Karyn Lee Boyar

Faculty

Karyn Lee Boyar headshot

Karyn Lee Boyar

Clinical Assistant Professor

1 212 992 9361

433 First Avenue
Room 415
New York, NY 10010
United States

Karyn Lee Boyar's additional information

Karyn Boyar is an assistant clinical professor at NYU Rory Meyers College of Nursing. 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.

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
Hillman Alumni Association
National League of Nursing
Sigma Theta Tau

Faculty Honors Awards

Hillman Scholar

Publications

Bringing Research to Life for Undergraduate Nursing Students Using a Design Thinking Model

Seltzer Uribe, J., Boyar, K., & Ramos, S. R. (2020). In K. Rodriguez, K. Boyar, & E. Ea (Eds.), Innovative use of concept care planning in a large class. Innovative strategies in teaching nursing. Springer.

Innovative use of concept care planning in a large class

Rodriguez, K., Boyar, K., & Ea, E. (2020). In E. Ea & C. Alfes (Eds.), Innovative strategies in teaching nursing: Exemplars of optimal learning outcomes. Springer.

Making QSEN visible in the classroom: Innovative use of in-class care mapping activity

Rodriguez, K., Boyar, K., Weidel, J., & Ea, E. (2016). QSEN Institute Teaching Strategy (online).

Essential tremor versus parkinson disease: Make the right diagnosis

Boyar, K. (2014). Nurse Practitioner, 39(9), 13-16. 10.1097/01.NPR.0000452984.51256.1a

Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson's disease

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Abstract
Abstract
We conducted a meta-analysis of Parkinson's disease genome-wide association studies using a common set of 7,893,274 variants across 13,708 cases and 95,282 controls. Twenty-six loci were identified as having genome-wide significant association; these and 6 additional previously reported loci were then tested in an independent set of 5,353 cases and 5,551 controls. Of the 32 tested SNPs, 24 replicated, including 6 newly identified loci. Conditional analyses within loci showed that four loci, including GBA, GAK-DGKQ, SNCA and the HLA region, contain a secondary independent risk variant. In total, we identified and replicated 28 independent risk variants for Parkinson's disease across 24 loci. Although the effect of each individual locus was small, risk profile analysis showed substantial cumulative risk in a comparison of the highest and lowest quintiles of genetic risk (odds ratio (OR) = 3.31, 95% confidence interval (CI) = 2.55-4.30; P = 2 × 10-16). We also show six risk loci associated with proximal gene expression or DNA methylation.

A randomized clinical trial of high-dosage coenzyme Q10 in early parkinson disease no evidence of benefit

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Abstract
Abstract
IMPORTANCE Coenzyme Q10 (CoQ10), an antioxidant that supports mitochondrial function, has been shown in preclinical Parkinson disease (PD) models to reduce the loss of dopamine neurons, and was safe and well tolerated in early-phase human studies. A previous phase II study suggested possible clinical benefit. OBJECTIVE To examine whether CoQ10 could slow disease progression in early PD. DESIGN, SETTING, AND PARTICIPANTS A phase III randomized, placebo-controlled, double-blind clinical trial at 67 North American sites consisting of participants 30 years of age or older who received a diagnosis of PD within 5 years and who had the following inclusion criteria: the presence of a rest tremor, bradykinesia, and rigidity; a modified Hoehn and Yahr stage of 2.5 or less; and no anticipated need for dopaminergic therapy within 3 months. Exclusion criteria included the use of any PD medication within 60 days, the use of any symptomatic PD medication for more than 90 days, atypical or drug-induced parkinsonism, a Unified Parkinson’s Disease Rating Scale (UPDRS) rest tremor score of 3 or greater for any limb, a Mini-Mental State Examination score of 25 or less, a history of stroke, the use of certain supplements, and substantial recent exposure to CoQ10. Of 696 participants screened, 78 were found to be ineligible, and 18 declined participation. INTERVENTIONS The remaining 600 participants were randomly assigned to receive placebo, 1200 mg/d of CoQ10, or 2400 mg/d of CoQ10; all participants received 1200 IU/d of vitamin E. MAIN OUTCOMES AND MEASURES Participants were observed for 16 months or until a disability requiring dopaminergic treatment. The prospectively defined primary outcome measure was the change in total UPDRS score (Parts I-III) from baseline to final visit. The study was powered to detect a 3-point difference between an active treatment and placebo. RESULTS The baseline characteristics of the participants were well balanced, the mean age was 62.5 years, 66%of participants were male, and the mean baseline total UPDRS score was 22.7. A total of 267 participants required treatment (94 received placebo, 87 received 1200 mg/d of CoQ10, and 86 received 2400 mg/d of CoQ10), and 65 participants (29 who received placebo, 19 who received 1200 mg/d of CoQ10, and 17 who received 2400 mg/d of CoQ10) withdrew prematurely. Treatments were well tolerated with no safety concerns. The study was terminated after a prespecified futility criterion was reached. At study termination, both active treatment groups showed slight adverse trends relative to placebo. Adjusted mean changes (worsening) in total UPDRS scores from baseline to final visit were 6.9 points (placebo), 7.5 points (1200 mg/d of CoQ10; P =.49 relative to placebo), and 8.0 points (2400 mg/d of CoQ10; P =.21 relative to placebo). CONCLUSIONS AND RELEVANCE Coenzyme Q10 was safe and well tolerated in this population, but showed no evidence of clinical benefit. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00740714.

