Christopher Chen
· Professor (BME, MSE)Boston University · Environmental Health
Active 1959–2024
About
Christopher Chen, MD, PhD, is the William F. Warren Distinguished Professor of Biomedical Engineering at Boston University College of Engineering. His laboratory seeks to understand how adhesive, mechanical, and biochemical interactions drive cell and tissue function, with the goal of building biomimetic tissues as experimental models of disease and physiology, and directing tissue remodeling and regeneration. Dr. Chen’s research focuses on how the cooperation between adhesive, mechanical, and biochemical signaling influences tissue organization during development, adaptation to physical stresses, and disease progression. His work involves the development and application of innovative technologies such as microfluidics, microelectromechanical systems (MEMS), nanofabrication, mechanobiology, biomaterials, and synthetic and stem cell biology. These efforts aim to provide new tools for biomedicine, gain insights into the control of cell and tissue function, and advance the fields of stem cell biology, tissue vascularization, cardiac tissue engineering, and cancer research. Dr. Chen is also the founding director of the Biological Design Center at Harvard’s Wyss Institute and holds additional roles including Deputy Director of the NSF Engineering Research Center in Cellular Metamaterials and co-PI of the NSF Science and Technology Center for Engineering Mechanobiology. His interdisciplinary work bridges technology, cell biology, and medicine, with a mission to impact research, medicine, and education through innovative approaches.
Research topics
- Medicine
- Internal medicine
- Pathology
- Biology
- Gerontology
- Bioinformatics
- Nursing
- Neuroscience
- Genetics
- Psychiatry
- Environmental health
- Psychology
- Economic growth
- Intensive care medicine
Selected publications
The Lancet Neurology · 2023 · 628 citations
- Medicine
- Environmental health
- Economic growth
Framework for Clinical Trials in Cerebral Small Vessel Disease (FINESSE)
JAMA Neurology · 2022 · 78 citations
- Medicine
- Pathology
- Bioinformatics
Importance: Cerebral small vessel disease (SVD) causes a quarter of strokes and is the most common pathology underlying vascular cognitive impairment and dementia. An important step to developing new treatments is better trial methodology. Disease mechanisms in SVD differ from other stroke etiologies; therefore, treatments need to be evaluated in cohorts in which SVD has been well characterized. Furthermore, SVD itself can be caused by a number of different pathologies, the most common of which are arteriosclerosis and cerebral amyloid angiopathy. To date, there have been few sufficiently powered high-quality randomized clinical trials in SVD, and inconsistent trial methodology has made interpretation of some findings difficult. Observations: To address these issues and develop guidelines for optimizing design of clinical trials in SVD, the Framework for Clinical Trials in Cerebral Small Vessel Disease (FINESSE) was created under the auspices of the International Society of Vascular Behavioral and Cognitive Disorders. Experts in relevant aspects of SVD trial methodology were convened, and a structured Delphi consensus process was used to develop recommendations. Areas in which recommendations were developed included optimal choice of study populations, choice of clinical end points, use of brain imaging as a surrogate outcome measure, use of circulating biomarkers for participant selection and as surrogate markers, novel trial designs, and prioritization of therapeutic agents using genetic data via Mendelian randomization. Conclusions and Relevance: The FINESSE provides recommendations for trial design in SVD for which there are currently few effective treatments. However, new insights into understanding disease pathogenesis, particularly from recent genetic studies, provide novel pathways that could be therapeutically targeted. In addition, whether other currently available cardiovascular interventions are specifically effective in SVD, as opposed to other subtypes of stroke, remains uncertain. FINESSE provides a framework for design of trials examining such therapeutic approaches.
