Uploaded August 2024 | Updated September 2026, 2 weeks ago
The older you get the scarier the prospect of Alzheimer’s disease becomes because the one the one thing we know about this disease for sure is that it is age related. The cause of Alzheimer’s is not known, but the hallmark of the disease is the buildup of two different proteins in the brain, called beta-amyloid and tau. However, not everyone with Alzheimer’s has a buildup of these proteins and not everyone who has a buildup gets the disease. There are no truly effective treatments although donepezil (Aricept) provides a small benefit in mental function but does not alter the progression of the disease. Two recently approved drugs offer a glimmer of hope because they may slow the decline by destroying amyloid proteins.
Donanemab and lecanemab are “monoclonal antibodies” that are produced by injecting mice with amyloid proteins that then stimulate their immune system to generate a variety of B cells to produce a host of antibodies. Through a sequence of complex steps, the B cells that produce the desired antibody that recognizes the problematic proteins are isolated and “cloned” or copied. These then produce a large population of cells from which the monoclonal antibodies are harvested. They are called monoclonal because they derive only from one type of B cell. Donanemab is administered via intravenous infusion but lecanemab can be injected.
While the results of trials are statistically significant, they are less than spectacular. After 18 months of use, these monoclonals showed about a 30% slower rate of cognitive decline than a placebo. That translates to a 0.5 point difference on an 18 point cognitive scale. A minor difference.
Researchers are also working on a vaccine against Alzheimer’s that would stimulate the immune system to produce antibodies that would link to the amyloid and tau proteins and mark them for destruction by white blood cells. This is challenging because our bodies naturally produce amyloid and tau proteins so that the immune system does not recognize them as foreign. However, it turns out that it is when these proteins, long chains of amino acids, fold in an irregular fashion that they congregate to produce the amyloid plaques and neurofibrillary tangles that characterize Alzheimer’s disease. The task is to incorporate the appropriately folded proteins into a vaccine. A number of companies are working on such vaccines, but this is a long-term project.
The older you get the scarier the prospect of Alzheimer’s disease becomes because the one the one thing we know about this disease for sure is that it is age related. The cause of Alzheimer’s is not known, but the hallmark of the disease is the buildup of two different proteins in the brain, called beta-amyloid and tau. However, not everyone with Alzheimer’s has a buildup of these proteins and not everyone who has a buildup gets the disease. There are no truly effective treatments although donepezil (Aricept) provides a small benefit in mental function but does not alter the progression of the disease. Two recently approved drugs offer a glimmer of hope because they may slow the decline by destroying amyloid proteins.
Donanemab and lecanemab are “monoclonal antibodies” that are produced by injecting mice with amyloid proteins that then stimulate their immune system to generate a variety of B cells to produce a host of antibodies. Through a sequence of complex steps, the B cells that produce the desired antibody that recognizes the problematic proteins are isolated and “cloned” or copied. These then produce a large population of cells from which the monoclonal antibodies are harvested. They are called monoclonal because they derive only from one type of B cell. Donanemab is administered via intravenous infusion but lecanemab can be injected.
While the results of trials are statistically significant, they are less than spectacular. After 18 months of use, these monoclonals showed about a 30% slower rate of cognitive decline than a placebo. That translates to a 0.5 point difference on an 18 point cognitive scale. A minor difference.
Researchers are also working on a vaccine against Alzheimer’s that would stimulate the immune system to produce antibodies that would link to the amyloid and tau proteins and mark them for destruction by white blood cells. This is challenging because our bodies naturally produce amyloid and tau proteins so that the immune system does not recognize them as foreign. However, it turns out that it is when these proteins, long chains of amino acids, fold in an irregular fashion that they congregate to produce the amyloid plaques and neurofibrillary tangles that characterize Alzheimer’s disease. The task is to incorporate the appropriately folded proteins into a vaccine. A number of companies are working on such vaccines, but this is a long-term project.
