The underlying causes of Alzheimer's disease are still mostly unknown, but significant research funding has gone into research for ways to prevent or halt disease progression. Estimates attribute roughly half of new dementia cases each year to Alzheimer's with prevalence ranging from 0.4% to 1.6% depending on which region of the world. However, in exciting new research findings from the Washington University School of Medicine, a team of scientist have shown that antibodies targeting the APOE protein can clear away the amyloid plaques building up in Alzheimer's patients. APOE plays an important role in transporting cholesterol and fats throughout the body and is found in blood as well as in the amyloid plaques. The most promising antibody, HAE-4, not only cuts the level of plaques in the brain in half, but has no impact on the APOE in blood, which has a different structure and whose removal would lead to undesirable side effects.
As with many neurodegenerative diseases, no Alzheimer's treatments exist that prevent onset or reverse disease progression. Patients are often left trying to manage symptoms. This development is an exciting step toward finding preventative therapy, but also highlights the need for early detection. Researchers are now planning further additional studies to determine safety and suitability for eventual clinical trials in humans and to explore other similar antibodies as well.
Plaques of a brain protein called amyloid beta are a characteristic sign of Alzheimer's disease. But nestled within the plaques are small amounts of another Alzheimer's protein: APOE. Now, researchers have shown that an antibody not only targets APOE for removal but sweeps away plaques in mice. The findings could lead to a way to halt the brain damage triggered by amyloid plaques while the disease is still in its early stages, perhaps before symptoms appear.