Science/Tech

Miracle Molecule Reverses Alzheimer's and Restores Memory in Mice

Alzheimer's disease patient sits in an armchair in her house.
New study claims tests that predict heart disease and stroke could also foresee memory loss and risk of dementia. Nacho Doce/Reuters

Part of the reason that Alzheimer's disease is so difficult to watch in a loved one is that, with no cure, the person gradually turns into a shell of who they once were. One molecule may change all of that. In a study performed on mice, TFP5 was injected into mice that were exhibiting symptoms of the debilitating disease. Researchers found that the miracle molecule reversed symptoms of Alzheimer's and restored memory loss.

As described in the article published in The FASEB Journal, the study separated two mice suffering from the equivalent of human Alzheimer's disease into two groups. One group of mice was injected with TFP5, while the other was injected with a saline placebo. After receiving the injection of TFP5, the mice's symptoms drastically reduced by 70 to 80 percent and they exhibited improved memory. The injection also did not appear to cause any adverse effects, like weight loss, anxiety or signs of toxicity. On the other hand, the mice that were injected with the placebo degenerated as usual.

Researchers believe that the reason that TFP5 had such a positive effect is that it is derived from the regulator of an important brain enzyme called cyclin-dependant kinase 5, or Cdk5. In brains impacted by Alzheimer's disease, the brain produces too much of the enzyme, helping to lead to plaques and tangles characteristic of neurological disorder. The injection of TFP5 "inhibits abnormal Cdk5 hyperactivity" but does not limit normal Cdk5 activity.

Of course what works in mice may not be effective in humans. Regardless, researchers are optimistic. "The next step is to find out if this molecule can have the same effects in people, and if not, to find out which molecule will," The FASEB Journal editor-in-chief Gerald Weissman said in a statement. "Now that we know that we can target the basic molecular defects in Alzheimer's disease, we can hope for treatments far better - and more specific - than anything we have today."

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