R1514Q substitution in Lrrk2 is not a pathogenic Parkinson's disease mutation

Nichols, W. C., Marek, D. K., Pauciulo, M. W., Pankratz, N., Halter, C. A., Rudolph, A., Shults, C. W., Wojcieszek, J., Foroud, T., Shults, C., Marshall, F., Oakes, D., Rudolph, A., Shinaman, A., Marder, K., Conneally, P. M., Foroud, T., Halter, C., Lyons, K., Siemers, E., Factor, S., Higgins, D., Evans, S., Shill, H., Stacy, M., Danielson, J., Marlor, L., Williamson, K., Jankovic, J., Hunter, C., Simon, D., Ryan, P., Scollins, L., Saunders-Pullman, R., Boyar, K., Costan-Toth, C., Ohmann, E., Sudarsky, L., Joubert, C., Friedman, J., Chou, K., Fernandez, H., Lannon, M., Galvez-Jimenez, N., Podichetty, A., Lewitt, P., DeAngelis, M., O’Brien, C., Seeberger, L., Dingmann, C., Judd, D., Marder, K., Fraser, J., Harris, J., Bertoni, J., Peterson, C., Chouinard, S., Panisset, M., Hall, J., Poiffaut, H., Calabrese, V., Roberge, P., Wojcieszek, J., Belden, J., Halter, C., Jennings, D., Marek, K., Mendick, S., Reich, S., Dunlop, B., Jog, M., Horn, C., Rao, J., Cook, M., Uitti, R., Turk, M., Ajax, T., Mannetter, J., Panisset, M., Hall, J., Sethi, K., Carpenter, J., Ligon, K., Narayan, S., Woodward, L., Blindauer, K., Petit, J., Elmer, L., Aiken, E., Davis, K., Schell, C., Wilson, S., Velickovic, M., Koller, W., Phipps, S., Feigin, A., Gordon, M., Hamann, J., Licari, E., Marotta-Kollarus, M., Shannon, B., Winnick, R., Simuni, T., Kaczmarek, A., Williams, K., Wolff, M., Fernandez, M., Hubble, J., Kostyk, S., Campbell, A., Reider, C., Camicioli, R., Carter, J., Andrews, P., Morehouse, S., Stone, C., Mendis, T., Grimes, D., Gray, P., Haas, K., Sutton, J., Hutchinson, B., Young, J., Rajput, A., Rajput, A., Klassen, L., Shirley, T., Manyam, B., Simpson, P., Whetteckey, J., Wulbrecht, B., Truong, D., Pathak, M., Luong, N., Tra, T., Tran, A., Vo, J., Lang, A., Kleiner-Fisman, G., Nieves, A., So, J., Podskalny, G., Giffin, L., Atchison, P., Allen, C., Martin, W., Wieler, M., Suchowersky, O., Klimek, M., Hermanowicz, N., Niswonger, S., Shults, C., Fontaine, D., Aminoff, M., Christine, C., Diminno, M., Hevezi, J., Dalvi, A., Kang, U., Richman, J., Uy, S., Young, J., Dalvi, A., Sahay, A., Schwieterman, D., Leehey, M., Culver, S., Derian, T., Demarcaida, T., Belber, S., Rodnitzky, R., Dobson, J., Pahwa, R., Lyons, K., Gales, T., Thomas, S., Shulman, L., Weiner, W., Dustin, K., Singer, C., Koller, W., Lyons, K., Weiner, W., Zelaya, L., Tuite, P., Hagen, V., Rolandelli, S., Schacherer, R., Gordon, P., Werner, J., Serrano, C., Roque, S., Kurlan, R., Berry, D., Gardiner, I., Hauser, R., Sanchez-Ramos, J., Zesiewicz, T., Delgado, H., Price, K., Rodriguez, P., Pfeiffer, R., Davis, L., Pfeiffer, B., Dewey, R., Hayward, B., Meacham, M., Walker, F., Hunt, V., Racette, B., Good, L., Rundle, M., Watts, A., Wang, A., Ross, T., Bennett, S., Kamp, D., & Julian-Baros, E. (2007). Movement Disorders, 22(2), 254-256. 10.1002/mds.21233
Abstract
Abstract
Mutations in LRRK2 were first reported as causing Parkinson's disease (PD) in late 2004. Since then, approximately a dozen LRRK2 substitutions have been identified that are believed to be pathogenic mutations. The substitution of adenine for guanine at nucleotide 4541 (4541G>A) in LRRK2 was recently reported. This substitution resulted in the replacement of an arginine at position 1514 with a glutamine (R1514Q). Although this substitution was not found in a large cohort of controls, its pathogenicity could not be verified. We have now genotyped the R1514Q substitution in a sample of 954 PD patients from 429 multiplex PD families. This substitution was identified in 1.8% of the PD patients; however, the majority of the PD sibships segregating this substitution were discordant for this putative mutation. In addition, the R1514Q substitution was detected in 1.4% of neurologically evaluated, control individuals. These data suggest that the R1514Q variant is not a pathogenic LRRK2 mutation. We believe it is imperative that the causative nature of any newly identified genetic variant be determined before it is included in any panel for diagnostic testing.

