Carey Mulligan
Carey Mulligan said her grandmother was diagnosed with Alzheimer's 10 years ago (Reuters)

Actress Carey Mulligan has shared her family's experience of Alzheimer's as researchers announce they have pinpointed a trigger that causes the disease.

Mulligan, who stars as Daily Buchanan in the recently released Baz Lurhmann film The Great Gatsby, said her grandmother suffers from Alzheimer's and has not recognised her for around five years.

Supporting the Alzheimer's Society Dementia Awareness Week, Mulligan told Channel 4: "People need to be more aware in their daily lives of people who could be suffering from Alzheimer's.

"To be aware that somebody who can't count their change in a shop when they are trying to buy a newspaper is not someone being old and doddery. They might potentially be suffering from Alzheimer's and they might just need some help and assistance.

"I feel very confident and strongly that the work a lot of organisations are doing in terms of research could lead to us finding a cure or treatment for this that will work."

In what scientists believe is a breakthrough in Alzheimer's research, a team from the University of Cambridge has identified a catalytic trigger that causes the onset of the disease.

Alzheimer's begins when the fundamental structure of a protein molecule changes, which then causes a chain reaction that results in the death of neurons in the brain.

The team believes this find could lead to earlier diagnosis of diseases like Alzheimer's and Parkinson's and offers new opportunities in drug therapies.

magnified a million times, of amyloid fibril, the type of protein structures that are formed in Alzheimer’s
Magnified image of amyloid fibril, the type of protein structures that are formed in Alzheimer’s (Tuomas Knowles)

Explaining the process, the researchers said: "Protein molecules are made in cellular 'assembly lines' that join together chemical building blocks called amino acids in an order encoded in our DNA. New proteins emerge as long, thin chains that normally need to be folded into compact and intricate structures to carry out their biological function.

"Under some conditions, however, proteins can 'misfold' and snag surrounding normal proteins, which then tangle and stick together in clumps which build to masses, frequently millions, of malfunctioning molecules that shape themselves into unwieldy protein tendrils."

The abnormal structures are called amyloid fibrils, which cause protein deposits (plaques) in the brain and were once believed to cause Alzheimer's.

However, Chris Dobson and the team from Cambridge have since found this is not the case.

They found that once a small but "critical" level of abnormal protein clumps have formed, a chain reaction is triggered, which multiplies the number of protein composites and activates new focal points.

This secondary process results in juvenile tendrils that contain small and highly diffusible protein molecules called "toxic oligomers". These molecules move around the brain, kill neurons and ultimately cause loss of memory and other symptoms of Alzheimer's.

Researcher Tuomas Knowles said: "There are no disease modifying therapies for Alzheimer's and dementia at the moment, only limited treatment for symptoms. We have to solve what happens at the molecular level before we can progress and have real impac

"We've now established the pathway that shows how the toxic species that cause cell death, the oligomers, are formed. This is the key pathway to detect, target and intervene - the molecular catalyst that underlies the pathology."