Brain Aging
Dr. Dennis de Bakker
Nexus Group Leader
I am an experimental biologist with a strong interest in identifying novel strategies to prevent neurodegenerative diseases.
Overview
Novel strategies to prevent neurodegenerative diseases
Turquoise killifish spontaneously develop age-related brain degeneration phenotypes, including protein aggregation, neuroinflammation, and neuronal loss. In our lab, we aim to identify and target the mechanisms underlying brain degeneration in killifish in order to delay or prevent the onset of these age-related phenotypes. If successful, insights gained from killifish may ultimately inform similar preventive approaches in humans suffering from neurodegenerative diseases.
To identify and target the mechanisms driving killifish brain degeneration, we employ a wide range of methodologies, including immunohistochemistry, confocal microscopy, RNA sequencing, proteomics (LC–MS), quantitative trait locus (QTL) analysis, CRISPR-mediated mutagenesis, pharmacological interventions, and behavioral testing.
More About Us
Outstanding Questions
Lab News
Carl-Zeiss-Stiftung funds research project to develop new strategies for preventing neurodegenerative diseases
At the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, a new research group led by experimental biologist Dr Dennis de Bakker began work in January 2026. This was made possible by the Carl-Zeiss-Stiftung Nexus programme, which offers postdocs the opportunity to establish their own interdisciplinary research group. The funding amounts to up to 1.5 million euros for a period of five years. The primary goal of the research group is to uncover the mechanisms of brain ageing through cross-species comparisons.
Storing defective energy: How the aging brain remains efficient
An international research team led by the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, and the University of Tennessee Health Science Center, Memphis, USA, has uncovered new insights into healthy brain aging. Researchers found that aging leads to the accumulation of defective energy molecules in the brains of aged mice, like humans, and identified the responsible genetic sequence. Importantly, no evidence was found that this accumulation would impair brain function, highlighting that age-related brain changes are not necessarily harmful.
