About
Benjamin Michael Miller is an Assistant Professor of Political Science at the University of Illinois, with additional appointments in the Unit for Criticism and Interpretive Theory and the Department of Classics. His research primarily focuses on democratic citizenship and the role citizens should play in preserving and improving the functioning of democracy. He is particularly interested in identifying the skills and value commitments necessary for citizens to fulfill their obligations effectively. Much of his work analyzes the history of political thought, with a special emphasis on Aristotle's conception of good citizenship. Miller critically examines Aristotle's theory of virtue, arguing in his forthcoming book, "Against Aristotelian Character Education: Practical Wisdom, Flourishing, and Liberal Democracy" (2025), that Aristotle's theory is fundamentally illiberal and incompatible with the liberal democratic principle of respecting pluralism. Miller is also deeply engaged in interdisciplinary work at the intersection of political philosophy and empirical political science. He highlights the divergence between philosophical and empirical understandings of what constitutes a good democratic citizen. While empirical literature often focuses on voting behavior and policy-matching, Miller contends that historical political thought does not support this as the main role of citizens. Instead, he emphasizes that citizens' obligations are grounded in liberal value commitments, advocating for leaders and laws that serve the interests of all citizens rather than particular interests. His research aims to bridge these traditions by integrating political philosophy concepts into empirical studies on political sophistication, democratic backsliding, and affective polarization. Miller argues that addressing contemporary concerns about citizens' hostility and support for authoritarian leaders requires incorporating philosophical theories of good citizenship into empirical research. Miller holds a Ph.D. from Stanford University in Philosophy, along with master's degrees from Stanford's Graduate School of Education and the University of Auckland's Department of Philosophy. He also earned dual bachelor's degrees in Philosophy & Religion and Psychology from Northeastern University. His teaching portfolio includes courses on political theory, justice in the law, classical political thought, citizenship and diversity, ancient philosophy, and social justice related to children and families. Miller's work contributes to a deeper understanding of the role of citizens as gatekeepers of democracy, emphasizing the importance of treating all individuals as free and equal within a liberal democratic framework.
Research topics
- Medicine
- Internal medicine
- Biology
- Psychology
- Neuroscience
- Pathology
- Genetics
- Bioinformatics
- Oncology
- Psychiatry
- Nuclear medicine
- Machine Learning
- Computer Science
- Gerontology
- Artificial Intelligence
- Theoretical computer science
- Clinical psychology
- Developmental psychology
- Data science
- Mathematics
- Chemistry
- Econometrics
- Audiology
Selected publications
Aristotelian Pluralism Is the Wrong Sort of Pluralism
2025-07-02
book-chapter1st authorCorrespondingThe Problem with Practical Wisdom
2025-07-02
book-chapter1st authorCorrespondingVirtue Requires Understanding the Nature of Value
2025-07-02
book-chapter1st authorCorrespondingNeo-Aristotelian Flourishing and the Problem of Paternalism
2025-07-02
book-chapter1st authorCorrespondingVirtue Requires Knowing What Political Experts Know
2025-07-02
book-chapter1st authorCorrespondingVirtue Requires Extensive Value Knowledge
2025-07-02
book-chapter1st authorCorresponding2025-07-02
book-chapter1st authorCorrespondingDoubly-Robust Quantile Treatment Effects with Staggered Interventions 
SSRN Electronic Journal · 2025-01-01
preprintOpen access1st authorCorrespondingDoubly-Robust Quantile Treatment Effect Estimation : Online supplement
SSRN Electronic Journal · 2024-01-01
articleOpen access1st authorCorrespondingTowards cascading genetic risk in Alzheimer’s disease
Brain · 2024 · 11 citations
- Oncology
- Internal medicine
- Medicine
Alzheimer's disease typically progresses in stages, which have been defined by the presence of disease-specific biomarkers: amyloid (A), tau (T) and neurodegeneration (N). This progression of biomarkers has been condensed into the ATN framework, in which each of the biomarkers can be either positive (+) or negative (-). Over the past decades, genome-wide association studies have implicated ∼90 different loci involved with the development of late-onset Alzheimer's disease. Here, we investigate whether genetic risk for Alzheimer's disease contributes equally to the progression in different disease stages or whether it exhibits a stage-dependent effect. Amyloid (A) and tau (T) status was defined using a combination of available PET and CSF biomarkers in the Alzheimer's Disease Neuroimaging Initiative cohort. In 312 participants with biomarker-confirmed A-T- status, we used Cox proportional hazards models to estimate the contribution of APOE and polygenic risk scores (beyond APOE) to convert to A+T- status (65 conversions). Furthermore, we repeated the analysis in 290 participants with A+T- status and investigated the genetic contribution to conversion to A+T+ (45 conversions). Both survival analyses were adjusted for age, sex and years of education. For progression from A-T- to A+T-, APOE-e4 burden showed a significant effect [hazard ratio (HR) = 2.88; 95% confidence interval (CI): 1.70-4.89; P < 0.001], whereas polygenic risk did not (HR = 1.09; 95% CI: 0.84-1.42; P = 0.53). Conversely, for the transition from A+T- to A+T+, the contribution of APOE-e4 burden was reduced (HR = 1.62; 95% CI: 1.05-2.51; P = 0.031), whereas the polygenic risk showed an increased contribution (HR = 1.73; 95% CI: 1.27-2.36; P < 0.001). The marginal APOE effect was driven by e4 homozygotes (HR = 2.58; 95% CI: 1.05-6.35; P = 0.039) as opposed to e4 heterozygotes (HR = 1.74; 95% CI: 0.87-3.49; P = 0.12). The genetic risk for late-onset Alzheimer's disease unfolds in a disease stage-dependent fashion. A better understanding of the interplay between disease stage and genetic risk can lead to a more mechanistic understanding of the transition between ATN stages and a better understanding of the molecular processes leading to Alzheimer's disease, in addition to opening therapeutic windows for targeted interventions.
Recent grants
Cell Differentiation and Organogenesis in Aspergillus
NSF · $375k · 2003–2009
NIH · $358k · 1990
NIH · $52.5M · 2019
NIH · $96.6M · 2002–2028
NIH · $6.3M · 2019–2024
Frequent coauthors
- 1860 shared
Howard J. Rosen
University Memory and Aging Center
- 1677 shared
Gil D. Rabinovici
University Memory and Aging Center
- 1631 shared
Adam L. Boxer
University Memory and Aging Center
- 1515 shared
Joel H. Kramer
University of California, San Francisco
- 1463 shared
William W. Seeley
University of California, San Francisco
- 965 shared
Lea T. Grinberg
University of California, San Francisco
- 862 shared
Maria Luisa Gorno‐Tempini
University of California, San Francisco
- 818 shared
Keith A. Johnson
Massachusetts General Hospital
Education
- 2015
PhD, Philosophy
Stanford University
Awards & honors
- Clarence A. Berdahl Excellent Undergraduate Teaching Award i…
- Clarence A. Berdahl Excellent Undergraduate Teaching Award i…
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