High cholesterol may be linked to dementia, new research suggests.
Cholesterol in the brain speeds up the formation of protein plaques that have previously been associated with Alzheimer’s disease by 20 times, a study by Cambridge University found today.
As The Daily Mail reports, researchers believe their findings may pave the way for new Alzheimer’s treatments that target these toxic protein clusters.
It is unclear whether such cholesterol comes from dietary sources, such as processed foods, with previous research suggesting this form of the fatty substance cannot enter the brain.
The researchers believe certain people may have a gene that leads to the development of cholesterol in the brain.
Around 850,000 people in the UK have dementia, of which approximately 62 per cent suffer from Alzheimer’s.
The Cambridge researchers, along with scientists from Lund University, Sweden, found that when cell membranes are exposed to cholesterol in the lab it triggers the clumping of the Alzheimer’s protein, which is known as amyloid-beta.
Amyloid-beta, which is normally present in very small amounts in the brain, attaches to cholesterol-containing lipid molecules.
Once attached to these lipid molecules, which are sticky, amyloid-beta is more likely to clump together and cause protein aggregates.
Before attaching to lipid molecules, amyloid-beta is carried around by proteins such as ApoE, which has previously been linked to Alzheimer’s.
ApoE becomes less effective as people age, therefore the researchers believe maintaining this protein’s function may prevent dementia.
Lead author Professor Michele Vendruscolo, from Cambridge University, said: ‘The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol’s role in Alzheimer’s disease through the regulation of its interaction with amyloid-beta.
‘We’re not saying that cholesterol is the only trigger for the aggregation process, but it’s certainly one of them.
‘We now need to understand in more detail how the balance of cholesterol is maintained in the brain in order to find ways to inactivate a trigger of amyloid-beta aggregation.’
The findings were published in the journal Nature Chemistry.
