Bio


Internship & Residency Stanford University School of Medicine
MD, University of Washington
MPH, The George Washington University
BA, Mount Holyoke College

Academic Appointments


  • Clinical Assistant Professor, Medicine

Honors & Awards


  • Brooke Gabster Award for Patient Care, Stanford Medicine (2022)
  • Department of Medicine Most Outstanding Student Award, University of Washington (2020)
  • Member, Alpha Omega Alpha Honor Society (2019)
  • Member, Arnold P Gold Humanism Honor Society (2018)

Boards, Advisory Committees, Professional Organizations


  • Women in Medicine Leadership Council Representative, Stanford Medicine (2021 - 2023)
  • Stanford IM HEARS, Co-lead (2022 - 2023)
  • Executive Board Member, Unite For Sight (2013 - Present)

All Publications


  • Cancer Survivorship at Stanford Cancer Institute. Journal of cancer survivorship : research and practice Smith, S. M., Steele, N., Kim, J., Yurkiewicz, I. R., Benedict, C., Trivedi, R., Heathcote, L. C., Simon, P. J., Bugos, K., Clayton, A., Palesh, O., Schapira, L. 2024

    Abstract

    The Stanford Cancer Survivorship Program is a key initiative of Stanford Cancer Institute. The program's mission is to improve the experience and outcomes of patients and family caregivers throughout all phases of the cancer trajectory by advancing survivorship research, clinical care, and education. The four pillars of the program include clinical care delivery with a focus on primary care-survivorship collaboration and expanding specialty services, education and training of healthcare professionals, transdisciplinary patient-oriented research, and community engagement. Cross-cutting areas of expertise include the following: (a) adolescents and young adults (AYAs), (b) mental health and patient self-management, (c) integration of primary care, and (d) postgraduate medical education. The clinical care model includes embedded survivorship clinics within disease groups in outpatient clinics, novel clinics designed to address unmet needs such as sexual health for women, and primary care-based faculty-led survivorship clinics for patients undergoing active cancer care requiring co-management, those who have completed active therapy and those at high risk for cancer due to genetic risk. Educational initiatives developed to date include an online course and medical textbook for primary care clinicians, a lecture series, monthly research team meetings, and rotations for medical trainees. Patient-facing activities include webinars and a podcast series designed to promote awareness, thus expanding the provision of expert-vetted information. Ongoing research focuses on oncofertility and family building after cancer, improving communication for AYAs, changing mindsets to improve quality of life through targeted digital interventions, increasing capacity to care for cancer survivors, and strengthening collaboration with community partners. IMPLICATIONS FOR CANCER SURVIVORS: Stanford's Cancer Survivorship Program includes a robust transdisciplinary and interdisciplinary research, training and clinical platform that is committed to advancing access and improving care for people living with and beyond cancer, through innovation in design and care delivery.

    View details for DOI 10.1007/s11764-023-01523-w

    View details for PubMedID 38183579

    View details for PubMedCentralID 9545782

  • The Patient Resident NEW ENGLAND JOURNAL OF MEDICINE Rabinowitz Steele, N. Z. 2022; 386 (11): 1010-1011

    View details for DOI 10.1056/NEJMp2116289

    View details for Web of Science ID 000767893900001

    View details for PubMedID 35275479

  • An Anomalous Cause of Pulmonary Hypertension. Annals of the American Thoracic Society Steele, N. Z., Luks, A. M. 2021; 18 (9): 1571-1576

    View details for DOI 10.1513/AnnalsATS.202102-113CC

    View details for PubMedID 34468285

  • Applicability of the Zenith Inner Branched Arch Endograft JOURNAL OF ENDOVASCULAR THERAPY Burke, C. R., Kratzberg, J. A., Yoder, A. D., Steele, N. Z., Aldea, G. S., Sweet, M. P. 2020; 27 (2): 252–57

