Rudolf Jaenisch, M.D.

Member, Whitehead Institute for Biomedical Research
Professor of Biology, Massachusetts Institute of Technology

Rudolf Jaenisch is a founding member of the Whitehead Institute in Cambridge, MA. His research focuses on understanding epigenetic regulation of gene expression (the biological mechanisms that affect how genetic information is converted into cell structures but that don’t alter the genes in the process). He is a pioneer of genetic manipulation, stem cell biology, and disease modeling. His recent work has focused on understanding the mechanisms of induced pluripotency and the modeling of neurodegenerative disorders using human induced pluripotent stem cells.

Jaenisch received his doctorate in medicine from the University of Munich in 1967. Before coming to Whitehead, he was head of the Department of Tumor Virology at the Heinrich Pette Institute at the University of Hamburg. He has coauthored more than 375 research papers and has received numerous prizes and recognitions, including an appointment to the National Academy of Sciences in 2003. 

Funded Research

Project Description Researchers Funding
Modeling DNA Methylation Changes in Alzheimer’s Disease Using Human-Induced Pluripotent Stem Cells

Alzheimer’s disease is associated with changes to DNA methylation, a modification of DNA that can alter the expression of genes in the brain. How DNA methylation changes contribute to Alzheimer’s disease, however, has been hard to determine. Our proposed work aims to study the causes of DNA methylation changes in Alzheimer’s disease and aims to better understand how these changes might affect Alzheimer’s disease patients.

2016 to 2017

CIRCUITS: Whole Genome Characterization of DNA Methylation Changes in the Aged and Alzheimer’s Disease Human Brain

Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder. Both normal aging and Alzheimer’s disease have been correlated with changes to the patterns of DNA methylation in the brain. DNA methylation is an epigenetic mark with the capacity to stably alter gene expression. The importance of changes to DNA methylation in AD has been difficult to assess. This proposed work would characterize the alterations of genome-wide DNA methylation patterns in post-mortem human neurons in the context of normal aging and AD.