June 24, 2024

Claire Story

11th Grade

Dominican Academy

Alzheimer’s disease is, unfortunately, a common yet destructive neurological disease. This disease destroys the memory and cognitive skills of affected individuals, leading to memory loss, behavioral changes, trouble completing simple tasks, and getting lost easily. It is mainly caused by amyloid plaques, neurofibrillary tangles, and misconnected neurons in the brain. Diagnosing Alzheimer’s consists of preliminary cognitive tests, such as a Mini-Mental State Examination (MMSE), and interviews with family members; the next steps in the diagnosis include extensive neuro-imaging and fluid-based examinations. Alzheimer’s can be early-onset, occurring in a person’s thirties to sixties, or late-onset, starting in a person’s mid-sixties. Depending on age, an individual may live anywhere from three to ten years after diagnosis. Because of this and the severe symptoms associated with Alzheimer’s, this disease is incredibly emotionally taxing on both affected individuals as well as their loved ones. Based on an estimate from 2021, six million Americans ages 65 and above will be diagnosed with Alzheimer’s. Although it is the most common cause of dementia, there is a distinction between the two: dementia is a general word for deteriorating cognitive skills that interfere with daily tasks while Alzheimer’s is a specific disease causing dementia that gets worse over time. Sometimes, healthcare providers do not recognize that dementia has other causes that lead to costly mistreatment of patients. It is crucial to properly diagnose the causes of disease, and when the diagnosis is Alzheimer’s disease, specific treatments aimed at the underlying cause are possible.

Lecanemab is the newest discovery in potential Alzheimer's treatments. According to David Knopman and Linda Hershey in their Neurology issue, lecanemab works “against a pathological sequence variant within the amyloid sequence in APP (amyloid precursor protein) that binds to soluble amyloid protofibrils” (613). It is an anti-amyloid monoclonal antibody (AAMA) that works differently from current therapeutic drugs, which temporarily improve symptoms but are far from curing the underlying disease. A study by the New England Journal of Medicine consisted of an 18-month phase 3 trial. Of the 1795 participants, 898 received lecanemab while 897 received a placebo. After eighteen months of bi-weekly IV infusions, the participants who received lecanemab were shown to have lesser amounts of amyloid in their brains. According to David Knopman and Linda Hershey in their Neurology piece, the new drug “delayed cognitive and functional worsening by approximately 5 months in an 18-month double-blind, placebo-controlled trial” (610). The change in CDR-SB score was also lower when using lecanemab, displaying the observable benefits of the drug. Because of these successes, the United States Food and Drug Association (FDA), declared an accelerated approval of lecanemab on January 6, 2023. However, lecanemab is still far from a perfect solution

Lecanemab has presented logistical, financial, and clinical issues. First, the majority of Alzheimer’s patients are not eligible for the treatment; only about eight percent may receive the drug and it can only be administered to patients in the severity range of the participants in the trial. Even if a patient is eligible, they still must come to terms with the heavy financial burden of the treatment. Lecanemab, on its own, costs $26,500 each year, approximately $14.50 daily. According to Rita Rubin, MA, it also requires “every-other-week infusions plus multiple magnetic resonance imaging (MRI) scans” (E2), further adding to the cost. In addition, not enough healthcare providers have enough experience or knowledge of how to administer the drug, or even determine the severity of the disease, to face the significant number of affected patients. The patient’s region may also come into play, leading to more obstacles for Black individuals when seeking AAMA therapy.

Furthermore, if financial and logistical issues were not detrimental factors already, according to Stephen Nadeau in his Neurology issue, the “use of several amyloid monoclonal antibodies…has been associated with progressive loss of cerebral and hippocampal volume and ventricular enlargement” (2). In addition, in the clinical trial, there was an overall 21.5 percent risk of bleeding or inflammation in the brain on MRI scans, collectively known as Amyloid-related Imaging Abnormalities (ARIA). The implications of these findings still need to be explored.

Overall, lecanemab is a promising yet uncertain pathway to new preventative measures for Alzheimer’s disease. Perhaps treating patients before they develop signs of dementia will become a future strategy. Although the phase 3 trial was successful and resulted in approval by the FDA, many questions remain as to its optimal use. As for now, it is most important to properly diagnose the disease before administering any form of treatment. For those eligible and able to obtain the treatment, lecanemab may be an effective measure in lessening the effects of Alzheimer’s. It is encouraging to discover a cure for such a heartbreaking disease and, of course, hopeful that an all-encompassing solution is soon found.