• Pre-Collegiate Global Health Review

The Possible Prevention of Alzheimer’s Disease in Developing Countries

By Avisha Garg, Heritage High School & Academies of Loudoun, Leesburg, Virginia, USA

The most common form of dementia, Alzheimer's Disease (AD), is ranked as the third leading cause of death in elderly people living in the United States (NIH National Institute on Aging (NIA), 2019). With no treatment or prevention of this progressive, neurodegenerative disease, millions of people worldwide will continue to succumb to the cognitive defects and life-threatening effects of AD (National Library of Medicine, 2021).

Figure 1. Age-standardized prevalence (per 100,000) for Alzheimer’s Disease and other dementias by location (The Lancet Neurology, 2016).

AD is a type of dementia that is caused by the loss of cholinergic neurons and abnormal function of proteins in the brain, leading to neurofibrillary tangles within the brain. The loss of neurons leads to a 40-90% depletion of acetylcholine (ACh), a neurotransmitter that plays a major role in cognitive and motor functions. A decrease of acetylcholine in the brain causes major issues with memory and information processing, leading to AD. Currently, a cure for AD and similar dementias has not yet been discovered (Ferreira-Vieira, Guimaraes, Silva, & Ribeiro, 2016). Because of its interesting drug potential, acetylcholine serves as a pathway to a promising prevention or treatment of AD.

AD is a growing global concern in developing countries. The primary increase of people living with AD and other dementias is predicted to take place in low income and middle-income countries (NIH, 2012). A preventative or cure for this neurodegenerative disease is thus crucial as the world’s population continues to age.

When a patient is diagnosed with AD, they are given inhibitors to decrease the breakdown of acetylcholine, keeping more of it active in neuronal synapses. Commonly prescribed examples include Donepezil, Galantamine, and Rivastigmine (Alzheimer's Association, 2021). Research has shown that using such inhibitors to treat AD shows moderate effects on improving cognitive deficits and slowing neurodegeneration in patients (NIH, 2009). Galantamine, a widely used acetylcholinesterase inhibitor, showed a positive cognitive effect on 14 percent of 100 patients using this drug. Although this is a significant number of patients with improvements, a more permanent and reliable treatment is much needed.

The lack of acetylcholine could be prevented or reversed by the consumption of its precursor, choline. Dietary choline combines with acetyl-coA through an enzymatic reaction, creating acetylcholine. Choline is typically highly accessible; most people consume this vital nutrient on a daily basis in foods such as egg yolks, peanuts, dairy products, and fish (Publishing, 2012). Choline supplements are also available for those without access to natural sources. The recommended daily intake (RDI) of choline is 550 mg for adult men and 425 mg for adult women, yet in 2013-2014, it was found that the American average daily intake 402 mg and 278 mg, respectively (NIH, 2021). These results show that many Americans are not meeting the RDI of choline, therefore making those with pre-existing risk factors to AD more susceptible to the disorder.

Educating people about the possible preventative measure of incorporating choline into daily diets should become a global health priority. Many developing countries have high rates of poverty and a healthcare system that is not prepared for an increase in dementia cases (NIH, 2012). If this neurocognitive disease can be easily prevented by the citizens of these countries, they should be informed about recommended measures as early as possible to ensure partial protection from AD. Additionally, there are options for people with a hereditary history of AD to determine whether or not they possess the APOE-e4 gene, which would increase their risk of developing AD (NIH National Institute on Aging (NIA), 2019). Genetic testing may not be available in most low-income countries, but if made accessible in countries with a predicted growth of AD cases, those who test positive for this gene could take extra precautions to decrease their chances of developing AD. Throughout the globe, all people should be encouraged to take preventive measures for AD for their cognitive well-being and to avoid its other associated challenges.

However, rigorous research and clinical trials will need to be conducted before reassuring patients that their risk of AD would be lowered by consuming choline. AD is also attributed to causes besides a depletion of the chemical acetylcholine, including vascular damage, inflammation in the brain, and atrophy of certain parts of the brain. While it has been shown that dietary choline increases levels of acetylcholine, it has not been proven that an increase of acetylcholine completely prevents or treats AD. Educating people across the world about this simple way to possibly prevent AD is a priority. The prevention of Alzheimer’s Disease is far overdue, and this simple way to reverse and stop the effects done by early onset AD could affect millions of lives globally.


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