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  • Writer's pictureAriff Zaidi

Will you forget your loved ones?

Edited by Sanaya Narula.

What is your name?

Who is your first love?

Where did you first meet them?

I believe that most of you can swiftly answer these three seemingly simple questions. But believe it or not, some people even grapple with the first one, especially those diagnosed with dementia - the loss of cognitive functioning like thinking, remembering, and reasoning.¹ Alzheimer's is the most common cause of dementia, accounting for 60-80 % of the cases.²

Alzheimer's disease is quite well-known for its symptoms, but do we comprehend the horde of turbulent events inside the brain of an Alzheimer's patient? In this article, I will be discussing the emergence of Alzheimer’s from the cellular level and how it inflames to be fatal.

Alzheimer’s disease, a neurodegenerative disorder characterised by cognitive and behavioural impairment, is estimated to affect more than 44 million people worldwide.³ A neurodegenerative disease is a pathological condition that involves the progressive destruction of neurons.⁴ Other prominent neurodegenerative diseases include Parkinson's, Huntington's, and Amyotrophic lateral sclerosis (ALS). Until today, the aetiology (the causes of a disease or condition) of neurodegenerative diseases and their relentless progression is still unknown but scientists are concerned with the role of genetics and environmental factors in their causation.

Alzheimer's disease was named after Alois Alzheimer, a clinical psychiatrist and neuroanatomist credited with discovering the ailment. In 1906, he monitored one of his patients, a woman in her fifties, who was admitted to hospital due to her paranoia, progressive sleep and memory disturbance, aggression and confusion.⁵ After her death five years later, he took a specimen from her brain and reported distinctive plaques and neurofibrillary tangles in the brain histology, which are still believed to be the hallmarks of Alzheimer's disease.

The plaque deposits and neurofibrillary tangles are identified as beta-amyloid peptides and tau, a microtubule-binding protein. These two features are believed to induce the disintegration of brain structures.

The beta-amyloid peptides are derived from amyloid precursor protein (APP) which researchers suggest will help the migration of neurons in the brain during early development. Naturally, APP undergoes processing catalysed by enzymes to form smaller fragments of proteins. These fragments are soluble amyloid precursor protein (sAPP) and amyloid beta peptide.6 Studies have shown that sAPP might serve growth-promoting properties and aid the formation of neurons in the brain. It can also inhibit the function of specific proteins. On the other hand, beta-amyloid peptides are likely to be involved in neural plasticity (the ability of neurons to adapt). However, in Alzheimer’s patients, the APP gene mutates which causes the formation of longer and chemically stickier beta-amyloid peptides.⁶ They can cluster together just outside neurons to create neuritic plaque, causing neurological impulses to be disrupted. As a result, the neurons are unable to interact with one another. These plaques, when combined, will provoke inflammation and thereby damage surrounding neurons.

Unlike beta-amyloid peptides, which accumulate outside the neuron, tau proteins remain within the cell. Tau protein is originally a part of a cell's cytoskeleton. One function of the intracellular (inside of the cell) cytoskeleton is to transport cellular components from one part of the cell to another.⁷ Tau protein ensures that the cytoskeleton maintains its structure and does not disassemble. In Alzheimer's disease patients, the enzyme kinase is activated to transport a phosphate group to the tau protein. The hyperphosphorylated* tau protein subsequently changes shape. Eventually, tau protein stops supporting the cytoskeleton, and combines with other tau proteins to construct neurofibrillary tangles.⁸ Rupture of the cytoskeleton will impede the neurotransmission mechanisms of neurons. Tau protein aggregation is also thought to cause apoptosis or cell death.⁹ One thing about neurons is that they cannot regenerate when they die - it is a definite ride or die for them.

* Hyperphosphorylated refers to a biochemical with saturated phosphorylation sites due to addition of a maximum phosphate group to the substance.

As this process continues, the brain will eventually shrink. In actuality, our brain shrinks throughout healthy ageing, but it does not lose a substantial number of neurons. With Alzheimer's disease, the damage is extensive because many neurons cease to function. At first, a patient with Alzheimer's will experience brain atrophy (loss of neurons) in parts of the brain such as the entorhinal cortex and hippocampus.¹⁰ Because the hippocampus is essential for the formation of new memories, Alzheimer’s patients at this stage will develop short-term memory loss, an infamous trait of the disease. Then, it will affect the cerebral cortex, which is crucial for language, reasoning, and social behaviour. Eventually, the control centres governing heart rate and breathing are overpowered, resulting in death.

Since research regarding how Alzheimer’s arises in the first place is still ongoing, scientists are yet to establish definitive preventative measures for the condition. However, several studies have suggested a few ways to reduce the risk of getting Alzheimer’s.¹¹ First, we need to reduce the risk of getting cardiovascular disease. Numerous autopsy studies have shown that 80% of Alzheimer’s patients also have cardiovascular diseases, but the reason behind this is still unknown. To maintain your cardiovascular health, it is advisable to stop smoking, drink less alcohol, and exercise regularly in the form of moderate-intensity aerobic activities like brisk walking. It is also essential to be mentally active and have strong social connections. Experts have suggested that constant social and mental stimulation will form stronger neural connections in the brain. This can be achieved through activities like reading, trying new hobbies and even actively participating in volunteering activities.

In conclusion, although this disease was first discovered quite a long time ago, scientists are still hammering away to unravel the truths of this mysterious illness and the ultimate way to treat it. Future advances in brain imaging, neural network and pharmacology may reveal breakthroughs to better treat neurological disorders, but until then, please continue to support those who are now facing the illness. Be sure to support agencies like Alzheimer's Disease Foundation to help them promote public awareness. Those with Alzheimer's may forget their loved ones one day, but we should never forget them - the ones who held us in their memories until their last synapse!



  1. National Institute on Aging. (2021). What Is Dementia? Symptoms, Types, and Diagnosis. National Institute on Aging.

  2. Alzheimer's Association. (2022). What Is Alzheimer’s? Alzheimer’s Disease and Dementia; Alzheimer’s Association.


  4. Przedborski, S., Vila, M., & Jackson-Lewis, V. (2003). Series Introduction: Neurodegeneration: What is it and where are we? Journal of Clinical Investigation, 111(1), 3–10.

  5. Hippius, H., & Neundörfer, G. (2003). The discovery of Alzheimer’s disease. Dialogues in Clinical Neuroscience, 5(1), 101–108.

  6. APP gene: MedlinePlus Genetics. (2022, April 11).

  7. Lecture 16: Transport, Cytoskeleton, and Motors. (2019, February 6). Biology LibreTexts.

  8. Medeiros, R., Baglietto-Vargas, D., & LaFerla, F. M. (2010). The Role of Tau in Alzheimer’s Disease and Related Disorders. CNS Neuroscience & Therapeutics, 17(5), 514–524.

  9. Gendron, T. F., & Petrucelli, L. (2009). The role of tau in neurodegeneration. Molecular Neurodegeneration, 4(1), 13.

  10. What Happens to the Brain in Alzheimer's Disease? (2022, April 21). National Institute on Aging.

  11. NHS Choices. (2019). Prevention - alzheimer’s disease. NHS.

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