By Andrea Flores Esparza
Many of us have experienced memory loss in one way or another; forgetting where we left our keys or forgetting what we wanted to say. However, these do not seriously affect our every-day lives. Memory and cognitive thinking are controlled by the brain through the transmission of signals across neuronal synapses; when these begin to experience physical damage, the brain’s ability to perform these tasks weakens. Dementia is a chronic syndrome in which brain functions, such as memory and thinking skills, deteriorate over time prejudicing daily activities (NHS, 2018). According to the World Health Organisation (WHO), there are approximately 50 million people diagnosed with dementia from which 60-70% of those patients also suffer from Alzheimer’s disease (WHO, 2020). Alzheimer’s disease is a form of dementia that is characterised by the cause of neuronal cell death and/or its locality in the brain (Fillit, H. 2017). People suffering from Alzheimer’s disease experience brain damage that consequently affects their memory, thinking as well as behavioural skills. Although the majority of the cases of Alzheimer’s disease are elderly, it is not considered as a normal consequence of aging (WHO, 2020).
Alzheimer’s disease was first identified in 1906 after an autopsy conducted by Dr. Alois Alzheimer. He suggested that the patient had died from “an unusual mental illness” involving loss of cognitive thinking, memory and language (NIA, 2019). Even though the cause of Alzheimer’s is not yet established, scientists have discovered genetic, environmental, health and lifestyle factors that can influence the onset of the disease. Early-onsets are primarily linked to genetic mutations; however, research has discovered that late-onsets can be due to changes in the brain (NIA, 2019). According to Lisa Genova’s TED-Talk, “What you can do to prevent Alzheimer’s”, these alterations occur throughout decades without being noticed nor expressed in the individual’s behaviour. These changes eventually reach the “tipping point”, eliciting a cascade of molecular transformations that triggers clinical symptoms (Genova, L. 2017).
Scientists have discovered that the brains of Alzheimer’s patients contain abnormal amyloid plaques and neurofibrillary bundles of tau proteins (NIA, 2019). In physiological conditions, the peptide known as beta-amyloid is secreted into the synapse alongside the neurotransmitter and is subsequently broken down by microglia. However, for unknown reasons, beta-amyloid begins to accumulate in the synaptic cleft forming sticky aggregates known as amyloid plaques that eventually degrade the synapse (Genova, L. 2017). Moreover, the physiological role of tau proteins, predominately located in neurons, involves the stabilisation of the internal microtubules. Nonetheless, in patients with Alzheimer’s disease, these proteins become hyperphosphorylated as they are abnormally shaped and misfolded, forming tangled bundles causing the cellular damage of neurons (Ellison, M.J. 2019; Genova, L. 2019). These changes are first identified in the hippocampus, the centre for memory and learning (Fillit H., 2017). Neuronal cell death in this region of the brain causes patients to be unable to access their memory as signals cannot longer be transmitted, so instead of questioning themselves “where are my keys?” they will begin to question “what are keys used for?”.
Since Alzheimer’s disease is uncurable and irreversible once “the tipping point” of beta-amyloid and tau accumulation is reached, scientists have mainly focused on preventative medicine. The usual lifestyle factors of having a healthy diet, exercising and appropriate sleeping schedule have been shown to delay the onset of Alzheimer’s. However, the most amusing factor that has been revealed as the one of the most effective ways to prevent and/or delay Alzheimer’s is actually the constant acquisition of knowledge. Learning is involved with the cognitive reserve and neural plasticity of the brain, meaning that it creates and strengthens neuronal connections and thus prevent massive brain damage (Genova, L. 2017). In this manner, regardless of the presence of amyloid plaques and neurofibrillary bundles, highly intellectual individuals would buffer the effects of neuronal degeneration as they constantly form new synapses by learning new things.
Some studies have had promising results suggesting effective preventative behaviours, one of the most successful being the research study known as “The Nun Study” conducted by the University of Minnesota (1986-2009). This investigation involved 600 Catholic nuns over the age of 75 who dedicate their lives to prayer and education. As part of their religious mission, the nuns agreed to donate their brains to the University of Minnesota for research on Alzheimer’s. Prior to their death, the congregation to which these nuns belong to, known as the School Sisters of Notre Dame, provided the research team with the autobiographies the participants had written before joining when they were around 20 years of age (i.e. five decades before). This study found that some nuns who, despite sharing the brain morphology of someone who would have suffered from Alzheimer’s, did not experience any symptoms while they were alive. Furthermore, they also discovered a negative correlation between the extensive vocabulary used in the nuns’ autobiography and their brain damage, nuns who had a more extensive vocabulary displayed the least brain damage. Other studies have also shown positive results, including the study from the University of California – Irvine in which mice were divided into groups that dictated whether they were given “learning sessions” discovered that mice that were allowed to learn experienced a delay in the formation of plaques and bundles in their neurons (University of California – Irvine, 2007).
Though there is still a lot to discover with regards to neuronal diseases such as Alzheimer’s, these innovative discoveries may lead the way for preventative medicine and/or therapy for patients who are susceptible of developing this chronic disease. The fact that constant learning takes part in the formation of new synapses as well as the strengthening of pre-existing ones offers an applicable way to buffer the effects of Alzheimer’s as there is no treatment available besides medications that can aim to improve the livelihood of these patients.
References:
Ellison, M.J. Tau Protein and Alzheimer’s Disease: What’s the Connection? [Internet]. BrightFocus Foundation. May 2019. Available from: https://www.brightfocus.org/alzheimers-disease/article/tau-protein-and-alzheimers-disease-whats-connection. Accessed date: 28 September 2020.
Fillit H. Dementia & Alzheimer’s Disease: What’s the difference? [Internet]. Alzheimer’s Matters Blog. June 2020.Available from: https://www.alzdiscovery.org/news-room/blog/dementia-alzheimers-disease-whats-the-difference?gclid=Cj0KCQjwqrb7BRDlARIsACwGad79bcjltQsmxSVhwacPQt4eb-qlPLXnFYv9iViogCxKNyvg9vJzQv0aAr-VEALw_wcB. Accessed date: 25 September 2020.
Genova L. What you can do to prevent Alzheimer’s. United States: TED; 2017. https://www.ted.com/talks/lisa_genova_what_you_can_do_to_prevent_alzheimer_s/details?language=en. Accessed date: 28 September 2020.
National Health Services (NHS). Alzheimer’s disease [Internet]. NHS.uk. May 2018. Available from: https://www.nhs.uk/conditions/alzheimers-disease/#:~:text=Alzheimer’s%20disease%20is%20the%20most,skills%20and%20other%20mental%20abilities. Accessed date: 28 September 2020.
National Institute of Aging (NIA). Alzheimer’s Disease Fact Sheet [Internet]. National Institute of Health (NIH). May 2019. Available from: https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet#causes. Accessed date: 28 September 2020.
University of California – Irvine. “Learning Slows Physical Progression Of Alzheimer’s Disease.” ScienceDaily. ScienceDaily, January 2007. <www.sciencedaily.com/releases/2007/01/070123182024.htm>. Accessed date: 28 September 2020.
World Health Organisation (WHO). Dementia [Internet]. WHO.int. September 2020. Available from: https://www.who.int/news-room/fact-sheets/detail/dementia. Accessed date: 27 September 2020.
Imperial Bioscience Review 