The amyloid-beta protein begins to form clumps in Alzheimer’s disease
“The study focused on the amyloid-beta protein in Alzheimer’s disease, but the new antibody design could be used to other disease-causing clumps as well. In the long run, we hope that the new format will open up new avenues for the development of future treatments, not only for Alzheimer’s disease, but also for other diseases in which proteins begin to aggregate, such as Parkinson’s disease “Fadi Rofo, a doctoral student and the study’s first author, agrees.
Alzheimer’s disease (AD) is responsible for 60–70% of dementia cases. Given the severity of the disease and the growing number of patients, researching effective treatments for Alzheimer’s disease has become a top priority. Currently available medications for Alzheimer’s disease treatment, such as cholinesterase inhibitors and an antagonist of the N-methyl-D-aspartate receptor, can only temporarily reduce dementia symptoms but not stop or reverse disease development. Many multinational drug companies have done numerous clinical trials on amyloid clearance therapy based on the amyloid hypothesis, but none have been successful.
The problem with the current therapy techniques being explored in patient research is that antibodies attach to large clumps considerably more strongly than small clumps. Small clumps are equally as hazardous as huge ones, and many people believe they are even more deadly since they can move around more. The goal of this research was to create an antibody that could attach to both big and small amyloid-beta clumps. Antibodies bind tightly to their targets thanks to the avidity effect. This necessitates the simultaneous binding of both arms of the antibody to the same target.The researchers have created a new antibody structure with shorter distances between the arms so that it may attach to smaller aggregates, according to the current study. The new format also includes more binding sites to increase the strength of the connection.