Alzheimer's, Dementia & Mental Health
Memory Loss Prevented in Alzheimer’s Disease Mice by
Daily dose of fisetin keeps mice - even those with
genetic mutations linked to Alzheimer's - from experiencing memory and
learning deficits as they age
Jan. 27, 2014 – Memory loss and learning
impairments have been stopped in mice that normally develop these
Alzheimer’s symptoms less than a year after they are born, according to
scientists at the Salk Institute for Biological Studies. It was
accomplished by a daily dose of fisetin, a flavonol compound, found in
fruits and vegetables, which they say has already been proven to enhance
The fisetin did not, however, alter the formation
of amyloid plaques in the brain, accumulations of proteins which are
commonly blamed for
Alzheimer's disease. The new finding suggests a way to treat
Alzheimer's symptoms independently of targeting amyloid plaques.
"We had already shown that in normal animals,
fisetin can improve memory," says Pamela Maher, a senior staff scientist
Cellular Neurobiology Laboratory who led the new study. "What we
showed here is that it also can have an effect on animals prone to
More than a decade ago, Maher discovered that
fisetin helps protect neurons in the brain from the effects of aging.
She and her colleagues have since - in both isolated cell cultures and
mouse studies - probed how the compound has both antioxidant and
anti-inflammatory effects on cells in the brain. Most recently, they
found that fisetin turns on a cellular pathway known to be involved in
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Alzheimer's, Dementia & Mental Health
"What we realized is that fisetin has a number of
properties that we thought might be beneficial when it comes to
Alzheimer's," says Maher.
So Maher - who works with
Dave Schubert, the head of the Cellular Neurobiology Lab - turned to
a strain of mice that have mutations in two genes linked to Alzheimer's
disease. The researchers took a subset of these mice and, when they were
only three months old, began adding fisetin to their food. As the mice
aged, the researchers tested their memory and learning skills with water
mazes. By nine months of age, mice that hadn't received fisetin began
performing more poorly in the mazes. Mice that had gotten a daily dose
of the compound, however, performed as well as normal mice, at both nine
months and a year old.
"Even as the disease would have been progressing,
the fisetin was able to continue preventing symptoms," Maher says.
In collaboration with scientists at the
University of California, San Diego, Maher's team next tested the
levels of different molecules in the brains of mice that had received
doses of fisetin and those that hadn't.
In mice with Alzheimer's symptoms, they found,
pathways involved in cellular inflammation were turned on. In the
animals that had taken fisetin, those pathways were dampened and
anti-inflammatory molecules were present instead. One protein in
particular - known as p35 - was blocked from being cleaved into a shorter
version when fisetin was taken. The shortened version of p35 is known to
turn on and off many other molecular pathways. The results were
published December 17, 2013, in the journal
Studies on isolated tissue had hinted that fisetin
might also decrease the number of amyloid plaques in Alzheimer's
affected brains. However, that observation didn't hold up in the mice
studies. "Fisetin didn't affect the plaques," says Maher. "It seems to
act on other pathways that haven't been seriously investigated in the
past as therapeutic targets."
Next, Maher's team hopes to understand more of the
molecular details on how fisetin affects memory, including whether there
are targets other than p35.
"It may be that compounds like this that have more
than one target are most effective at treating Alzheimer's disease,"
says Maher, "because it's a complex disease where there are a lot of
things going wrong."
They also aim to develop new studies to look at how
the timing of fisetin doses affect its influence on Alzheimer's.
"The model that we used here was a preventive
model," explains Maher. "We started the mice on the drugs before they
had any memory loss. But obviously human patients don't go to the doctor
until they are already having memory problems." So the next step in
moving the discovery toward the clinic, she says, is to test whether
fisetin can reverse declines in memory once they have already appeared.
Other researchers on the paper were Antonio Currais,
Marguerite Prior, Richard Dargusch, Jennifer Ehren, and David Schubert
of the Salk Institute and Aaron Armando and Oswald Quehenberger of the
University of California at San Diego.
The work was supported by grants from the
Alzheimer's Association, Paul Slavik, the National Institutes of Health,
the Alzheimer's Drug Discovery Foundation, and the George E. Hewitt
Studies at Salk Institute over the past few years
have shown fisetin can target multiple organs, which they say suggests
that a single drug could be used to mitigate numerous medical
Salk report in 2011 found it reduced the complications of diabetes.
most abundantly in strawberries and to a lesser extent in other fruits
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world's
preeminent basic research institutions, where internationally renowned
faculty probe fundamental life science questions in a unique,
collaborative, and creative environment. Focused both on discovery and
on mentoring future generations of researchers, Salk scientists make
groundbreaking contributions to our understanding of cancer, aging,
Alzheimer's, diabetes and infectious diseases by studying neuroscience,
genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with
numerous honors, including Nobel Prizes and memberships in the National
Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas
Salk, M.D., the Institute is an independent nonprofit organization and
Salk Institute for Biological Studies
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