In the early stages of Alzheimer's disease, patients typically suffer a major loss of
the brain connections necessary for memory and information processing. Now, a
combination of nutrients that was developed at MIT has shown the potential to
improve memory in Alzheimer's patients by stimulating growth of new brain
In a clinical trial of 225 Alzheimer's patients, researchers found that a cocktail of
three naturally occurring nutrients believed to promote growth of those
connections, known as synapses, plus other ingredients (B vitamins,
phosopholipids and antioxidants), improved verbal memory in patients with mild
"If you can increase the number of synapses by enhancing their production, you
might to some extent avoid that loss of cognitive ability," says Richard Wurtman,
the Cecil H. Green Distinguished Professor of Brain and Cognitive Sciences, who
did the basic research that led to the new experimental treatment. He is an author
of a paper describing the new results in the journal Alzheimer's and Dementia.
There is currently no cure for Alzheimer's disease, though some medications can
slow the progression of the disease. In particular, many U.S. patients take
cholinesterase inhibitors, which increase levels of acetylcholine, a neurotransmitter
important for learning and memory.
While those treatments target the symptoms of Alzheimer's, Wurtman hopes to
attack what he believes is the root cause of the disease: loss of synapses. The
three nutrients in his dietary cocktail - uridine, choline and the omega-3 fatty acid
DHA (all normally present in breast milk) - are precursors to the fatty molecules
that make up brain cell membranes, which form synapses.
In animal studies, Wurtman has shown that these nutrients boost the number of
dendritic spines (small outcroppings of neural membranes). When those spines
contact another neuron, a synapse is formed.
Three additional clinical studies in Alzheimer's patients are now underway, one in
the United States and two in Europe. Results are expected to be available between
2011 and 2013.
The first clinical study was sponsored by the French company Danone, known in
the United States as Dannon; the study was conducted primarily in Europe and was
led by Philip Scheltens, director of the Alzheimer Center at Vrije Universiteit
Medical Center in Amsterdam. Wurtman and MIT have patented the mixture of
nutrients used in the study, and Nutricia Advanced Medical Nutrition, a unit of
Danone, holds the exclusive license on the patent.
Patients with mild Alzheimer's drank the cocktail (made in the form of a nutrient
drink called Souvenaid, with the collaboration of Danone) or a control beverage
daily for 12 weeks. Patients who received the nutrients showed a statistically
significant level of improvement compared to control subjects: 40 percent of the
treated patients improved performance in a test of verbal memory (memory for
words, as opposed to memory of locations or experiences) known as the
Wechsler Memory Scale, while 24 percent of patients who received the control
drink improved their performance. Among those who received the cocktail, patients
with the mildest cases of Alzheimer's showed the most improvement.
The drink appeared to have no effect on patients' performance in another
commonly used evaluation for Alzheimer's patients, the ADAS-cog test. Wurtman
believes that is because ADAS-cog is a more general assessment that tests for
orientation and movement/spatial memory as well as cognition. So in subjects with
early Alzheimer's who show principally cognitive changes, more than the 225
subjects in the first study will probably be required to yield significant ADAS-cog
changes after Souvenaid. The 500 subjects in the ongoing study in the United
States may be sufficient.
John Growdon, a neurologist at Massachusetts General Hospital, says that trying to
regrow synapses is an innovative strategy and offers a complementary approach to
two other lines of attack in treating Alzheimer's: targeting the amyloid plaques that
accumulate in patients' brains, and minimizing the damage done by toxic
metabolites that build up in Alzheimer's-affected brains.
"I don’t think any one approach has a monopoly, and that's good," Growdon says.
"You need to have a lot of different approaches because no one knows what's
going to work."
Wurtman believes his approach to Alzheimer's may eventually prove beneficial in
treating other diseases. If these nutrients prove to be successful in Alzheimer's
patients, "then you can think about other diseases in which there are too few
synapses," such as Parkinson's disease, he says. "There are a lot of diseases
associated with synapse deficiency."
Contact: Anne Traftongillooly@mit.edu
MIT News Office
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