Tanis and research colleagues recently uncovered fresh information on the possible effect of food on Alzheimer’s disease, a devastating, progressive brain illness that affects and over 6 million people. Whenever nematodes develop Alzheimer’s disease, they don’t wriggle. In Prof Jessica Tanis’s laboratory, whatever let worm with condition keeps their wriggle.
Interesting Data From A Worm Study On Vitamin B12 And Alzheimer’s
It must be noted here that Alzheimer’s is the disease with the highest increasing rate in terms of patients across the USA. Gradually, the average age of the patient is also declining, which is taken seriously by the experts. The new study will help them to analyze the level of vitamin B12 and its effects on the patients who are countering this health issue.
During 36 hours of reaching maturity, worms are paralyzed due to the development of beta-amyloid, a deadly peptide linked to Alzheimer’s disease. Whereas the worm in one Petri plate in Tanis’s laboratory is made motionless, the worm in the neighboring petri dish continued to squirm, which the researchers noted as “body bends.”
“It was an observation my master’s student Kirsten Kervin made,” said Tanis, an assistant professor in the Department of Biological Sciences. “She repeated the experiment again and again, with the same results.”
Tanis added that after decades of investigation, the group has ultimately discovered a significant variation. Although all of the worms are fed E. coli, it was discovered that only one strain of E. coli has greater vitamin B12 concentrations than another. Tanis’ investigation is originally centered on hereditary variables, but she shifted her focus to this vitamin and its protective factor.
“As humans, we have immense genetic diversity and such complex diets that it makes it hard to decipher how one dietary factor is affecting the onset and progression of Alzheimer’s,” Tanis said. “That’s where the worms are amazing. The worms we use all have the same genetic background, they react to amyloid beta-like humans do, and we can exactly control what they eat so that we can get down to the molecular mechanisms at work.”
C. elegans is a thin, translucent worm measuring less than a millimeter in length that resides in soil and feeds on microorganisms. Those worms have been used as a reference species and the topic of various researches throughout the 1970s, even though it is an easier platform to research molecular genetics and illnesses than people.
Vitamin B12 requires the activity of a particular enzyme known as methionine synthase, according to researchers. B12 seems to have no impact unless that protein is present, according to Tanis. Furthermore, supplementing the meal with the vitamin solely helped if the mice were B12 deficient. Providing extra B12 to animals had normal amounts accomplishes little to benefit them. The researchers also discovered the vitamin B12 does not influence the worms’ levels of amyloid-beta.
The accumulation of beta-amyloid in the brain of Alzheimer’s patients generates harmful consequences in cell differentiation, leading to decreased vitality, the disintegration of mitochondria, the cell’s power plants, and oxidative from an abundance of free – radicals. Tanis claims that the identical phenomenon occurs in C. elegans, but in a couple of hours. In the worm, amyloidosis beta induces paralytic.
“Right now, there is no effective treatment for Alzheimer’s disease,” Tanis said. “There are certain factors that you cannot change the fact that your age and you cannot change a genetic predisposition to Alzheimer’s disease. But one thing you can control is what you eat. If people could change their diet to affect the onset of disease, that would be fantastic. That’s something my lab is excited to continue to explore.”
