Written by Natalie Tran and Edited by Kevin Liu
Alzheimer’s disease, the sixth leading cause of death in the United States, is a common neurological disease caused by the accumulation of plaque and “tangles” in the brain [1]. This disease, which leads to the gradual death of neurons, disrupts communication within individual parts of the brain. This can be likened to the flow of electricity–when one electrical post is unable to function, the flow of electricity is compromised. However, unlike a damaged electrical post, which severs electrical flow only in the area of impact, neuron death spreads and ultimately leads to the death of surrounding neurons. Gradually, Alzheimer’s disease manifests and results in adverse symptoms such as the inability to remember or perform basic tasks [2].
Currently, drugs help repress the symptoms of Alzheimer’s disease. One common type of treatment medication is a cholinesterase inhibitor. Neurons communicate with each other via “packets” of chemicals called neurotransmitters that code different messages. Acetylcholine is one such transmitter and its job is to code for memory. Since cholinesterase is an enzyme that breaks down acetylcholine, cholinesterase inhibitors stop the cholinesterase from doing its job and leave more acetylcholine for the neuron to accept [3]. Findings show that individuals on cholinesterase-inhibitor medication show minimal improvement in cognition and memory [4]. However, cholinesterase inhibitors can produce adverse effects such as nausea and anorexia, which are detrimental to the already-weak older patients [5].
However, a new discovery may revolutionize future treatment for individuals with Alzheimer’s disease: oligomannate. Derived from brown algae, oligomannate alleviates Alzheimer’s symptoms by targeting the gut instead of the brain. Within the gut is a microbiome of bacteria that affect our body’s production of certain amino acids. An imbalance of good and bad bacteria in the gut microbiome can increase the production of certain amino acids, which promote the rise of T Helper 1 Cells (Th1) [6]. The main role of Th1 cells is to protect the body from pathogens by promoting inflammation [7]. However, the excess of Th1 cells can lead to unnecessary inflammation, such as that of the nerve tissue, which then causes quicker progression of the disease. Oligomannate focuses on the initial step of this process: it helps balance the gut microbiome [6]. A balanced gut microbiome reduces the production of excess Th1 cells, leading to reduced neuroinflammation and slower and less severe manifestations of Alzheimer’s disease.
Overall, this new approach to Alzheimer’s treatment is unique because it is suggestive of the influence of the gut microbiome on wellness, and can slow the development of Alzheimer’s disease. Because this study has shown an unexpected correlation between the gut microbiome and brain function, it might encourage more detailed investigations on microbiomes present elsewhere in the body, and their influences on other bodily systems. Furthermore, this study may act as a stepping stone to a healthier way of treating Alzheimer’s disease – a way that limits harmful side effects. Secondly, unlike cholinesterase inhibitors, which only mitigate the symptoms of Alzheimer’s, oligomannate wholistically reduces the cognitive regression of Alzheimer’s. Those participating in the study have shown improvements in cognitive abilities [6].
Although this study’s preliminary findings are revolutionary, more studies must be performed in order for the findings of this study to be implicated in the mainstream. The impact that oligomannate can have on future treatments is both, novel and profound.
References:
1. “Facts and Figures.” Alzheimer’s Disease and Dementia, www.alz.org/alzheimers-dementia/facts-figures.
2. “What Is Alzheimer’s Disease?” National Institute on Aging, U.S. Department of Health and Human Services, 16 May 2017, www.nia.nih.gov/health/what-alzheimers-disease.
3. “Drug Treatments for Alzheimer’s Disease Cholinesterase Inhibitors.” Dementia.org, 2018, www.dementia.org.au/files/helpsheets/Helpsheet-DementiaQandA01-CholinesteraseInhibitors_english.pdf.
4. “FDA-Approved Treatments for Alzheimer’s.” Alz.org, Aug. 2019, www.alz.org/media/documents/fda-approved-treatments-alzheimers-ts.pdf.
7. Romagnani S., (1999). Th1/Th2 cells., Inflammatory Bowel Discussion, 5: 285-294.