The Comprehensive Clinical Trials Unit at UCL



DESPIAD: Depletion of Serum Amyloid P Component In Alzheimer’s Disease

4 November 2020

Alzheimer’s disease (AD) is the most common cause of dementia, affecting around 30 million individuals worldwide. It is caused by the abnormal build-up of various proteins in the brain to form what are known as amyloid plaques. The plaques are toxic to brain cells, and eventually cause their death, leading to the gradual decline in day-to-day memory and other mental functions.

Serum amyloid P component (SAP) is a normal protein that occurs in everyone. It is produced in the liver and travels via the blood stream to reach other organs including the brain. Although only very small amounts of SAP enter the brain, it binds to the abnormal proteins in the brains of patients with AD.

It forms part of the amyloid plaques and prevents them from breaking down. Therefore, preventing SAP from binding amyloid plaques may lead to faster breakdown of the amyloid plaques and so delay the progression of Alzheimer’s disease. There is also evidence that SAP directly damages brain cells and may contribute to the development of Alzheimer’s disease.

Removal of SAP may reduce this damage to brain cells. A new drug has been developed, called Miridesap, which eliminates SAP almost completely from the blood and thereby stops SAP from reaching the brain. Miridesap may also remove the SAP already present in the brain. This may reduce the brain damage caused by the disease.

The aim of this study is to explore the safety, tolerability and potential effectiveness of Miridesap in patients with mild AD

Trial status: Ongoing. Open for recruitment.
Funder: National Institute for Health Research
Sponsor: University College London