    Abstract

    Purpose: To evaluate the clinical and anatomical features of patients with arch pathology to better understand the applicability of the Zenith inner branched arch endograft (IBAE). Materials and Methods: A retrospective review was performed of 60 consecutive patients (mean age 62.5 years; 42 men) who presented with nonruptured aortic arch pathology at a single institution between 2009 and 2016. Patients were stratified into standard (no previous cardiac surgery, <80 years old, and no significant medical comorbidity), high (previous cardiac surgery or significant comorbidity), or prohibitive risk (turned down for operative intervention) for operative intervention. Anatomical measurements of the aorta were obtained on computed tomography scans; anatomical suitability was based on the device's instructions for use. Results: Overall, 27 (45%) patients had anatomy amenable to treatment with the existing IBAE. Inadequate proximal seal length and large ascending aortic diameters were the primary reasons for anatomical unsuitability. Shortening the inner curve seal zone from 25 to 15 mm and increasing the proximal seal zone diameter from 38 to 42 mm increased anatomical suitability to include 49 (82%) patients. Of these, 31 were in the high-risk cohort and 7 were deemed prohibitive risk; therefore, IBAE would have been strongly considered in these 38 patients. Conclusion: Based on anatomical criteria alone, nearly half of patients with aortic arch pathology have anatomy suitable to the Zenith IBAE in its current design. Arch branch vessel anatomy was not a limitation of the device. From a clinical standpoint, if endovascular repair were reserved for those at high or prohibitive risk for open repair, approximately 30% of patients would likely benefit from the IBAE in its current form.

    View details for DOI 10.1177/1526602820909487

    View details for Web of Science ID 000523901600015

    View details for PubMedID 32186260

  • Primary Care Provider Attitudes and Practices Evaluating and Managing Patients with Neurocognitive Disorders JOURNAL OF GENERAL INTERNAL MEDICINE Bernstein, A., Rogers, K. M., Possin, K. L., Steele, N. R., Ritchie, C. S., Miller, B. L., Rankin, K. P. 2019; 34 (9): 1691–92

    View details for DOI 10.1007/s11606-019-05013-7

    View details for Web of Science ID 000483539200010

    View details for PubMedID 31044411

    View details for PubMedCentralID PMC6712190

  • Genetic variation across RNA metabolism and cell death gene networks is implicated in the semantic variant of primary progressive aphasia SCIENTIFIC REPORTS Bonham, L. W., Steele, N. R., Karch, C. M., Broce, I., Geier, E. G., Wen, N. L., Momeni, P., Hardy, J., Miller, Z. A., Gorno-Tempini, M., Hess, C. P., Lewis, P., Miller, B. L., Seeley, W. W., Manzoni, C., Desikan, R. S., Baranzini, S. E., Ferraris, R., Yokoyama, J. S., Hernandez, D. G., Nalls, M. A., Rohrer, J. D., Ramasamy, A., Kwok, J. J., Dobson-Stone, C., Schofield, P. R., Halliday, G. M., Hodges, J. R., Piguet, O., Bartley, L., Thompson, E., Haan, E., Hernandez, Ruiz, A., Boada, M., Borroni, B., Padovani, A., Cruchaga, C., Cairns, N. J., Benussi, L., Binetti, G., Ghidoni, R., Forloni, G., Albani, D., Galimberti, D., Fenoglio, C., Serpente, M., Scarpini, E., Clarimon, J., Lleo, A., Blesa, R., Waldo, M., Nilsson, K., Nilsson, C., Mackenzie, I. A., Hsiung, G. R., Mann, D. A., Grafman, J., Morris, C. M., Attems, J., Griffiths, T. D., McKeith, I. G., Thomas, A. J., Pietrini, P., Huey, E. D., Wassermann, E. M., Baborie, A., Jaros, E., Tierney, M. C., Pastor, P., Razquin, C., Ortega-Cubero, S., Alonso, E., Perneczky, R., Diehl-Schmid, J., Alexopoulos, P., Kurz, A., Rainero, Rubino, E., Pinessi, L., Rogaeva, E., St George-Hyslop, P., Rossi, G., Tagliavini, F., Giaccone, G., Rowe, J. B., Schlachetzki, J. M., Uphill, J., Collinge, J., Mead, S., Danek, A., Van Deerlin, V. M., Grossman, M., Trojanowski, J. Q., van der Zee, J., Cruts, M., Van Broeckhoven, C., Cappa, S. F., Leber, Hannequin, D., Golfier, Vercelletto, M., Brice, A., Nacmias, B., Sorbin, S., Bagnoli, S., Piaceri, Nielsen, J. E., Hjermind, L. E., Riemenschneider, M., Mayhaus, M., Ibach, B., Gasparoni, G., Pichler, S., Gu, W., Rossor, M. N., Fox, N. C., Warren, J. D., Spillantini, M. G., Morriss, H. R., Rizzu, P., Heutink, P., Snowden, J. S., Rollinson, S., Richardson, A., Gerhard, A., Bruni, A. C., Maletta, R., Frangipane, F., Cupidi, C., Bernardi, L., Anfossi, M., Gallo, M., Conidi, M. E., Smirne, N., Rademakers, R., Baker, M., Dickson, D. W., Graff-Radford, N. R., Petersen, R. C., Knopman, D., Josephs, K. A., Boeve, B. F., Parisi, J. E., Karydas, A. M., Rosen, H., van Swieten, J. C., Dopper, E. P., Seelaar, H., Pijnenburg, Y. L., Scheltens, P., Logroscino, G., Capozzo, R., Novelli, Puca, A. A., Franceschi, M., Postiglione, A., Milan, G., Sorrentino, P., Kristiansen, M., Chian, H., Graff, C., Pasquier, F., Rollin, A., Deramecourt, Lebouvier, T., Kapogiannis, D., Ferrucci, L., Pickering-Brown, S., Singleton, A. B., Int FTD-Genomics Consortium 2019; 9: 10854

