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Editor’s note: The following is a press release from the
Buck Institute for Research on Aging. It
is posted in full. http://www.thebuck.org/buck-news/reversal-memory-loss-ad
Pre and post testing show reversal of memory loss from
Alzheimer's disease in ten patients
Small trial from the Buck Institute and UCLA succeeds
using systems approach to memory disorders
Results from quantitative MRI and neuropsychological testing show unprecedented improvements in ten patients with early Alzheimer’s disease (AD) or its precursors following treatment with a programmatic and personalized therapy. Results from an approach dubbed metabolic enhancement for neurodegeneration are now available online in the journal Aging.
The study, which comes jointly from the Buck Institute for
Research on Aging and the UCLA Easton Laboratories for Neurodegenerative
Disease Research is the first to objectively show that memory loss in patients
can be reversed, and improvement sustained, using a complex, 36-point
therapeutic personalized program that involves comprehensive changes in diet,
brain stimulation, exercise, optimization of sleep, specific pharmaceuticals
and vitamins, and multiple additional steps that affect brain chemistry.
“All of these patients had either well-defined mild
cognitive impairment (MCI), subjective cognitive impairment (SCI) or had been
diagnosed with Azheimer's disease before beginning the program,” said author
Dale Bredesen, MD, a professor at the Buck Institute and professor at the
Easton Laboratories for Neurodegenerative Disease Research at UCLA, who noted
that patients who had had to discontinue work were able to return to work and
those struggling at their jobs were able to improve their performance. “Follow
up testing showed some of the patients going from abnormal to normal.”
In another instance, a 69-year old professional man and
entrepreneur, who was in the process of 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 improvement in memory. A life-long 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;
results showed marked improvements in all categories with his long-term recall
increasing from the 3rd to 84th percentile. He is 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.
All but one of the ten patients included in the study are at
genetic risk for AD, carrying at least one copy of the APOE4 allele. 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.” Sixty-five percent of the
Alzheimer’s cases in this country involve APOE4; with seven million people
carrying two copies of the ApoE4 allele.
Bredesen’ s systems-based approach to reverse memory loss
follows the abject failure of monotherapies designed to treat AD and the
success of combination therapies to treat other chronic illnesses such as
cardiovascular disease, cancer and HIV. Bredesen says decades of biomedical
research, both in his and other labs, have revealed that an extensive network
of molecular interactions is involved in AD pathogenesis, 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,” Bredesen 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 ten
patients is unprecedented, providing additional objective evidence that this
programmatic approach to cognitive decline is highly effective,” Bredesen 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.
Cognitive decline is often listed as the major concern of
older adults. Already, Alzheimer’s disease affects approximately 5.4 million
Americans and 30 million people globally. Without effective prevention and
treatment, the prospects for the future are bleak. By 2050, it’s estimated that
160 million people globally will have the disease, including 13 million
Americans, leading to potential bankruptcy of the Medicare system. Unlike
several other chronic illnesses, Alzheimer’s disease is on the rise--recent
estimates suggest that AD has become the third leading cause of death in the
United States behind cardiovascular disease and cancer.
Dr. Bredesen’s book describing for a broad audience the
interventions described in this paper, will be released by Penguin Random House
in May 2017. Dr. Bredesen hopes to eventually transform the perception and
reality of Alzheimer’s disease from a death sentence to a preventable and
reversible condition.
Citation: Reversal of Cognitive Decline in Alzheimer’s
Disease
Other collaborators on the study include Edwin C. Amos,
Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, and Jamila
Ahdidan. Multiple entities provided
support for the research which supported the study. They include the National
Institutes of Health (AG16570, AG034427 and AG036975). Please see paper for the
complete list.
The Buck Institute for Research on Aging is the U.S.’s first
independent research organization devoted to Geroscience – focused on the
connection between normal aging and chronic disease. Based in Novato, CA, The
Buck is dedicated to extending “Healthspan”, the healthy years of human life
and does so utilizing a unique interdisciplinary approach involving
laboratories studying the mechanisms of aging and those focused on specific
diseases. Buck scientists strive to discover new ways of detecting, preventing
and treating age-related diseases such as Alzheimer’s and Parkinson’s, cancer,
cardiovascular disease, macular degeneration, osteoporosis, diabetes and
stroke. In their collaborative research,
they are supported by the most recent developments in genomics, proteomics,
bioinformatics and stem cell technologies. For more information:
www.thebuck.org
The Easton Laboratories for Neurodegenerative Disease
Research are part of the UCLA Department of Neurology which encompasses more
than 26 disease-related research programs. This includes all of the major
categories of neurological diseases and methods, encompassing neurogenetics and
neuroimaging as well as health services research. The 140 faculty members of
the Department are distinguished scientists and clinicians who have been ranked
#1 in NIH funding for 9 consecutive years beginning in 2002. The Department is
dedicated to understanding the human nervous system and improving the lives of
people with neurological diseases, focusing on three key areas:
patient/clinical care, research, and education. For more information, see
http://www.neurology.ucla.edu/
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