Despite many promising leads, new treatments for Alzheimer’s are slow to emerge. Current Alzheimer’s treatments temporarily improve symptoms of memory loss and problems with thinking and reasoning.
These Alzheimer’s treatments boost the performance of chemicals in the brain that carry information from one brain cell to another. They include cholinesterase inhibitors and the medicine memantine (Namenda). However, these treatments don’t stop the underlying decline and death of brain cells. As more cells die, Alzheimer’s disease continues to progress.
Experts are cautious but hopeful about developing treatments that can stop or delay the progression of Alzheimer’s. Experts continue to better understand how the disease changes the brain. This has led to the research of potential Alzheimer’s treatments that may affect the disease process.
Future Alzheimer’s treatments may include a combination of medicines. This is similar to treatments for many cancers or HIV/AIDS that include more than one medicine.
These are some of the strategies currently being studied.
Taking aim at plaques
Some of the new Alzheimer’s treatments target clumps of the protein beta-amyloid, known as plaques, in the brain. Plaques are a characteristic sign of Alzheimer’s disease.
Strategies aimed at beta-amyloid include:
Recruiting the immune system. Medicines known as monoclonal antibodies may prevent beta-amyloid from clumping into plaques. They may also remove beta-amyloid plaques that have formed. They do this by helping the body clear them from the brain. These medicines mimic the antibodies your body naturally produces as part of your immune system’s response to foreign invaders or vaccines.
The U.S. Food and Drug Administration (FDA) has approved lecanemab (Leqembi) and donanemab (Kisunla) for people with mild Alzheimer’s disease and mild cognitive impairment due to Alzheimer’s disease.
Clinical trials found that the medicines slowed declines in thinking and functioning in people with early Alzheimer’s disease. The medicines prevent amyloid plaques in the brain from clumping.
Lecanemab is given as an IV infusion every two weeks. Your care team likely will watch for side effects and ask you or your caregiver how your body reacts to the drug. Side effects of lecanemab include infusion-related reactions such as fever, flu-like symptoms, nausea, vomiting, dizziness, changes in heart rate and shortness of breath.
Donanemab is given as an IV infusion every four weeks. Side effects of the medicine may include flu-like symptoms, nausea, vomiting, headache and changes in blood pressure. Rarely, donanemab can cause a life-threatening allergic reaction and swelling.
Also, people taking lecanemab or donanemab may have swelling in the brain or may get small bleeds in the brain. Rarely, brain swelling can be serious enough to cause seizures and other symptoms. Also in rare instances, bleeding in the brain can cause death. The FDA recommends getting a brain MRI before starting treatment. The FDA also recommends periodic brain MRIs during treatment for symptoms of brain swelling or bleeding.
People who carry a certain form of a gene known as APOE e4 appear to have a higher risk of these serious complications. The FDA recommends testing for this gene before starting treatment.
If you take a blood thinner or have other risk factors for brain bleeding, talk to your healthcare professional before taking lecanemab or donanemab. Blood-thinning medicines may increase the risk of bleeds in the brain.
More research is being done on the potential risks of taking lecanemab and donanemab. Other research is looking at how effective the medicines may be for people at risk of Alzheimer’s disease, including people who have a first-degree relative, such as a parent or sibling, with the disease.
The monoclonal antibody solanezumab did not show benefits for individuals with preclinical, mild or moderate Alzheimer’s disease. Solanezumab did not lower beta-amyloid in the brain, which may be why it wasn’t effective.
Preventing destruction. A medicine initially developed as a possible cancer treatment — saracatinib — is now being tested in Alzheimer’s disease.
In mice, saracatinib turned off a protein that allowed synapses to start working again. Synapses are the tiny spaces between brain cells through which the cells communicate. The animals in the study experienced a reversal of some memory loss. Human trials for saracatinib as a possible Alzheimer’s treatment are now underway.
Production blockers. These therapies may reduce the amount of beta-amyloid formed in the brain. Research has shown that beta-amyloid is produced from a “parent protein” in two steps performed by different enzymes.
Several experimental medicines aim to block the activity of these enzymes. They’re known as beta- and gamma-secretase inhibitors. Recent studies showed that the beta-secretase inhibitors did not slow cognitive decline. They also were associated with significant side effects in those with mild or moderate Alzheimer’s. This has decreased enthusiasm for the medicines.
Edited By Zanda Hilger, LPC, Founder, Family Caregiver & Program Manager for Family Caregivers Online
We hope this information is helpful to you in the important work you do as a family caregiver.
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