Mutations in LRRK2 other than G2019S are rare in a north-American based sample of familial Parkinson's didease

Pankratz, N., Pauciulo, M. W., Elsaesser, V. E., Marek, D. K., Halter, C. A., Rudolph, A., Shults, C. W., Foroud, T., Nichols, W. C., Shults, C., Marshall, F., Oakes, D., Shinaman, A., Marder, K., Conneally, P. M., Lyons, K., Siemers, E., Factor, S., Higgins, D., Evans, S., Shill, H., Stacy, M., Danielson, J., Marlor, L., Williamson, K., Jankovic, J., Hunter, C., Simon, D., Ryan, P., Scollins, L., Saunders-Pullman, R., Boyar, K., Costan-Toth, C., Ohmann, E., Sudarsky, L., Joubert, C., Friedman, J., Chou, K., Fernandez, H., Lannon, M., Galvez-Jimenez, N., Podichetty, A., Lewitt, P., DeAngelis, M., O’Brien, C., Seeberger, L., Dingmann, C., Judd, D., Fraser, J., Harris, J., Bertoni, J., Peterson, C., Chouinard, S., Panisset, M., Hall, J., Poiffaut, H., Calabrese, V., Roberge, P., Wojcieszek, J., Belden, J., Halter, C., Jennings, D., Marek, K., Mendick, S., Reich, S., Dunlop, B., Jog, M., Horn, C., Rao, J., Cook, M., Uitti, R., Turk, M., Ajax, T., Mannetter, J., Sethi, K., Carpenter, J., Ligon, K., Narayan, S., Woodward, L., Blindauer, K., Petit, J., Elmer, L., Aiken, E., Davis, K., Schell, C., Wilson, S., Velickovic, M., Koller, W., Phipps, S., Feigin, A., Gordon, M., Hamann, J., Licari, E., Marotta-Kollarus, M., Shannon, B., Winnick, R., Simuni, T., Kaczmarek, A., & Williams, K. (2006). Movement Disorders, 21(12), 2257-2260. 10.1002/mds.21162
Abstract
Abstract
A total of 956 individuals with Parkinson's disease (PD) from 430 multiplex PD pedigrees were screened for 12 previously reported, pathogenic LRRK2 mutations: R793M, L1114L, I1371V, R1441C, R1441G, R1441H, Y1699C, M1869T, I2012T, I2020T, G2385R, and IVS31 +3G>A. Previous screening identified the LRRK2 G2019S mutation in 5% of our families. Only 1 of the 12 newly screened mutations, R1441C, was detected in a single family in our patient cohort. These results indicate that, although the G2019S mutation remains the most common mutation identified in familial PD patients, other mutations in LRRK2 are infrequent

Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia

Pankratz, N., Byder, L., Halter, C., Rudolph, A., Shults, C. W., Conneally, P. M., Foroud, T., Nichols, W. C., Lyons, K., Marder, K., Marshall, F., Oakes, D., Rudolph, A., Shinaman, A., Siemers, E., Wojcieszek, J., Belden, J., Carter, J., Camicioli, R., Andrews, P., Panisset, M., Hall, J., Hubble, J., Fernandez, M., Reider, C., Rajput, A., Rajput, A., Shirley, T., Mendis, T., Grimes, D. A., Gray, P., Ramos, C. S., Roque, S., Pfeiffer, R., Pfeiffer, B., Elmer, L., Davis, K., Friedman, J., Fernandez, H., Lannon, M., Reich, S., Dunlop, B., Seeberger, L., O’Brien, C., Judd, D., Hauser, R., Zesiewicz, T., Delgado, H., Fontaine, D., Jennings, D., Marek, K., Mendick, S., Aminoff, M., DiMinno, M., Lewitt, P., De Angelis, M., Pahwa, R., Thomas, S., Truong, D., Pathak, M., Tran, A., Rodnitzky, R., Dobson, J., Koller, W., Weiner, W., Lyons, K., Kurlan, R., Berry, D., Bertoni, J., Peterson, C., Martin, W., Wieler, M., Tuite, P., Schacherer, R., Harris, J., Jankovic, J., Hunter, C., Lang, A., Kleimer-Fisman, G., Nieves, A., So, J., Factor, S., Evans, S., Manyam, B., Wulbrecht, B., Walker, F., Hunt, V., Gordon, M. F., Hamman, J., Kang, U. J., Young, J., Blindauer, K., Petit, J., Rao, J., Cook, M., Stacy, M., Williamson, K., Pullman, R. S., & Boyar, K. (2006). Movement Disorders, 21(1), 45-49. 10.1002/mds.20663
Abstract
Abstract
The ε4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; P = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; P = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology.

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.