Could Antidepressants Be Used to Slow Alzheimer Disease?

By: Dr. Pascale Michelon

Anti-depressants ‘could slow onset of Alzheimer’s disease’ (BBC): Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer’s patients. Scientists said they hoped the study could help prevent the disease.

How many hopeful titles like this one have you read recently in the media? Scientific results tend to get in the news very fast these days, especially as far as Alzheimer’s disease is concerned. Often, the research is only beginning and patients and their family should learn to be critical readers.

Here are a few reasons not to get excited too fast about the present study.

Pippa Stephens, at BBC News, reports: ”Researchers at the University of Pennsylvania and Washington University School of Medicine …bred mice with Alzheimer’s disease and looked at the levels of the peptide – or protein component – amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer’s. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number.

The 23 people used in the study were aged between 18 and 50 and were “healthy”, researchers said. They were given a single dose of citalopram, and the levels of AB in their cerebrospinal fluid was monitored, according to the study. Researchers said AB levels dropped by 38% in the 37-hour period after treatment, compared to a placebo test.”

This is an interesting result with potential. However there are at least 4 reasons not to get too excited: 

  1. The mice model of Alzheimer’s is useful to try to understand the disease but does not exactly correspond to what happens in humans. Testing the concept in humans is essential.
  2. The human sample tested in that study was very small: it was a kind of concept study to test the idea. A larger study is of course necessary.
  3. The antidepressant was not tested on people actually diagnosed with Alzheimer’s but on young and healthy people. Targeting actual patients is the next step.
  4. Previous studies that tried to reduce the levels of the AB protein have shown that it is actually not enough to fight against Alzheimer’s.

Other questions remain such as the length of the effect, etc. If you would like to learn more on how to decode scientific studies reported in the media, check out chapter 2 of The SharpBrains Guide to Brain Fitness: Be a Coach, Not a Patient.

Using your brain is part of staying sharp and building brain reserve. What a better way to do so than being a critical news reader?!

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