Quenching the Burning

Memories

A glimmer of hope for Alzheimer's patients

Written by: Amy Yao | Edited by: Miranda Huang | Graphic Design by: Dora Meiwes

It is estimated that more than 6 million people in the US have Alzheimer’s disease, the most common form of dementia. Given its prevalence, it's likely that many of us have family members who have been affected by it, or at least heard of someone who has. So what exactly is this disease, and what does recent research reveal about it? 

The most well-known symptom of Alzheimer's disease is memory loss. Although the impact in the beginning may be negligible, as time and the disease progresses, the memory loss begins to become more severe, and other symptoms also surface, such as difficulties with reasoning and decision-making. The disease may also affect the personality and behavior of the sufferer, sometimes resulting in mood swings, distrust of others, and aggression. People affected by Alzheimer's disease may eventually forget the names of family members and everyday objects, slowly regressing to the point of not being able to take care of themselves, at which point it falls to those around them to ensure their basic survival. 

But care for them is expensive–one source estimates that the total lifetime cost of care for a person living with dementia is nearly $400,000, a colossal number. Most devastatingly, there is no cure for Alzheimer's disease. Or is there? Alzheimer's is characterized by the appearance of abnormal lumps and tangles in the brain, scientifically known as amyloid plaques and neurofibrillary tangles. These structures eventually cause brain cells to die, thus disrupting the normal functioning of the brain. So, what if we remove the plaques and tangles before they build up to the point of the disease's onset? 

A recent paper, published in mid-March this year, has the answer. Researchers found that an experimental drug, known as gantenerumab, was able to reduce amyloid plaques in the brain. They conducted the study on a group of people who are "destined” to develop the disease at around 30-50 years of age, due to a rare, inherited genetic mutation that causes the excess production of amyloid in the brain, practically "guaranteeing" that plaques will begin to build up. It was found in a group of such participants that receiving the drug for an average of eight years lowered the risk of developing symptoms from around 100% to about 50%, a significant decrease. 

The genetic disease that affects the participants is known as Dominantly Inherited Alzheimer's Disease (DIAD). Although the mutation causing this condition is rare, occurring in less than 1% of all Alzheimer's disease cases, the pathological features of DIAD are close to the most common, sporadically occurring form of Alzheimer's disease, so it's likely that any discoveries made on DIAD could be applied to the more common forms of Alzheimer' as well. 

Of course, gantenerumab is not a miracle cure. The drug, although effective on one group of participants, had little effect on some other groups of participants who had either not been on the drug for as long or only started the drug after symptoms began to develop. This likely indicates that for the drug to be effective, any treated patients must begin taking it years before the onset, which may be infeasible because the onset of other forms of Alzheimer's disease may be hard to predict. In addition, gantenerumab has also caused some side effects, though none were life-threatening. 

Despite these limitations, there seems to be enough reason to be hopeful. With this study setting the precedent, other research is sure to follow, and we can expect the discovery of many more preventions and treatments for Alzheimer's disease. Perhaps one day, we will reach the point where those affected by this condition can live a normal and healthy lifespan like those without it, and this memory-destroying disease will become history. 

These articles are not intended to serve as medical advice. If you have specific medical concerns, please reach out to your provider.