Rebecca A Betensky | NYU School of Global Public Health

Rebecca Betensky

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Chair of the Department of Biostatistics

Professor of Biostatistics

Prior to NYU, Dr. Betensky was Professor of Biostatistics at the Harvard T.H. Chan School of Public Health. She was director of the Harvard Catalyst (Clinical and Translational Science Award) Biostatistics Program; director of the Data and Statistics Core for the Massachusetts Alzheimer’s Disease Research Center; and director of the Biostatistics Neurology Core at Massachusetts General Hospital. Previously, she was the Biostatistics Program Leader for the Dana-Farber/Harvard Cancer Center.

Dr. Betensky’s research focuses on methods for the analysis of censored and truncated outcomes and covariates, which frequently arise from the subsampling of cohort studies. She has a long-time interest in clinical trials, and has written on the evaluation of biomarkers and the use and interpretation of p-values. She has collaborated extensively in studies in neurologic diseases, and serves as statistical editor for Annals of Neurology.

Dr. Betensky was awarded, and directed for 15 years, an NIH T32 training program in neurostatistics and neuroepidemiology for pre- and post-doctoral students in biostatistics and epidemiology and for clinician-scientists. She previously directed Harvard’s Biostatistics programs to promote and support diversity at all levels in the field of quantitative public health. She was also a member of the BMRD Study Section for review of NIH statistical methodology grants; on committees for the Institute of Medicine; and a co-chair of the technical advisory committee for the scientific registry of transplant recipients.

Dr. Betensky an elected Fellow of the American Statistical Association and of the International Statistical Institute, and is a past recipient of the Spiegelman Award from the American Public Health Association. She currently serves as a member of the Board of Scientific Counselors for Clinical Science and Epidemiology at the National Cancer Institute.

Education

AB, Mathematics, Harvard University, Cambridge, MA

PhD, Statistics, Stanford University, Stanford, CA

Areas of research and study

Biology

Biostatistics

Neuroepidemiology

Neurology

Neurostatistics

Translational science

Publications

Transformation model estimation of survival under dependent truncation and independent censoring

Wide Range of Clinical Outcomes in Patients with Gliomatosis Cerebri Growth Pattern: A Clinical, Radiographic, and Histopathologic Study

An optimal Wilcoxon–Mann–Whitney test of mortality and a continuous outcome

Biomarker validation with an imperfect reference: Issues and bounds

Hypothesis Tests for Neyman's Bias in Case–Control Studies

Immunophenotyping of pediatric brain tumors: correlating immune infiltrate with histology, mutational load, and survival and assessing clonal T cell response

Integration of risk factors for Parkinson disease in 2 large longitudinal cohorts

Interaction between caffeine and polymorphisms of glutamate ionotropic receptor NMDA type subunit 2A (GRIN2A) and cytochrome P450 1A2 (CYP1A2) on Parkinson's disease risk

Intravenous thrombolysis in unwitnessed stroke onset: MR WITNESS trial results

Inverse probability weighted Cox regression for doubly truncated data

Multicrossover Randomized Controlled Trial Designs in Alzheimer Disease

Neuronal calcineurin transcriptional targets parallel changes observed in Alzheimer disease brain

Permutation tests for general dependent truncation

PET staging of amyloidosis using striatum

Polygenic pleiotropy and potential causal relationships between educational attainment, neurobiological profile, and positive psychotic symptoms

Probing tumor microenvironment in patients with newly diagnosed glioblastoma during chemoradiation and adjuvant temozolomide with functional MRI

rBPI21 (opebacan) promotes rapid trilineage hematopoietic recovery in a murine model of high-dose total body irradiation

Reader response: Systematic review and statistical analysis of the integrity of 33 randomized controlled trials

Tau induces blood vessel abnormalities and angiogenesis-related gene expression in P301L transgenic mice and human Alzheimer's disease

