Small Study Shows Memory Loss from Alzheimer’s Can Be Reversed

A small trial of 10 patients has found that broad-based treatment with personalized therapy can reverse memory loss from Alzheimer’s disease.

Results from quantitative MRI and neuropsychological testing show “unprecedented” improvements in the patients with early Alzheimer’s disease (AD) or its precursors following the treatment, according to researchers from the Buck Institute for Research on Aging and the University of California, Los Angeles (UCLA) Easton Laboratories for Neurodegenerative Disease Research.

The study, published in the journal Aging, shows that memory loss can be reversed, and improvement sustained, using a 36-point therapeutic personalized program that involves changes in diet, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry, researchers said.

“All of these patients had either well-defined mild cognitive impairment (MCI), subjective cognitive impairment (SCI), or had been diagnosed with AD before beginning the program,” said Dale Bredesen, M.D., a professor at the Buck Institute and professor at the Easton Laboratories for Neurodegenerative Disease Research at UCLA. “Follow-up testing showed some of the patients going from abnormal to normal.”

Bredesen noted that some patients who had to discontinue work were able to return to work and those struggling at their jobs were able to improve their performance.

According to the researchers, one of the more striking cases was a 66-year-old man whose neuropsychological testing was compatible with a diagnoses of MCI and whose PET scan showed reduced glucose utilization indicative of AD. An MRI showed hippocampal volume at only the 17th percentile for his age.

After 10 months on the protocol, a follow-up MRI showed a dramatic increase of his hippocampal volume to the 75th percentile, with an associated absolute increase in volume of nearly 12 percent, the researchers reported.

In another instance, a 69-year-old entrepreneur who was shutting down his business went on the protocol after 11 years of progressive memory loss. After six months, his wife, co-workers, and he noted an improvement in his memory. A lifelong ability to add columns of numbers rapidly in his head returned and he reported an ability to remember his schedule and recognize faces at work.

After 22 months on the protocol he returned for follow-up quantitative neuropsychological testing. The results showed marked improvements in all categories with his long-term recall increasing from the third to 84th percentile, according to the researchers, who add he is now expanding his business.

Another patient, a 49-year-old woman who noted progressive difficulty with word finding and facial recognition went on the protocol after undergoing quantitative neuropsychological testing at a major university. She had been told she was in the early stages of cognitive decline and was therefore ineligible for an Alzheimer’s prevention program.

After several months on the protocol she noted a clear improvement in recall, reading, navigating, vocabulary, mental clarity, and facial recognition. Her foreign language ability had returned.

Nine months after beginning the program she did a repeat of the neuropsychological testing at the same university site. She no longer showed evidence of cognitive decline, according to the researchers.

All but one of the 10 patients included in the study are at genetic risk for AD, carrying at least one copy of the APOE4 allele, the researchers said. Five of the patients carry two copies of APOE4, which gives them a 10-12 fold increased risk of developing AD.

“We’re entering a new era,” said Bredesen. “The old advice was to avoid testing for APOE because there was nothing that could be done about it. Now we’re recommending that people find out their genetic status as early as possible so they can go on prevention.”

He added that 65 percent of the Alzheimer’s cases in the U.S. involve APOE4, with seven million people carrying two copies of the ApoE4 allele.

According to Bredesen, decades of biomedical research has revealed that an extensive network of molecular interactions is involved in Alzheimer’s disease, suggesting that a broader-based therapeutic approach may be more effective.

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well — the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much,” he said.

“We think addressing multiple targets within the molecular network may be additive, or even synergistic, and that such a combinatorial approach may enhance drug candidate performance, as well.”

While encouraged by the results of the study, Bredesen admits more needs to be done.

“The magnitude of improvement in these 10 patients is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective,” he said. “Even though we see the far-reaching implications of this success, we also realize that this is a very small study that needs to be replicated in larger numbers at various sites.”

Plans for larger studies are underway, he added.

“The Bredesen Protocol,” Bredesen’s book describing the interventions described in the study, will be released by Penguin Random House in May 2017.

Janice Wood

Published by Meg Duke

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