Evaluation of the neuroprotective actions of adiponectin in dementia

Appropriate communication between brain cells determines how we think and behave. In Alzheimer’s disease (AD), communication between brain cells is impaired, resulting in memory deficits. AD-related memory deficits are linked to the build-up of a protein called tau, which ultimately inhibits communication between brain cells. Consequently, identifying agents that limit tau build-up and prevent its unwanted effects on brain cell communication is likely to be beneficial in AD. 

Adiponectin is a metabolic hormone secreted by fat cells that readily accesses the brain and can influence important brain functions. Recent studies suggest that adiponectin has therapeutic benefits as it reverses memory deficits in rodent models of AD. But the protective effects of adiponectin and its effects on tau build up, and brain cell communication are unclear. Here, we propose to address this key gap in our knowledge. We will assess the neuroprotective actions of adiponectin using various cellular and animal models that replicate the unwanted effects of tau protein that occur in AD. Additionally, we will evaluate the cell signalling pathways that are key to adiponectin’s protective actions. This will increase our understanding of the brain effects of adiponectin and provide valuable information on the therapeutic potential of adiponectin in AD.

Funded PhD Project (UK Students Only)

Cunningham Trust funded the project for 3 years.

Proposed Start date: September 2026.

Stipend: £23,000 for first year.