    Abstract

    The semantic variant of primary progressive aphasia (svPPA) is a clinical syndrome characterized by neurodegeneration and progressive loss of semantic knowledge. Unlike many other forms of frontotemporal lobar degeneration (FTLD), svPPA has a highly consistent underlying pathology composed of TDP-43 (a regulator of RNA and DNA transcription metabolism). Previous genetic studies of svPPA are limited by small sample sizes and a paucity of common risk variants. Despite this, svPPA's relatively homogenous clinicopathologic phenotype makes it an ideal investigative model to examine genetic processes that may drive neurodegenerative disease. In this study, we used GWAS metadata, tissue samples from pathologically confirmed frontotemporal lobar degeneration, and in silico techniques to identify and characterize protein interaction networks associated with svPPA risk. We identified 64 svPPA risk genes that interact at the protein level. The protein pathways represented in this svPPA gene network are critical regulators of RNA metabolism and cell death, such as SMAD proteins and NOTCH1. Many of the genes in this network are involved in TDP-43 metabolism. Contrary to the conventional notion that svPPA is a clinical syndrome with few genetic risk factors, our analyses show that svPPA risk is complex and polygenic in nature. Risk for svPPA is likely driven by multiple common variants in genes interacting with TDP-43, along with cell death,x` working in combination to promote neurodegeneration.

    View details for DOI 10.1038/s41598-019-46415-1

    View details for Web of Science ID 000477698600012

    View details for PubMedID 31350420

    View details for PubMedCentralID PMC6659677

  • Frequency of frontotemporal dementia gene variants in C9ORF72, MAPT, and GRN in academic versus commercial laboratory cohorts. Advances in genomics and genetics Steele, N. Z., Bright, A. R., Lee, S. E., Fong, J. C., Bonham, L. W., Karydas, A., Karbassi, I. D., Pribadi, M., Meservey, M. A., Gallen, M. C., Ramos, E. M., Liaquat, K., Hoffman, C. C., Krasner, M. R., Dodge, W., L Miller, B., Coppola, G., Rankin, K. P., Yokoyama, J. S., Higgins, J. J. 2018; 8: 23-33

