With many twists, turns and controversies, getting to the bottom of Alzheimer's disease has been a rapidly evolving pursuit. In the latest crook in the research road, scientists have found a new insight into the interaction between proteins associated with the disease. The report, which appears in the journal ACS Chemical Neuroscience, could have important implications for developing novel treatments.
Witold K. Surewicz, Krzysztof Nieznanski and colleagues explain that for years, research has suggested a link between protein clumps, known as amyloid-beta plaques, in the brain and the development of Alzheimer's, a devastating condition expected to affect more than 10 million Americans by 2050.
But how they inflict their characteristic damage to nerve cells and memory is not fully understood. Recent studies have found that a so-called prion protein binds strongly to small aggregates of amyloid-beta peptides. But the details of how this attachment might contribute to disease — and approaches to treat it — are still up for debate. To resolve at least part of this controversy, Surewicz's team decided to take a closer look.
Contrary to previous studies, they found that the prion protein also attaches to large fibrillar clumps of amyloid-beta and do not break them down into smaller, more harmful pieces, as once thought. This finding bodes well for researchers investigating a novel approach to treating Alzheimer's — using prion-protein-based compounds to stop these smaller, toxic amyloid-beta pieces from forming, the authors conclude.