News | Thursday, 3rd September 2015

Post-stroke protein linked with dementia

Increased risk of Alzheimer’s disease following attack

The uptake of mCRP by brain neurons is seen here

A PROTEIN strongly linked with the increased risk of dementia in stroke patients could hold the key to developing an antibody.

Healthcare scientists at Manchester Metropolitan University have identified a protein that is released in large amounts following a stroke and has a direct influence on neurodegeneration.

It is known that patients who suffer a stroke are up to 12 times more likely to develop Alzheimer’s disease and researchers propose to block the monomeric C-reactive protein (mCRP) to stop its harmful post-stroke effects.

In their findings, published today in Scientific Reports, researchers outline how mCRP is laid down in the brain in large quantities through damaged blood vessels. They suggest that the protein could be involved in creating abnormal blood vessel development following a stroke and consequently play a pivotal role in causing dementia.


Professor Mark Slevin, Professor of Cell Pathology at Manchester Met, said: “The results are exciting because they show us a possible route to developing an antibody that would prevent the worst of stroke-related vascular dementia and Alzheimer’s disease. Within 10 years of a stroke, around 40 per cent of people develop dementia so the benefits could be huge.

“The protein appears to have a direct role in inducing haemorrhagic angiogenesis – blood vessel rupture – and directly inducing dementia. The exact mechanisms of how neurodegeneration is caused following a stroke is unknown. We know the protein is always present, floating in our circulation system, but we found that you get it in large quantities after a stroke.”

Using in-vitro tissue cultures, researchers demonstrated how the protein stimulates abnormal vessel production that is linked to neurodegenerative disease. Further tests showed that Alzheimer’s disease was present in mice which had been introduced to the protein.

The therapeutic hypothesis proposes to block the downstream effects of mCRP with an antibody, thereby nullifying its neurodegenerative effects.


Prof Slevin added: “We’re aiming to produce an antibody that would be delivered to the brain via the immune system that will either breakdown or bind to the mCRP as soon as possible after a stroke. It would be insoluble, possibly using nanotechnology as a delivery mechanism.”

Professor Slevin, who is also Director of Manchester Met’s Healthcare Research Centre, led the study with collaborators from Europe, USA and Saudi Arabia.



The paper, Monomeric C-reactive protein – a key molecule driving the development of Alzheimer’s disease associated with brain ischemia, was published in Scientific Reports on Thursday, September 3, 2015, and is available online:

For more information or to interview Prof Mark Slevin, contact Press Officer Chris Morris on 0161 247 2184 or email

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