Like a bad seed that overtakes an entire garden, a single abnormal protein may spoil other proteins nearby and begin the progression of Alzheimer’s disease, a new study suggests.
Recent research has suggested that a protein called amyloid-beta is a likely culprit in causing the disease. Healthy brain cells produce this protein in small amounts and regularly clear away any excess. But in brains plagued by Alzheimer’s disease, the protein becomes misshapen and clumps, hindering its removal.
Though this clumping process has been well studied, scientists know little about what corrupts the protein and makes clumps spread across the brain. To investigate, Lary C. Walker of Emory University in Atlanta and his colleagues injected the brains of young mice with diluted samples of brain tissue from Alzheimer’s patients. The mice were of a type that’s genetically predisposed to develop a form of the disease.
Rather than develop amyloid-beta clumps after age 10 months, as brains of these mice typically do, the organs of the infected mice were ridden with clumps within 4 months.
A closer look suggested that the brain extracts from Alzheimer’s patients acted as amyloid-beta seeds, encouraging the growth of clumps around them. Normal amyloid-beta that came in close contact with these seeds appeared to have become similarly misshapen, multiplying and spreading the problem proteins. Mice injected with diluted brain tissue from a healthy elderly person or from healthy old mice didn’t develop the clumps more quickly than usual.
The researchers suggest in the Sept. 22 Science that misshapen amyloid-beta might arise spontaneously in people, spreading its corruption through contact with healthy protein. This process resembles the destructive interactions of other proteins called prions. If researchers can find a way to catch the bad amyloid-beta proteins early, says Walker, they might stop Alzheimer’s disease in its tracks.