Could ageing brain cells increase our risk of Alzheimer’s?

Research project: Which age-related changes in astrocytes contribute to Alzheimer’s disease?

Lead investigator: Dr Nathaniel Woodling
Institution: University College London
Grant type: Junior Fellowship
Duration: 36 months
Amount: £225,000.00

Why did we fund this research? 

Comment from a member of our Research Network:

'[This project is] looking for an answer to a very clear question which would seem capable of narrowing down research in the future and targeting research for prevention.’

What do we already know?

There are two main types of brain cell inside the brain. The neuron is responsible for sending thoughts around the brain and creating actions such as kicking a ball - but neurons can’t do this on their own. 

The second type of brain cell, glia, support the neuron in everything they do – one of which is the astrocyte. The astrocyte is a star shaped cell that reaches out, supporting neurons and their connections with other cells. They also mop up excess chemicals that neurons release when they are communicating with one another. Importantly they form a protective barrier between the brain and the blood, keeping the brain safe.

All our cells, including neurons and astrocytes need to be able to react to a changing environment. To do this they need to send instructions to both themselves and to other cells. These instructions are bundles of genetic information and are known as RNA. 

Previous research from Dr Woodling’s group has suggested that astrocytes are very vulnerable to ageing. Could this be part of the reason that age is such a major risk factor for dementia?

What does this project involve?

Dr Woodling will use fruit flies to look at the effect of toxic amyloid on the brain and on astrocytes. Though the brains of fruit flies are many times smaller and very different from ours, fruit flies can be a useful way to study the effects of amyloid protein, a key hall mark of Alzheimer's. 

Dr Woodling will look at the RNA produce by astrocytes in the brains of fruit flies that have toxic amyloid. They will compare this with information that other researchers have uncovered about the response of the brain to toxic amyloid.

By carefully increasing or decreasing RNA made by astrocytes Dr Woodling will be able to uncover which RNA instructions can help the fruit fly brain function better despite the presence of toxic amyloid and so increase the lifespan of the fly. The RNA that works best will be taken further into future research studies.

How will this help people living with dementia?

This research will reveal new genetic targets that could be targeted by drug treatments to protect against dementia. All going well, a new treatment of this kind would take several years to get through clinical trials.

This project will help to shed light on a little understood area of research and offers inspiration to other researchers and hope for people affected by dementia in the future.