There is no getting around it – Alzheimer’s Disease is devastating. It affects the lives of not only those afflicted, but also their families and friends. And it’s not even one of those things that just weighs on the minds of those involved; it often becomes the center point in familial dynamics. Many times having a family member diagnosed with AD comes with months and years of assistance, planning for the future, and constant stress and worry. And this is for good reason – the disease affects the memory, thinking, and behavior of the patient, with the symptoms worsening over time. But recently, I have heard points being made that an AD diagnosis could possibly be something everyone experiences, whether they live long enough to develop it or not. Before discussing that, however, it’s important to understand what exactly goes wrong in the brains of AD patients.
Although the exact cause of AD has been extensively researched, it is still largely un
known. What has been examined is the connection to a faulty breakdown of amyloid precursor protein, or APP. APP is a single-pass transmembrane protein expressed at high levels in the brain that’s broken down into the AB oligomer (ABO) AB-40 by various enzymes. In a normal brain, APP is broken down into AB-42, a slightly larger ABO, about 5% of the time. . At low levels like this, AB-42 is cleared easily by the natural systems in the brain. However, in the brains of AD patients, APP is broken down into AB-42 about 40% of the time, which results in much higher levels of the larger oligomer. At these high concentrations, it begins to aggregate, which leads to the activation of the microglia in the brain. These microglia then destroy and remove cells in an attempt to clear the large AB-42 aggregations. This leads to neurodegeneration – a major factor in AD. Now, there are various other abnormal processes occurring in the brains of AD patients, but it is thought that the aggregation of large ABO’s in the brain could be the most significant.
So, does this eventually happen in everyone’s brain? Does everyone eventually begin to have AB-42 build up, microglia activation, subsequent neurodegeneration, and eventual memory loss and cognitive decline? Current research wo
uld suggest that the answer is no; however, I think it’s interesting to explore the possibility that the answer is actually yes. What if this process started with some people at an earlier age than others, or for some it doesn’t start until they would hypothetically turn 110 years old?
It’s a scary thought, that’s for sure. But it also raises a controversial question: should we continue funding AD research if everyone eventually gets it? Is there even a point? One side may say that the amount of money put into AD research is too high, and that even if we did find a “cure” for the disease, a different one would eventually take its place. Another side focuses on the severity of AD itself, how many people it affects, and how AD needs to be further studied. I, personally, take the second side. I think of the multitude of individuals and families that are affected by the specific effects of AD – memory loss and cognitive decline. Although I personally haven’t been affected by the disease, I cannot begin to imagine the toll it must take on those who have. To those backing the side that suggests researching AD is a waste, I can’t help but ask if there could possibly be a worse disease to take the place of AD. But, like many subjects in neuroscience, no clear-cut answer can be determined today. Therefore, the many scientists devoting their lives to trying to understand this disease should continue with their efforts, it is worth the research.
Alzheimer's Disease: A Disease Worth the Research
