Karyn Lee Boyar

Faculty

Karyn Lee Boyar headshot

Karyn Lee Boyar

CNE DNP

Clinical Associate Professor

1 212 992 9361

433 First Ave
New York, NY 10010
United States

Karyn Boyar is an assistant clinical professor at NYU Rory Meyers College of Nursing, the director for the Master in Clinical Nursing Research Program as well as a CNE, Certified Nurse Educator. As an educator and family nurse practitioner specializing in neurology and long-term care, she teaches both didactic and clinical courses and simulation. She has over 20 years of experience in healthcare and over ten years of experience in the clinical care and management of patients with Parkinson’s disease and Dystonia. Her background includes work on many research trials including original research on diet in the management of Parkinson’s disease. Boyar has created comprehensive outreach initiatives for people with Parkinson’s disease that include community symposia, support groups, and educational lectures and materials. She also created and taught unique movement classes with live music for people with Parkinson’s disease. 

Before joining the faculty at NYU, Boyar was the clinical specialty coordinator at Mount Sinai School of Medicine and the designated outreach coordinator for the National Parkinson Center of Excellence at the Robert and John M. Benheim Center for Movement Disorders.

Boyar earned her DNP from Pace University and MS and BS in nursing science from Pace University. Currently, she serves on the board of directors of the IARCN (International Association of Clinical Research Nurses) as a member-at-large. 

Her current scholarship focus' on bringing Design Thinking Models to life for undergraduate students in the large classroom.  She has presented her work on Design Thinking on the local, national and international levels and has written several book chapters disseminating this innovation in teaching.

DNP - Pace University (2014)
Family Nurse Practitioner /MS, Nursing - Pace University (2002)
BS, Nursing - Pace University (2001)

Primary care
Home care
Neurology

American Nurses Association
Eastern Nursing Research Society
National League of Nursing
Sigma Theta Tau
IACRN - International Association of Clinical Research Nurses
NPA - Nurse Practitioner Association of New York State
SONSIEL - Society of Nurse Scientist, Innovators, Entreprenurs & Leadership

Hillman Scholar

Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study

VanItallie, T. B., Nonas, C., Di Rocco, A., Boyar, K., Hyams, K., & Heymsfield, S. B. (2005). Neurology, 64(4), 728-730. 10.1212/01.WNL.0000152046.11390.45
Abstract
Abstract
Ketones may bypass the defect in complex I activity implicated in Parkinson disease (PD). Five of seven volunteers with PD were able to prepare a "hyperketogenic" diet at home and adhere to it for 28 days. Substituting unsaturated for saturated fats appeared to prevent cholesterol increases in four volunteers. Unified Parkinson's Disease Rating Scale scores improved in all five during hyperketonemia, but a placebo effect was not ruled out.

Evaluation of the role of Nurr1 in a large sample of familial Parkinson's disease

Nichols, W. C., Uniacke, S. K., Pankratz, N., Reed, T., Simon, D. K., Halter, C., Rudolph, A., Shults, C. W., Conneally, P. M., Foroud, T., Wojcieszek, J., Belden, J., Carter, J., Camicioli, R., Andrews, P., Panisset, M., Hall, J., Hubble, J., Fernandez, M., … Werner, J. (2004). Movement Disorders, 19(6), 649-655. 10.1002/mds.20097
Abstract
Abstract
Parkinson's disease (PD) is a common neurodegenerative disorder in humans with wide variability in the age of disease onset. Although the disease has been thought previously to occur sporadically in most patients, there is increasing evidence of a genetic contribution to the disorder. Recently, a polymorphic variant within intron 6 of the Nurr1 gene was reported to be associated with sporadic and familial PD. In an effort to identify susceptibility genes for PD, we have collected 783 PD patients from 372 families and 397 healthy controls from 217 families. PD patients and healthy controls were genotyped for the intron 6 insertion polymorphism by BseRI restriction endonuclease digestion. No significant difference in either homozygosity or heterozygosity for the 7048G7049 (IVS6 1361 +16insG) polymorphism was detected in the PD patient cohort as compared with the panel of healthy controls. Moreover, direct sequencing of exon 1 of the Nurr1 gene in PD patients failed to detect either of the two recently reported Nurr1 mutations identified in a small subset of a PD patient cohort. Taken together, these data suggest that genetic alteration at the Nurr1 locus is not a significant risk factor for the development of Parkinson's disease in our large sample of familial PD patients.

Genome-wide linkage analysis and evidence of gene-by-gene interactions in a sample of 362 multiplex Parkinson disease families

Pankratz, N., Nichols, W. C., Uniacke, S. K., Halter, C., Murrell, J., Rudolph, A., Shults, C. W., Conneally, P. M., Foroud, T., Truong, D., Pathak, M., Tran, A., Rodnitzky, R., Dobson, J., Koller, W., Weiner, W., Lyons, K., Kurlan, R., Berry, D., … Turk, M. F. (2003). Human Molecular Genetics, 12(20), 2599-2608. 10.1093/hmg/ddg270
Abstract
Abstract
Parkinson disease (PD) is the second most common neurodegenerative disorder. We studied 754 affected individuals, comprising 425 sibling pairs, to identify PD susceptibility genes. Screening of the parkin gene was performed in a subset of the sample having earlier age of PD onset or a positive LOD score with a marker in the parkin gene. All subjects were evaluated using a rigorous neurological assessment. Two diagnostic models were considered for genome-wide, non-parametric linkage analyses. Model I included only those individuals with a more stringent diagnosis of verified PD (216 sibling pairs) and resulted in a maximum LOD score of 3.4 on chromosome 2. Model II included all affected individuals (425 sibling pairs) and yielded a LOD score of 3.1 on the X chromosome. Our large sample was then employed to test for gene-by-gene (epistatic) interactions. A genome screen using the 23 families with PD patients having a mutation in only one allele of the parkin gene detected evidence of linkage to chromosome 10 (LOD = 2.3). The 85 families with a very strong family history of PD were employed in a genome screen and, in addition to strong evidence of linkage to chromosome 2 (LOD = 4.9), also produced a LOD of 2.4 on chromosome 14. A genome screen performed in the 277 families without a strong family history of PD detected linkage to chromosomes 10 (LOD = 2.4) and X (LOD = 3.2). These findings demonstrate consistent evidence of linkage to chromosomes 2 and X and also support the hypothesis that gene-by-gene interactions are important in PD susceptibility.

Significant linkage of Parkinson disease to chromosome 2q36-37

Pankratz, N., Nichols, W. C., Uniacke, S. K., Halter, C., Rudolph, A., Shults, C., Conneally, P. M., Foroud, T., Golbe, L., Koller, W., Lyons, K., Marder, K., Marshall, F., Oakes, D., Shinaman, A., Siemers, E., Wojcieszek, J., Belden, J., Carter, J., … Werner, J. (2003). American Journal of Human Genetics, 72(4), 1053-1057. 10.1086/374383
Abstract
Abstract
Parkinson disease (PD) is the second most common neurodegenerative disorder, surpassed in frequency only by Alzheimer disease. Elsewhere we have reported linkage to chromosome 2q in a sample of sibling pairs with PD. We have now expanded our sample to include 150 families meeting our strictest diagnostic definition of verified PD. To further delineate the chromosome 2q linkage, we have performed analyses using only those pedigrees with the strongest family history of PD. Linkage analyses in this subset of 65 pedigrees generated a LOD score of 5.1, which was obtained using an autosomal dominant model of disease transmission. This result strongly suggests that variation in a gene on chromosome 2q36-37 contributes to PD susceptibility.