    Abstract

    Frontotemporal lobar degeneration (FTLD) is a leading cause of dementia, and elucidating its genetic underpinnings is critical. FTLD research centers typically recruit patient cohorts that are limited by the center's specialty and the ways in which its geographic location affects the ethnic makeup of research participants. Novel sources of data are needed to get population estimates of the contribution of variants in known FTLD-associated genes.We compared FLTD-associated genetic variants in microtubule-associated protein tau (MAPT), progranulin (GRN), and chromosome nine open reading frame 72 (C9ORF72) from an academic research cohort and a commercial clinical genetics laboratory. Pathogenicity was assessed using guidelines of the American College of Medical Genetics and Genomics and a rule-based DNA variant assessment system. We conducted chart reviews on patients with novel or rare disease-associated variants.A total of 387 cases with FTLD-associated variants from the commercial (n=2,082) and 78 cases from the academic cohort (n=2,089) were included for analysis. In the academic cohort, the most frequent pathogenic variants were C9ORF72 expansions (63%, n=49), followed by GRN (26%, n=20) and MAPT (11%, n=9). Each gene's contribution to disease was similarly ranked in the commercial laboratory but differed in magnitude: C9ORF72 (89%, n=345), GRN (6%, n=24), and MAPT (5%, n=19). Of the 37 unique GRN/MAPT variants identified, only six were found in both cohorts. Clinicopathological data from patients in the academic cohort strengthened classification of two novel GRN variant as pathogenic (p.Pro166Leufs*2, p.Gln406*) and one GRN variant of unknown significance as a possible rare risk variant (p.Cys139Arg).Differences in gene frequencies and identification of unique pathogenic alleles in each cohort demonstrate the importance of data sharing between academia and community laboratories. Using shared data sources with well-characterized clinical phenotypes for individual variants can enhance interpretation of variant pathogenicity and inform clinical management of at-risk patients and families.

    View details for DOI 10.2147/AGG.S164047

    View details for PubMedID 31031559

    View details for PubMedCentralID PMC6483103

  • Protein network analysis reveals selectively vulnerable regions and biological processes in FTD NEUROLOGY-GENETICS Bonham, L. W., Steele, N. R., Karch, C. M., Manzoni, C., Geier, E. G., Wen, N., Ofori-Kuragu, A., Momeni, P., Hardy, J., Miller, Z. A., Hess, C. P., Lewis, P., Miller, B. L., Seeley, W. W., Baranzini, S. E., Desikan, R. S., Ferrari, R., Yokoyama, J. S., Int FTD-Genomics Consortium IFGC 2018; 4 (5): e266

    Abstract

    The neuroanatomical profile of behavioral variant frontotemporal dementia (bvFTD) suggests a common biological etiology of disease despite disparate pathologic causes; we investigated the genetic underpinnings of this selective regional vulnerability to identify new risk factors for bvFTD.We used recently developed analytical techniques designed to address the limitations of genome-wide association studies to generate a protein interaction network of 63 bvFTD risk genes. We characterized this network using gene expression data from healthy and diseased human brain tissue, evaluating regional network expression patterns across the lifespan as well as the cell types and biological processes most affected in bvFTD.We found that bvFTD network genes show enriched expression across the human lifespan in vulnerable neuronal populations, are implicated in cell signaling, cell cycle, immune function, and development, and are differentially expressed in pathologically confirmed frontotemporal lobar degeneration cases. Five of the genes highlighted by our differential expression analyses, BAIAP2, ERBB3, POU2F2, SMARCA2, and CDC37, appear to be novel bvFTD risk loci.Our findings suggest that the cumulative burden of common genetic variation in an interacting protein network expressed in specific brain regions across the lifespan may influence susceptibility to bvFTD.