The prognostic value of histopathologic lesions in native kidney biopsy specimens: Results from the Boston kidney biopsy cohort study

Threshold regression to accommodate a censored covariate

Time-to-event data with time-varying biomarkers measured only at study entry, with applications to Alzheimer's disease

APOE-related risk of mild cognitive impairment and dementia for prevention trials: An analysis of four cohorts

Qian, J., Wolters, F. J., Beiser, A., Haan, M., Ikram, M. A., Karlawish, J., Langbaum, J. B., Neuhaus, J. M., Reiman, E. M., Roberts, J. S., Seshadri, S., Tariot, P. N., Woods, B. M. C., Betensky, R. A., & Blacker, D. (n.d.).

Publication year

2017

Journal title

PLoS Medicine

Volume

Issue

10.1371/journal.pmed.1002254

Abstract

Abstract

Background: With the onset of prevention trials for individuals at high risk for Alzheimer disease, there is increasing need for accurate risk prediction to inform study design and enrollment, but available risk estimates are limited. We developed risk estimates for the incidence of mild cognitive impairment (MCI) or dementia among cognitively unimpaired individuals by APOE-e4 dose for the genetic disclosure process of the Alzheimer’s Prevention Initiative Generation Study, a prevention trial in cognitively unimpaired APOE-e4/e4 homozygote individuals. Methods and findings: We included cognitively unimpaired individuals aged 60–75 y, consistent with Generation Study eligibility criteria, from the National Alzheimer’s Coordinating Center (NACC) (n = 5,073, 158 APOE-e4/e4), the Rotterdam Study (n = 6,399, 156 APOE-e4/e4), the Framingham Heart Study (n = 4,078, 67 APOE-e4/e4), and the Sacramento Area Latino Study on Aging (SALSA) (n = 1,294, 11 APOE-e4/e4). We computed stratified cumulative incidence curves by age (60–64, 65–69, 70–75 y) and APOE-e4 dose, adjusting for the competing risk of mortality, and determined risk of MCI and/or dementia by genotype and baseline age. We also used subdistribution hazard regression to model relative hazard based on age, APOE genotype, sex, education, family history of dementia, vascular risk, subjective memory concerns, and baseline cognitive performance. The four cohorts varied considerably in age, education, ethnicity/race, and APOE-e4 allele frequency. Overall, cumulative incidence was uniformly higher in NACC than in the population-based cohorts. Among APOE-e4/e4 individuals, 5-y cumulative incidence was as follows: in the 60–64-y age stratum, it ranged from 0% to 5.88% in the three population-based cohorts versus 23.06% in NACC; in the 65–69-y age stratum, from 9.42% to 10.39% versus 34.62%; and in the 70–75-y age stratum, from 18.64% to 33.33% versus 38.34%. Five-year incidence of dementia was negligible except for APOE-e4/e4 individuals and those over 70 y. Lifetime incidence (to age 80–85 y) of MCI or dementia for the APOE-e4/e4 individuals in the long-term Framingham and Rotterdam cohorts was 34.69%–38.45% at age 60–64 y, 30.76%–40.26% at 65–69 y, and 33.3%–35.17% at 70–75 y. Confidence limits for these estimates are often wide, particularly for APOE-e4/e4 individuals and for the dementia outcome at 5 y. In regression models, APOE-e4 dose and age both consistently increased risk, as did lower education, subjective memory concerns, poorer baseline cognitive performance, and family history of dementia. We discuss several limitations of the study, including the small numbers of APOE-e4/e4 individuals, missing data and differential dropout, limited ethnic and racial diversity, and differences in definitions of exposure and outcome variables. Conclusions: Estimates of the absolute risk of MCI or dementia, particularly over short time intervals, are sensitive to sampling and a variety of methodological factors. Nonetheless, such estimates were fairly consistent across the population-based cohorts, and lower than those from a convenience cohort and those estimated in prior studies—with implications for informed consent and design for clinical trials targeting high-risk individuals.