Evolutionary Perspectives On Alzheimer's Disease

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Meiyu Liu Evolutionary Medicine Professor Omar Cornejo Feb. 26th, 2024 Evolutionary Perspectives on Alzheimer’s Disease (AD) Introduction Alzheimer’s disease is a brain disorder that slowly destroys memory and thinking skills and the ability to carry out the simplest tasks. In the most common cases, the symptoms first appear in the patients’ mid-60s, which is considered the late-onset type. In very rare cases of early-onset type, the symptoms occur between a person’s 30s and mid-60s. This disease is named after the German doctor Alois Alzheimer. In 1901, a 51-year-old woman named Auguste Deter was sent to the Frankfurt Mental Hospital, where Dr. Alzheimer worked after her husband noticed her uncontrollable behaviors. In the beginning, she accused …show more content…
Dr. Alzheimer diagnosed this case as ‘presenile dementia’. In 1905, Auguste deteriorated in condition; she could not get out of bed by herself and was unable to do any daily activities including eating. In 1906, she lost all cognitive ability and died because of septicemia and pneumonia, aged 55 years old. Dr. Alzheimer conducted a biopsy of her brain immediately afterward and found many abnormal clumps and tangled bundles of fibers, which are still considered some of the main features of Alzheimer’s disease. One other feature is the loss of connections between nerve cells in the brain. Recently, scientists have found that evolution-caused gene changes in the human genus have made certain neurons in the brain more accepting of factors that trigger Alzheimer’s disease (AD). These changes include myelin breakdown, neuronal oxidative stress, epigenetic changes in the promoter region of genes related to synaptic plasticity, increased expression of genes related to synaptic activity and plasticity, and incomplete myelination [2][3]. This paper will focus on the mechanisms of Alzheimer’s disease and its evolutionary …show more content…
These proteins include but are not limited to beta-amyloid clumps into plaques between neurons and Tau accumulates in specific brain regions (neurofibrillary tangles) involved in memory. When the level of beta-amyloid reaches a tipping point, the tau proteins spread rapidly throughout the brain. Healthy neurons are internally supported by structures called microtubules, which help guide nutrients and molecules from the cell body to the axon and dendrites. Tau’s job is to bind and stabilize microtubules, but abnormal chemical changes in Alzheimer’s disease cause tau to detach from microtubules and stick to other tau molecules, forming tangles inside neurons, which block the transport system in neurons and harm the synaptic communication between neurons. The connection between networks of neurons may break down as the neurons get injured and stop working, which leads to the brain shrinking. At the final stage of Alzheimer’s disease, this process continues and causes a large amount of cell death and loss of brain
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