    View details for DOI 10.1212/NXG.0000000000000266

    View details for Web of Science ID 000447372900002

    View details for PubMedID 30283816

    View details for PubMedCentralID PMC6167176

  • Insulin-Like Growth Factor Binding Protein 2 Is Associated With Biomarkers of Alzheimer's Disease Pathology and Shows Differential Expression in Transgenic Mice FRONTIERS IN NEUROSCIENCE Bonham, L. W., Geier, E. G., Steele, N. R., Holland, D., Miller, B. L., Dale, A. M., Desikan, R. S., Yokoyama, J. S., Alzheimers Dis Neuroimaging Initia 2018; 12: 476

    Abstract

    There is increasing evidence that metabolic dysfunction plays an important role in Alzheimer's disease (AD). Brain insulin resistance and subsequent impairment of insulin and insulin-like growth factor (IGF) signaling are associated with the neurodegenerative and clinical features of AD. Nevertheless, how the brain insulin/IGF signaling system is altered in AD and the effects of these changes on AD pathobiology are not well understood. IGF binding protein 2 (IGFBP-2) is an abundant cerebral IGF signaling protein and there is early evidence suggesting it associates with AD biomarkers. We evaluated the relationship between protein levels of IGFBP-2 with cerebrospinal fluid (CSF) biomarkers and neuroimaging markers of AD progression in 300 individuals from across the AD spectrum. CSF IGFBP-2 levels were correlated with CSF tau levels and brain atrophy in non-hippocampal regions. To further explore the role of IGFBP2 in tau pathobiology, we evaluated the expression of IGFBP2 in different human and mouse brain cell types and brain tissue from two transgenic mouse models: the P301L-tau model of tauopathy and TASTPM model of AD. We observed significant differential expression of IGFBP2 in both transgenic mouse models relative to wild-type mice in cortex but not in hippocampus. In both humans and mice, IGFBP2 is most highly expressed in astrocytes. Taken together, our findings suggest that IGFBP-2 may be linked to tau pathology and provides further evidence for a relationship between metabolic dysregulation and neurodegeneration. Our results also raise the possibility that this relationship may extend beyond neurons.

    View details for DOI 10.3389/fnins.2018.00476

    View details for Web of Science ID 000438754300002

    View details for PubMedID 30061810

    View details for PubMedCentralID PMC6055061

  • The Brain Health Assessment for Detecting and Diagnosing Neurocognitive Disorders JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Possin, K. L., Moskowitz, T., Erlhoff, S. J., Rogers, K. M., Johnson, E. T., Steele, N. R., Higgins, J. J., Stiver, J., Alioto, A. G., Farias, S. T., Miller, B. L., Rankin, K. P. 2018; 66 (1): 150–56

    Abstract

    Brief cognitive screens lack the sensitivity to detect mild cognitive impairment (MCI) or support differential diagnoses. The objective of this study was to validate the 10-minute, tablet-based University of California, San Francisco (UCSF) Brain Health Assessment (BHA) to overcome these limitations.Cross-sectional.UCSF Memory and Aging Center.Older adults (N = 347) (neurologically healthy controls (n = 185), and individuals diagnosed with MCI (n = 99), dementia (n = 42), and as normal with concerns (n = 21)).The BHA includes subtests of memory, executive function and speed, visuospatial skills, and language and an optional informant survey. Participants completed the Montreal Cognitive Assessment (MoCA) and criterion-standard neuropsychological tests. Standardized structural 3T brain magnetic resonance imaging was performed in 145 participants.At a fixed 85% specificity rate, the BHA had 100% sensitivity to dementia and 84% to MCI; the MoCA had 75% sensitivity to dementia and 25% to MCI. The BHA had 83% sensitivity to MCI likely due to AD and 88% to MCI unlikely due to AD, and the MoCA had 58% sensitivity to MCI likely AD and 24% to MCI unlikely AD. The BHA subtests demonstrated moderate to high correlations with the criterion-standard tests from their respective cognitive domains. Memory test performance correlated with medial temporal lobe volumes; executive and speed with frontal, parietal, and basal ganglia volumes; and visuospatial with right parietal volumes.The BHA had excellent combined sensitivity and specificity to detect dementia and MCI, including MCI due to diverse etiologies. The subtests provide efficient, valid measures of neurocognition that are critical in making a differential diagnosis.

