Healthy Ageing Research
Key areas of ageing research
- Exploring changes in how our genomes are modified (the epigenome) during ageing
- Understanding how we respond to infection differently as we age
- Understanding the molecular mechanisms of ageing associated with declining competence of the immune system
- The effect of age on neuron survival
- Nutritional effects on signalling and ageing
- Using a systems biology approach to answer questions about how genome structure changes as a result of ageing and in response to external conditions
Key observations include:
- Determining the importance of changes in the axon survival factor Nmnat2 during ageing,
- Defining the importance of the aryl hydrocarbon receptor in the long term maintenance of tissue T cells
- Defining links between signalling pathways and epigenetic change pointing to mechanisms whereby nutrition and environment can interact with the epigenome.
Recent initiatives in Babraham’s ageing researchVaccination efficacy
ISP: Lymphocyte Signalling/Nuclear Dynamics
Group Leader: Michelle Linterman
Michelle’s group studies the age-related cellular and molecular changes that occur in immune cells (T cells) and contribute to the age-dependent decline in the strength of immune responses. Their work on the reduction in vaccination efficiency with age integrates with other work in the Immunology ISP, in addition it also complements the work on age-dependent changes in B cell function in the Nuclear Dynamics ISP.
Lymphocyte development and function
ISP: Lymphocyte Signalling
Group Leader: Martin Turner
The Turner group is working to understand how lymphocyte development and function is controlled by gene transcription, post-transcriptional control and signal transduction. Through funding from a BBSRC Strategic Longer and Larger (sLoLa) grant the Turner group is investigating how a class of regulators called RNA binding proteins controls processes fundamental to lymphocyte development and ageing.
Ageing research in C. elegans
Group Leader: Olivia Casanueva
Life expectancy is variable in many organisms, including humans. Obviously differences in the genetic background of individuals as well as variable environmental influences are important contributors to this variability. Surprisingly, however, lifespan is even variable in laboratory strains of C. elegans that lack genetic variability and that are grown in controlled environmental conditions. The main interest of my lab is to uncover the non-genetic sources of inter-individual variability in lifespan, using C. elegans as a model organism. We are studying the influence of epigenetic changes in the probability of life expectancy. These changes are stable, long-term alterations in the transcriptional potential of a gene that are not caused by changes in the DNA sequence. We propose that lifespan variation is at least in part a by-product of epigenetic sources of variability in the pathways that control longevity.
Regulation of the epigenome during ageing
Group Leader: Wolf Reik
We are interested in the possibility that components of the epigenome undergo regulated changes during ageing, and how this might be influenced by nutrition and transgenerational inheritance. In collaboration with the Nuclear Dynamics ISP we have begun to describe changes in chromatin organisation that occur in senescence and ageing, incorporating novel computational approaches.
Group Leaders: Oliver Florey and Nicholas Ktistakis
The Babraham Institute has a strong background in autophagy research as a key aspect of ageing. Autophagy is a pathway by which cells engulf and digest unnecessary cellular components, allowing them to be reused by the cell for energy in times of nutritional scarcity. This process becomes deregulated during ageing.
Our research has showed that the movement of mitochondria in nerves declines during normal ageing. Mitochondria are the part of the cell responsible for energy production. This decline is likely to contribute to age-related frailty, waning memory and could make an individual prone to degenerative disorders such as Alzheimer's. New work indicates that it may be possible to reverse this decline.