EXPERT REACTION: Different protein clumps for different 'types' of Alzheimer's

Alzheimer’s disease is a devastating condition that is characterised by loss of memory and ultimately more widespread issues and it is ultimately devastating. It is the second leading cause of death in Australia. The toll of this disease on the individuals affected, their families and their carers is substantial; additional to the huge economic burden of this disorder. There are no treatments that can slow or reverse this devastating condition and as a consequence it is urgent that solutions are found to help slow it down.

The cause of Alzheimer’s is largely unknown, and much attention has focused on clumps that are found in the brains of sufferers, called plaques. These plaques are made up of a substance called amyloid-beta peptide. More recently, there has been interest in substances found in the Alzheimer’s brain called amyloid fibrils. The study by Robert Tycko, John Collinge and colleagues, just published in Nature, suggests that variations in the structure of amyloid-beta peptide deposits that develop in the brain tissue of patients with Alzheimer's disease are associated with different clinical subtypes of the disease. The authors show that a single specific structure is dominant in samples from patients with either typical Alzheimer’s disease or the posterior cortical atrophy form, which is associated with disruptions of visual processing, whereas samples from patients with the rapidly progressive disease, in which disease progression occurs within months, display a range of different fibril structures. The findings can be taken to support one hypothesis of Alzheimer's disease: that different clinical subtypes might be associated with different amyloid-beta fibril structures.
 
However this study does not prove that plaques or amyloid cause Alzheimer’s disease. It is still possible that amyloid is a marker of disease rather than the unique cause. Recent clinical studies that have trialled drugs that remove amyloid have not shown the promise that has been hoped for, although other trials are in progress. For this and a host of other reasons, the role of amyloid fibrils and plaques in causing the disease remains unclear, and currently there are a number of alternative views of what may cause the disorder, including substantial evidence for a role of inflammation. Therefore there are numerous important studies progressing around the world to identify a range of alternative routes to treating this disease. I remain optimistic that a treatment will be found that slows the disease in the foreseeable future.
 
And it is urgent that cures are found.  There are more than 353,800 Australians living with dementia and 46.8 million worldwide. Without a medical breakthrough, the number of people with dementia in Australia is expected to be almost 900,000 by 2050.