Alzheimer's Disease

What is alzheimer's disease?

Alzheimer's Disease is a neurological disorder that slowly destroys a person's memory and cognition. As Alzheimer's disease progresses, people lose their ability to perform everyday tasks, such as eating and walking. Firstly, Alzheimer's begins to destroy the connections between neurons in the hippocampus (which is responsible for forming new memories) and in the entorhinal cortex (which relays sensory information to the hippocampus to form new memories). Then, it systemically affects other regions of the cerebral cortex, such as Wernicke's area (which is responsible for understanding language), and the frontal lobe, which may cause changes in personality, worsened judgement, and executive dysfunction. Ultimately, people with Alzheimer's disease gradually lose their ability to live independently, until they lose their ability to live at all without the proper medical care, support, and management of complications after diagnosis. 

Causes

Alzheimer’s disease is caused by a combination of genetic, lifestyle, and environmental factors that affect the brain over time. While the causes of Alzheimer’s disease are not yet fully understood, researchers are currently focused on two related proteins — amyloid-beta and tau. Amyloid-beta is a fragment of a larger protein called amyloid precursor protein (APP), which sits in neuronal cell membranes. In the brains of people with Alzheimer’s disease, different enzymes cut APP, leading to amyloid-beta (Aβ) breaking off. Normally, the brain clears away amyloid beta as it’s made. However, aging and certain genes slow this process down, allowing amyloid-beta monomers to float around until they bump into each other, forming small clusters known as oligomers, which then bundle together to form amyloid plaques. Amyloid-beta oligomers stick to the surface of neurons and interfere with receptors, weakening the connection between neurons, making it harder to recall memories or learn new information. Tau proteins support and stabilize microtubules, which allow vital nutrients and chemical messages to travel throughout neurons. In Alzheimer’s, amyloid-beta triggers enzymes to overlay tau with phosphate groups, causing tau to become hyperphosphorylated (which means that too many phosphate groups are attached to it) and lose its shape. This reduces tau’s ability to bind to microtubules, causing microtubules to become unstable and disintegrate, starving certain parts of neurons from essential materials. The detached tau proteins then stick together, forming twisted fibers called neurofibrillary tangles (NFTs) inside neurons, which interfere with normal cellular processes. As transport fails and NFTs accumulate, neurons become dysfunctional and die, leading to memory loss and cognitive decline.

Symptoms

Due to its progressive nature, the early symptoms of Alzheimer's disease can easily be confused for normal signs of aging. The most characteristic symptom of Alzheimer's disease is memory loss that disrupts daily life. This commonly shows up as difficulty recalling recently learnt information, forgetting important dates and events, and increased reliance on others. As the posterior cortex (parietal and occipital loves) gets damaged in later stages, people may experience trouble understanding visual images and spatial relationships. This shows up in daily life as difficulty with reading, judging distance, and balance. Other symptoms include problems with maintaining a conversation, social withdrawal, decreased judgement, and changes to mood and personality caused by the deterioration of the frontal lobe. In late-stage Alzheimer's, individuals lose their ability to respond to external stimuli, communicate, or control their movement. They require assistance for basic tasks and can no longer function independently. The immune system also declines, leaving individuals with Alzheimer's more vulnerable to infections, particularly pneumonia.

Treatment

There is currently no known cure for Alzheimer's disease, but modern medicine has made advancements in treatment, such as disease-modifying therapies like Leqembi and Kisunla, which are IV infusions and prevent the clumping of amyloid plaques in the brain. Other Alzheimer's medicines include cholinesterase inhibitors, which work by inhibiting breakdown of acetylcholine, maintaining efficient communication between neurons and stabilizing cognitive symptoms. Cholinesterase inhibitors are taken orally and may also improve behavioral symptoms, such as depression. Individuals with Alzheimer's disease also benefit from non-pharmacological approaches, which may include environmental modifications, structured routines, memory aids, a nutritious diet, and hydration.

Conclusion

Alzheimer's disease is a devasting neurological condition that robs individuals of their memory, identity, and autonomy, while simultaneously robbing their families of the person they once loved. While there is currently no known cure for Alzheimer's, care, patience, and compassion go a long way towards making individuals with the disease feel safe and heard. Raising awareness for Alzheimer's disease and supporting advancements in research and treatment are some of the most powerful tools we currently have against this cruel condition. 

Bibliography