Alzheimer's has affected more than 3 million people in the United States alone, with the belief that it will only increase in the upcoming years. Alzheimer's is a neurodegenerative disease that worsens over times, causing dementia, language/behavioral problems, and disorientation. This disease needs much more research to be done in order to be understood. There is a possibility that the risk may be genetic, or associated with a history of depression. There is also an association with beta-amyloid plaques and tangles.
The buildup of A-beta plaque causes the destruction of synapses, which results in cognitive decline and memory loss. Researchers at Harvard Medical School and Massachusetts General Hospital have proposed the hypothesis that A-beta’s purpose is to protect the brain from invading microbes. This idea originated from the similarities between A-beta and LL37, which is a protein that acts in the brain’s innate immune system killing harmful cells. The experiments began overexpressing A-beta in mice, and it was found that there was an increased resistance to infection and longer survival rates. It was most surprising that the plaques were able to form in 48 hours. Therefore, these new findings can conclude that as a person gets older, their immune systems get weaker so it is necessary that A-beta increases to prevent infection. However, the issue arises when the threshold is exceeded and the protective role of the protein turns into a neurotoxic one. The fact that A-beta could indeed have a positive role in the body can completely change the way scientists approach future treatments.
Dr. Sangram Sisodia recently discussed the use of antibiotics to reduce the levels of the disease in mice brains. Previous studies were able to determine that there may be a link between gut bacteria and reducing Alzheimer's. Sisodia looked at the use of antibiotics affecting globs of A-beta. It was found that the microbial shift in the gut affected the brain; those mice had fewer plaques compared to the control group. It is still not known how the bacteria signals to the brain to change the A-beta density. However, it is hypothesized that the bacteria could be changing the levels of immune system molecules in the blood. This may allow possible treatment options for people and provide an option for preventative measures for Alzheimer patients. Researchers have been able to explore many different hypothesis, and fortunately it is providing different treatment options for Alzheimer patients.
Works Cited:
Sanders, Laura. "Antibiotics Might Fight Alzheimer's Plaques." Science News. N.p., 10 Aug. 2016. <https://www.sciencenews.org/article/antibiotics-might-fight-alzheimer%E2%80%99s-plaques>.
Cepelewicz, Jordana. "Antimicrobial Mechanism Gone Rogue May Play a Role in Alzheimer's Disease." Scientific American. N.p., 25 May 2016. <https://www.scientificamerican.com/article/antimicrobial-mechanism-gone-rogue-may-play-role-in-alzheimer-s-disease/>.
Massachusetts General Hospital. "Human Amyloid-beta Acts as Natural Antibiotic in the Brain: Alzheimer's-associated Amyloid Plaques May Trap Microbes." ScienceDaily. ScienceDaily, 25 May 2016. <https://www.sciencedaily.com/releases/2016/05/160525161351.htm>.
Image: Marrs, Chandler. "Alzheimer's May Be a Brain Infection and Amyloid Beta Is an Antimicrobial." Hormones Matter. N.p., 01 Sept. 2016. <http://www.hormonesmatter.com/alzheimers-brain-infection-amyloid-beta-antimicrobial/>.
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