Currently, no
treatment can stop Alzheimer's disease, but now, a new study has offered hope
by showing that it possible to reverse memory loss in the patients.
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.
The
study of 10 patients, 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 AD before
beginning the program," said author Dale Bredesen, 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."
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, has revealed
that an extensive network of molecular interactions is involved in AD
pathogenesis, suggesting that a broader-based therapeutic approach may be more
effective.
The
study appears online in the journal Aging.
Representative
Image
Source:
ANI
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