimer Res., 13: 84-96, 2016. PMID: 26391046. NIHMSID #753420.

Strupp, B.J., Powers, B.E., Velazquez, R., Ash, J.A., Kelley, C.M., Alldred, M.J., Strawderman, M.S., Caudill, M.A., Mufson, E.J., and Ginsberg, S.D.: Maternal choline supplementation: A potential prenatal treatment for Down syndrome and Alzheimer’s disease. Curr Alzheimer Res. 13: 97-106, 2016. PMID: 26391045. NIHMSID #753474

Powers, B.E., Velazquez, R., Kelley, C.M., Ash, J.A., Strawderman, M.S., Alldred, M.J., Ginsberg, S.D., Mufson, E.J., and Strupp, B.J.: Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome. Brain Struct. Funct., 2015 Dec 30. [Epub ahead of print]. PMID: 26719290. NIHMSID #753351.



Selected Keywords:
choline, Down syndrome, nutrition and behavior, lead exposure, cocaine exposure, Fragile X syndrome, manganese neurotoxicity; epigenetics; maternal and child nutrition

The information on this bio page is taken from the CHE Annual Report.