Can lithium protect against damage in Alzheimer's disease?

Lead Investigator: Dr Oyinkansola Adesakin
Institution: University College London
Grant type: Research Fellowship 
Duration: 3 years 
Amount:  £216,956
Scientific Title: Protection against Abeta toxicity by lithium: investigation of the role of non-canonical, wnt-mediated  changes in neuorgenesis 

What do we already know?

One of the hallmarks of Alzheimer's disease is the build-up of plaques of a protein called amyloid-beta. This, along with the build-up of tangles of another protein called tau, causes nerve cells (neurones) to die, which leads to the symptoms seen in Alzheimer's disease.

Producing new brain cells (neurogenesis) is vital for healthy brain function, especially in creating new memories, and this ability is impaired in Alzheimer's disease.

Previously, a fruit-fly 'model' of Alzheimer's disease, which develops the amyloid-beta plaques, has been used to study the effects of amyloid in the brain. In this model, the amyloid has been shown to affect the flies' behaviour and survival. It has been shown that when these flies are given the drug lithium, their survival and behaviour is improved. Lithium is known to be important in neurogenesis.

What does this project involve?

This project will investigate if the effects seen in the fruit-fly model of Alzheimer's disease as a result of lithium are because of neurogenesis, or if there are other reasons for the improvements. The researchers will investigate if the lithium prevents amyloid-beta from being toxic to newly formed cells, and will also investigate the route by which lithium alters the toxicity of amyloid-beta.

This project will use both the fruit-fly model of Alzheimer's disease to investigate the effects of lithium within a living brain, and will also use human nerve cells grown within the laboratory to understand how the specific neurones found in a region of the brain commonly affected in Alzheimer's are altered.

How will this benefit people with dementia?

Understanding how lithium interacts with amyloid-beta to prevent it from being toxic to neurones would help researchers to better understand that causes of Alzheimer's disease, and would pave the way for new treatments.