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  • Writer's pictureEric Yoon

Early-Onset Alzheimer's- An Analysis

Updated: Oct 1, 2019

Early-Onset Alzheimer’s. The inexplicable feeling that your mind is missing something; something that guides your reality. It’s not that you’re a senior and simply suffering from old age- you’ve just turned 34, being the breadwinner to uphold a new family. Memory is supposed to deteriorate when you’re old, and yet you keep forgetting your keys. Keep yelling at your spouse for having said something they claim to have never said. Blanking on your children's name. This is Early-Onset Alzheimer’s disease: non-curable, progressive, and fatal to life.

Early-Onset Alzheimer’s, as fitting with its name, is a subset of Alzheimer’s disease that strikes those younger than 65. The five percent of Alzheimer’s patients that have it constitutes over 200,000 people, and they suffer from sustained memory loss and deteriorating cognitive function. A single cause of the disease is unknown, though a combination of genetic and environmental factors have been shown to give rise to the formation of Alzheimers. To be specific, Alzheimer’s disease destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior. Over time, the disease affects all parts of the brain.

The differences between Early-Onset Alzheimer’s and Late-Onset Alzheimer’s, though few, are important to note: for one, many cases of the early-onset form are caused by mutations in chromosomes 1, 14, or 21 of a person’s DNA. This leads to defects within proteins that are responsible for the breakdown of amyloid precursor protein (APP), allowing amyloid plaques to form and block communication between neurons. This is one of the defining characteristics of Alzheimer’s, and is shared among both forms; in Late-Onset Alzheimer’s, however, the formation of amyloid plaques is less clear due to latent activation in mutated genes. The Late-Onset type’s development is thus chalked to a mixture of genetic, environmental, and lifestyle factors. In both types of Alzheimer’s, amyloid plaques form between neurons and eventually kill the cells, leading to reduced brain function. Researchers have not found a specific gene that directly causes the late-onset form of the disease. However, one genetic risk factor—having one form of the apolipoprotein E (APOE) gene on chromosome 19—does increase a person's risk. APOE ε4 is the version of the gene that does increase risk for Alzheimer's and is also associated with an earlier age of disease onset; other forms of APOE play a neutral or even a beneficial role in delaying the start of Alzheimer's.

Another hallmark of Alzheimer’s are the emergence of neurofibrillary tangles, disrupting synaptic communication between neurons. These form from the dysfunction of tau, a protein responsible for the support of microtubules within the neurons to transport nutrients. For Alzheimer’s, tau fails to bind with the microtubules and instead binds to other tau, creating tangles that block the transport system and result in microtubule collapse, impeding upon normal function of the neurons.

On a macro scale, this leads to many symptoms of brain degradation like, as neurologist Adnan A. Awada reports, “memory loss, disorientation, language difficulties, visuospatial problems, apraxia… mood swings, delusions, hallucinations, [and] misbehavior.” It is key to note that there are differences between the symptoms of Early and Late Onset Alzheimer’s; in the same article, Awada states that “in the study of Toyota et al.,[1] behavioral and psychological symptoms were relatively fewer in EOAD than in LOAD, while there were no differences in cognitive functions or dementia severity between two groups. In the largest and most recent study from Korea,[4] apathy was more common in EOAD patients, while delusions were more prevalent in LOAD patients.”

What can be taken away from this? Like its parent disease, Early-onset Alzheimer’s is terrible and costly for anyone that develops it. It does not affect those under 30 years old (so teenagers are safe), but it still leaves individuals with a full life ahead of them with less time to indulge in their futures, even in comparison to normal Alzheimer’s. The characteristic difficulty in remembering events that just happened as well as the accompanying mood and personality changes grind not just on the person with Alzheimer’s but on friends and family as well.

When I researched the disease, I found myself thinking about how I take my life for granted and what it comes with. Perhaps this line of thought is pretentious, and is not exclusive to only Early-Onset Alzheimer’s, but the inevitable nature of the disease and how it slowly affects those who have it make it the quintessential topic to consider this. Not everyone is fortunate enough to be able to remember their best friend’s interests, what one does for work, and their own family members. Early-onset Alzheimer’s shows us that we don’t have the luxury of waiting later to do the things we want to do, and we can’t take for granted a wistful safety. Most of all, it shows that we can fight. Those with early-onset Alzheimer’s still battle to have a normal life with a career and family they support. If anything, that’s the reason for why this battle is worth continuing to the end.

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