Amyloid proteins in the brain have long been implicated as the culprit behind Alzheimer's disease. Amyloid are insoluble protein aggregates that arise from inappropriately folded proteins and polypeptides. These form tangles or plaques. They have been associated in the pathology of more than 20 serious neurodegenerative disorders, including Alzheimer's disease. They’re thought to disrupt the seamless workings of the neurons responsible for memory and movement.
Recent studies in the US and in Australia, have however found that amyloid may not be as destructive as previously thought.
Two recent US studies have found that amyloid proteins may in fact play a protective rather than a destructive role in the brain. The studies run by Professor Lawrence Steinman of Stanford University found that treating mice with multiple sclerosis (MS) with amyloid proteins reduced brain inflammation and reversed MS-related paralysis.
A second study extended the finding to show that small portions of several notorious amyloid-forming proteins (including tau and prion proteins) can also alleviate symptoms in mice with the condition — despite the fact that the fragments can and do form the long tendrils, or fibrils, previously thought harmful to nerve health. This supported previous research showing that Alzeimer's disease is much worse in animals born without the genes that produce amyloid.
He reported, "we were so fixated on the idea that amyloid is bad for the brain that if one goes back and looks at the old literature and the new literature, one finds there's a lot of publications where people have ignored these kinds of experiments in humans where, for instance, lower levels of amyloid are associated with earlier dementia".
In another recent Australian study run by Dr Bryce Vissel of the Garvan Institute of Medical Research, researchers have found that the amyloid plaques that are characteristic of Alzheimer's disease appear much later in the disease than previously thought, and after the development of cognitive symptoms. This indicates that neurodegenerative processes such as memory loss and executive dysfunction occur independently of amyloid plaques.
Instead it is proposed that inflammation in the brain is the leading cause of brain damage and neurodegeneration in Alzheimer's disease. Lawrence suggested that amyloid proteins may soak up harmful molecules that are responsible for inflammation.
The studies suggest that anti-amyloid therapies may not be the best way to manage the disease, and that therapies focusing on reducing inflammation may be more beneficial.