Lecanemab in Early Alzheimer’s Disease
New England Journal of Medicine · 2022 · 4966 citations
- Medicine
- Internal medicine
BACKGROUND: The accumulation of soluble and insoluble aggregated amyloid-beta (Aβ) may initiate or potentiate pathologic processes in Alzheimer's disease. Lecanemab, a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils, is being tested in persons with early Alzheimer's disease. METHODS: We conducted an 18-month, multicenter, double-blind, phase 3 trial involving persons 50 to 90 years of age with early Alzheimer's disease (mild cognitive impairment or mild dementia due to Alzheimer's disease) with evidence of amyloid on positron-emission tomography (PET) or by cerebrospinal fluid testing. Participants were randomly assigned in a 1:1 ratio to receive intravenous lecanemab (10 mg per kilogram of body weight every 2 weeks) or placebo. The primary end point was the change from baseline at 18 months in the score on the Clinical Dementia Rating-Sum of Boxes (CDR-SB; range, 0 to 18, with higher scores indicating greater impairment). Key secondary end points were the change in amyloid burden on PET, the score on the 14-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog14; range, 0 to 90; higher scores indicate greater impairment), the Alzheimer's Disease Composite Score (ADCOMS; range, 0 to 1.97; higher scores indicate greater impairment), and the score on the Alzheimer's Disease Cooperative Study-Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS-MCI-ADL; range, 0 to 53; lower scores indicate greater impairment). RESULTS: A total of 1795 participants were enrolled, with 898 assigned to receive lecanemab and 897 to receive placebo. The mean CDR-SB score at baseline was approximately 3.2 in both groups. The adjusted least-squares mean change from baseline at 18 months was 1.21 with lecanemab and 1.66 with placebo (difference, -0.45; 95% confidence interval [CI], -0.67 to -0.23; P<0.001). In a substudy involving 698 participants, there were greater reductions in brain amyloid burden with lecanemab than with placebo (difference, -59.1 centiloids; 95% CI, -62.6 to -55.6). Other mean differences between the two groups in the change from baseline favoring lecanemab were as follows: for the ADAS-cog14 score, -1.44 (95% CI, -2.27 to -0.61; P<0.001); for the ADCOMS, -0.050 (95% CI, -0.074 to -0.027; P<0.001); and for the ADCS-MCI-ADL score, 2.0 (95% CI, 1.2 to 2.8; P<0.001). Lecanemab resulted in infusion-related reactions in 26.4% of the participants and amyloid-related imaging abnormalities with edema or effusions in 12.6%. CONCLUSIONS: Lecanemab reduced markers of amyloid in early Alzheimer's disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events. Longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer's disease. (Funded by Eisai and Biogen; Clarity AD ClinicalTrials.gov number, NCT03887455.).
The Amyloid-β Pathway in Alzheimer’s Disease
Molecular Psychiatry · 2021 · 1733 citations
- Neuroscience
- Medicine
- Biology
Breakthroughs in molecular medicine have positioned the amyloid-β (Aβ) pathway at the center of Alzheimer's disease (AD) pathophysiology. While the detailed molecular mechanisms of the pathway and the spatial-temporal dynamics leading to synaptic failure, neurodegeneration, and clinical onset are still under intense investigation, the established biochemical alterations of the Aβ cycle remain the core biological hallmark of AD and are promising targets for the development of disease-modifying therapies. Here, we systematically review and update the vast state-of-the-art literature of Aβ science with evidence from basic research studies to human genetic and multi-modal biomarker investigations, which supports a crucial role of Aβ pathway dyshomeostasis in AD pathophysiological dynamics. We discuss the evidence highlighting a differentiated interaction of distinct Aβ species with other AD-related biological mechanisms, such as tau-mediated, neuroimmune and inflammatory changes, as well as a neurochemical imbalance. Through the lens of the latest development of multimodal in vivo biomarkers of AD, this cross-disciplinary review examines the compelling hypothesis- and data-driven rationale for Aβ-targeting therapeutic strategies in development for the early treatment of AD.
World‐Wide FINGERS Network: A global approach to risk reduction and prevention of dementia
Alzheimer s & Dementia · 2020 · 507 citations
- Gerontology
- Medicine
- Psychology
Reducing the risk of dementia can halt the worldwide increase of affected people. The multifactorial and heterogeneous nature of late-onset dementia, including Alzheimer's disease (AD), indicates a potential impact of multidomain lifestyle interventions on risk reduction. The positive results of the landmark multidomain Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) support such an approach. The World-Wide FINGERS (WW-FINGERS), launched in 2017 and including over 25 countries, is the first global network of multidomain lifestyle intervention trials for dementia risk reduction and prevention. WW-FINGERS aims to adapt, test, and optimize the FINGER model to reduce risk across the spectrum of cognitive decline-from at-risk asymptomatic states to early symptomatic stages-in different geographical, cultural, and economic settings. WW-FINGERS aims to harmonize and adapt multidomain interventions across various countries and settings, to facilitate data sharing and analysis across studies, and to promote international joint initiatives to identify globally implementable and effective preventive strategies.
Frequent coauthors
- 1173 shared
Saima Hilal
National University Health System
- 830 shared
Tien Yin Wong
Singapore National Eye Center
- 781 shared
Thiruma V. Arumugam
La Trobe University
- 741 shared
Narayanaswamy Venketasubramanian
Raffles Institution
- 737 shared
Christopher Levi
Hunter Medical Research Institute
- 720 shared
Mike B. Calford
- 720 shared
John Thundyil
Abbott (Singapore)
- 720 shared
Ferdinand Miteff
John Hunter Hospital
Education
- 2000
Ph.D., Materials Science and Engineering
Boston University
- 1995
M.D.
University of California, San Francisco
- 1991
B.S., Materials Science and Engineering
University of California, Berkeley
Awards & honors
- William F. Warren Distinguished Professor of Biomedical Engi…
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