    View details for DOI 10.1111/jgs.15208

    View details for Web of Science ID 000422998600024

    View details for PubMedID 29355911

    View details for PubMedCentralID PMC5889617

  • Fine-mapping of the human leukocyte antigen locus as a risk factor for Alzheimer disease: A case-control study PLOS MEDICINE Steele, N. R., Carr, J. S., Bonham, L. W., Geier, E. G., Damotte, V., Miller, Z. A., Desikan, R. S., Boehme, K. L., Mukherjee, S., Crane, P. K., Kauwe, J. K., Kramer, J. H., Miller, B. L., Coppola, G., Hollenbach, J. A., Huang, Y., Yokoyama, J. S. 2017; 14 (3): e1002272

    Abstract

    Alzheimer disease (AD) is a progressive disorder that affects cognitive function. There is increasing support for the role of neuroinflammation and aberrant immune regulation in the pathophysiology of AD. The immunoregulatory human leukocyte antigen (HLA) complex has been linked to susceptibility for a number of neurodegenerative diseases, including AD; however, studies to date have failed to consistently identify a risk HLA haplotype for AD. Contributing to this difficulty are the complex genetic organization of the HLA region, differences in sequencing and allelic imputation methods, and diversity across ethnic populations.Building on prior work linking the HLA to AD, we used a robust imputation method on two separate case-control cohorts to examine the relationship between HLA haplotypes and AD risk in 309 individuals (191 AD, 118 cognitively normal [CN] controls) from the San Francisco-based University of California, San Francisco (UCSF) Memory and Aging Center (collected between 1999-2015) and 11,381 individuals (5,728 AD, 5,653 CN controls) from the Alzheimer's Disease Genetics Consortium (ADGC), a National Institute on Aging (NIA)-funded national data repository (reflecting samples collected between 1984-2012). We also examined cerebrospinal fluid (CSF) biomarker measures for patients seen between 2005-2007 and longitudinal cognitive data from the Alzheimer's Disease Neuroimaging Initiative (n = 346, mean follow-up 3.15 ± 2.04 y in AD individuals) to assess the clinical relevance of identified risk haplotypes. The strongest association with AD risk occurred with major histocompatibility complex (MHC) haplotype A*03:01~B*07:02~DRB1*15:01~DQA1*01:02~DQB1*06:02 (p = 9.6 x 10-4, odds ratio [OR] [95% confidence interval] = 1.21 [1.08-1.37]) in the combined UCSF + ADGC cohort. Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4. Separate analyses of class I and II haplotypes further supported the role of class I haplotype A*03:01~B*07:02 (p = 0.03, OR = 1.11 [1.01-1.23]) and class II haplotype DRB1*15:01- DQA1*01:02- DQB1*06:02 (DR15) (p = 0.03, OR = 1.08 [1.01-1.15]) as risk factors for AD. We followed up these findings in the clinical dataset representing the spectrum of cognitively normal controls, individuals with mild cognitive impairment, and individuals with AD to assess their relevance to disease. Carrying A*03:01~B*07:02 was associated with higher CSF amyloid levels (p = 0.03, β ± standard error = 47.19 ± 21.78). We also found a dose-dependent association between the DR15 haplotype and greater rates of cognitive decline (greater impairment on the 11-item Alzheimer's Disease Assessment Scale cognitive subscale [ADAS11] over time [p = 0.03, β ± standard error = 0.7 ± 0.3]; worse forgetting score on the Rey Auditory Verbal Learning Test (RAVLT) over time [p = 0.02, β ± standard error = -0.2 ± 0.06]). In a subset of the same cohort, dose of DR15 was also associated with higher baseline levels of chemokine CC-4, a biomarker of inflammation (p = 0.005, β ± standard error = 0.08 ± 0.03). The main study limitations are that the results represent only individuals of European-ancestry and clinically diagnosed individuals, and that our study used imputed genotypes for a subset of HLA genes.We provide evidence that variation in the HLA locus-including risk haplotype DR15-contributes to AD risk. DR15 has also been associated with multiple sclerosis, and its component alleles have been implicated in Parkinson disease and narcolepsy. Our findings thus raise the possibility that DR15-associated mechanisms may contribute to pan-neuronal disease vulnerability.

    View details for DOI 10.1371/journal.pmed.1002272

    View details for Web of Science ID 000397906100024

    View details for PubMedID 28350795

    View details for PubMedCentralID PMC5369701