Breakthrough findings have unveiled new targets and biomarkers for novel therapies for Alzheimer’s Disease treatment – supporting a new understanding of the mechanism behind Alzheimer’s disease.
The study has suggested that amyloid beta deposits, long known to build up in the brains of Alzheimer’s patients, act as a scaffold for the accumulation of other proteins.
Because many of these proteins have known signalling functions, their presence around the amyloid accumulations, known as plaques, could be the culprit causing brain cell damage rather than the amyloid itself.
The findings from Emory University have been published in Cell Reports Medicine.
Challenging existing theories about the origins of Alzheimer’s
The team, led by researchers at the Goizueta Brain Health Institute has found strong evidence supporting a new understanding of the mechanism behind Alzheimer’s disease.
In the brains of those who suffer from Alzheimer’s, amyloids accumulate and build up into sticky plaque that disrupts brain functions and causes cognitive decline, however, it is unknown exactly how that occurs.
According to the most widely adopted hypothesis, the amyloid beta buildup disrupts cell-to-cell communication and activates immune cells in a process that eventually destroys brain cells.
In the study, Golde, director of the Emory Center for Neurodegenerative Disease in the Goizueta Institute, Levites, associate professor in Emory University’s School of Medicine, and their colleagues presented a new hypothesis, emphasising a different role for amyloid beta, a simple protein that forms in all brains but normally dissolves out by natural processes.
In experiments, the team identified more than 20 proteins that co-accumulate with amyloid beta in both the human brains with Alzheimer’s and the mice, and suspect they will find more as the research continues.
“Once we identified these new proteins, we wanted to know whether they were merely markers of Alzheimer’s or if they could actually alter the disease’s deadly pathology,” says Golde.
“To answer that, we focused on two proteins, midkine and pleiotrophin.
“Our research showed they accelerated amyloid aggregation both in the test tube and in mice. In other words, these additional proteins may play an important role in the process that leads to brain damage rather than the amyloid itself.
“This suggests they might be a basis for new therapies for this terrible brain affliction that’s been frustratingly resistant to treatment over the years.”
Multiple kinds of amyloid build up, besides amyloid beta, have been implicated in more than 30 human disorders affecting tissues and organs throughout the body.
This new research proposes a novel process by which Alzheimer’s develops, potentially allowing for fresh approaches to discovering treatment targets for other diseases as well.
