A Curative Prescription for ALS: Unlocking the Mechanism behind the Wen-Shen-Jian-Pi Treatment

Published on April 8, 2022

Imagine you have a magic potion, called Wen-Shen-Jian-Pi prescription, that can slow down the progression of a devastating disease. Well, scientists have discovered that this ancient Chinese remedy can actually delay the decline in motor function caused by Amyotrophic Lateral Sclerosis (ALS). Just like how a superhero swoops in to save the day, Wen-Shen-Jian-Pi prescription works its magic by reducing neuron degeneration in ALS model mice. In a study, researchers treated these mice with different doses of the prescription and observed remarkable improvements. The mice gained weight faster, showed increased activity, and performed better on motor tests compared to the control group. The number of damaged mitochondria and autophagosomes, which are indicators of disease progression, were significantly reduced in the treated mice. This suggests that Wen-Shen-Jian-Pi prescription has therapeutic potential for ALS patients. While more research is needed to assess its effectiveness in humans, this groundbreaking discovery opens up new possibilities for developing targeted ALS treatments. If you’re curious to dive deeper into this exciting advancement, check out the original research article!

ObjectiveTo study the mechanism of the effect of Wen-Shen-Jian-Pi (WSJP) prescription on an ALS model comprising mice knocked out for an encoding RNA editing, mice (AR2).MethodsTwenty-four transgenic AR2 mice were randomly divided into a vehicle group, a low dose WSJP group (15 mg), a medium-dose WSJP group (30 mg), and a high-dose WSJP group (45 mg) (all n = 6 per group). In the treatment groups, the WSJP prescription was given once a day while the vehicle group was fed the same volume of water. The weekly changes in body weight, rotarod test, and grip strength were used to detect the changes in the AR2 and changes of the number of normal mitochondria, abnormal mitochondria, and autophagosomes in injured spinal cord cells were used to evaluate the pathogenetic effects of WSJP treatment.ResultsThe WSJP-treated AR2 mice gained weight more quickly from 8 weeks, and showed active behavior and displayed significantly better constant rotarod scores and grip strengths during the experiment compared with those of the vehicle AR2 mice. The number of normal mitochondria in the WSJP-treated AR2 mice had significantly more normal mitochondria than the vehicle group, while the numbers of abnormal mitochondria and autophagosomes were greatly decreased compared with those in the vehicle group.ConclusionThe WSJP prescription could delay the decline in motor function of ALS model mice by reducing the degeneration of neurons. The potential of WSJP to treat ALS should be assessed in a clinical trial.

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