Neuroscience, diagnostic tools and numerous trials often hit the media — and the latest study, focusing on nutrition, is no exception.
Researchers at the Massachusetts Institute of Technology (MIT) have recently expanded on an earlier trial documenting a nutritional supplement and its effect on the connections between brain cells; a leading cause of memory loss in Alzheimer’s patients. MIT reports that the recent trial, published in the Journal of Alzheimer’s Disease, found that a cocktail of nutrients improved the memory capabilities of Alzheimer’s sufferers.
The connections between brain cells, known as synapses, are gradually lost as the degenerative disease takes root. The loss of these important connectors causes memory loss and the steadily degeneration of other cognitive faculties.
The nutritional supplement, called Souvenaid, appeared to stimulate the growth of new synapses — replacing those lost or damaged — according to Richard Wurtman, professor of brain and cognitive science at MIT.
Wurtman said:
“You want to improve the numbers of synapses, not by slowing their degradation — though of course you’d love to do that too — but rather by increasing the formation of the synapses.”
In order to stimulate this growth, three naturally occurring dietary compounds: choline, uridine and the omega-3 fatty acid DHA were mixed together. Along with specific proteins, these compounds make up brain-cell membranes, which in turn form synapses. However, to be effective, all of these precursors have to be administered at the same time.
The trial, conducted in Europe, followed 259 patients who consumed Souvenaid or a placebo over the course of six months. Over the first three months, all of the patients improved their verbal-memory performance. However, in the final three months, only the patients taking the nutritional supplement showed further improvement — whereas the placebo-taking patients slowly deteriorated.
According to the team, 97 percent of the trial patients followed the regimen correctly, and no serious side-effects were reported.
Electroencephalography (EEG) was used to measure each patient’s brain activity during the trial’s six-month timeframe. The researchers found that the Souvenaid drinkers’ patterns shifted; moving from standard dementia patterns to those considered more ‘normal’. As EEG patterns reflect synaptic activity, it seems the supplement may help promote new growth before the disease becomes advanced — not as a cure, but as a preventative measure.
Patients admitted to this study were in the early stages of Alzheimer’s disease, with an average of 25 on a scale of dementia that ranged from 1 to 30, with 30 the level for ‘normal’ brain activity. Early stage patients were chosen to a previous trial which found that the supplement does not work in the more advanced stages of the neurodegenerative disease.
A two-year trial of patients who are starting to show mild cognitive impairment — without being diagnosed with Alzheimer’s — has now begun. Wurtman believes that if the nutritional supplement appears to help delay impairment, then it could be prescribed to patients who show positive signs for the disease early on.
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