This month we have been focusing on brain health. Alzheimer’s Disease (AD) in particular, is the most common form of dementia, and nearly 5.8 million Americans are living with the disease (CanoHealth). AD was discovered and named in 1906. From the beginning, scientists have noted that memory loss is accompanied by many other symptoms, including agitation, wandering, nighttime disturbances, and delusions. Initially, sedatives were prescribed to help people with AD sleep. Antidepressant and antipsychotic medications were also used to help keep difficult symptoms at bay (Fisher Center for Alzheimer’s Research).
Treatments have always focused on managing symptoms. AD is a complex disease and it seems unlikely that one drug will cure all those affected by the wide variety of symptoms. However, in recent years, scientists are a better understanding of AD, and how it progresses and focusing efforts on new research that targets the pathway of disease progression.
Today, the first step in treatment for AD is the prescription of cholinesterase inhibiting drugs. These drugs target chemicals in the brain, but scientists do not fully understand why they work to manage symptoms. This works at the beginning stages of diagnosis when symptoms are mild to moderate. They can be incredibly helpful for keeping seniors with AD independent longer and supporting caregivers. However, brain chemistry can only be altered for so long, and there will come a point when these drugs are no longer effective. This is why treatments that stop the progression of AD are the top priority for new research.
Until recently, we did not know what causes AD, besides the obvious death of neurons in the brain. It has now become clear, that the build-up of a protein plaque called amyloid is a clear disease mechanism for AD. In June 2021, the FDA provided accelerated approval for use of the drug Aducanumab, the only disease-modifying medication currently approved to treat AD. This drug is a monoclonal antibody that works by targeting and breaking down the amyloid protein. It is thought that if these plaques are removed, neurons will stop dying, and the patient’s memory, thinking, and confusion will stop worsening.
As we mentioned before, AD is an incredibly complicated disease, and nearly 30% of patients do not develop amyloid plaques in the early stages. For this reason, Aducanumbab can only be utilized after a patient has a PET scan to confirm the presence of the plaques. The drug is also very expensive and administered intravenously every four weeks for the duration of the patient’s life. While this is problematic, it is also the first drug that attacks the disease progression instead of simply masking symptoms. New research is focusing on drugs that can be administered by injections in the skin, and treat a wider variety of patients diagnosed with AD.