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2007 December 26 Wednesday

Evidence For Omega 3 Fatty Acid Against Alzheimer's Disease

More evidence that fish oils really are good for you.

Many Alzheimer's researchers have long touted fish oil, by pill or
diet, as an accessible and inexpensive "weapon" that may delay or
prevent this debilitating disease. Now, UCLA scientists have confirmed
that fish oil is indeed a deterrent against Alzheimer's, and they have
identified the reasons why.

Reporting in the current issue of the Journal of Neuroscience, now
online, Greg Cole, professor of medicine and neurology at the David
Geffen School of Medicine at UCLA and associate director of UCLA's
Alzheimer Disease Research Center, and his colleagues report that the
omega-3 fatty acid docosahexaenoic acid (DHA) found in fish oil
increases the production of LR11, a protein that is found at reduced
levels in Alzheimer's patients and which is known to destroy the
protein that forms the "plaques" associated with the disease.

The plaques are deposits of a protein called beta amyloid that is
thought to be toxic to neurons in the brain, leading to Alzheimer's.
Since having high levels of LR11 prevents the toxic plaques from being
made, low levels in patients are believed to be a factor in causing
the disease.

I ate a large piece of Salmon on Christmas Day and now I feel even
better about it.

DHA also boosted LR11 in human cells grown in culture.

"We found that even low doses of DHA increased the levels of LR11 in
rat neurons, while dietary DHA increased LR11 in brains of rats or
older mice that had been genetically altered to develop Alzheimer's
disease," said Cole, who is also associate director of the Geriatric
Research Center at the Veterans Affairs Medical Center.

To show that the benefits of DHA were not limited to nonhuman animal
cells, the researchers also confirmed a direct impact of DHA on human
neuronal cells in culture as well. Thus, high levels of DHA leading to
abundant LR11 seem to protect against Alzheimer's, Cole said, while
low LR11 levels lead to formation of the amyloid plaques.

Since the oceans don't have enough fish in them we really need land
crops genetically engineered to have high levels of omega 3 fatty
acids.

Not convinced yet? See my previous posts Omega 3 Fatty Acids In Fish
Delay Alzheimer's In Mice, Fish In Diet Slows Rate Of Cognitive
Decline, Omega 3 Fatty Acids Might Slow Alzheimers Disease, and Omega
3 Fatty Acids Protect Against Parkinsons Disease? for more on brain
aging benefits of omega 3 fatty acids.

We need to slow the aging of our brains for the day when brain
rejuvenation therapies become available. The more neurons we have left
at that point the more that can be repaired and restored.

*  *  *
The Journal of Neuroscience, December 26, 2007, 27(52):14299-14307;
doi:10.1523/JNEUROSCI.3593-07.2007

Omega-3 Fatty Acid Docosahexaenoic Acid Increases SorLA/LR11, a
Sorting Protein with Reduced Expression in Sporadic Alzheimer's
Disease (AD): Relevance to AD Prevention

Qiu-Lan Ma,1,3 Bruce Teter,1,3 Oliver J. Ubeda,1,3 Takashi Morihara,
1,3,4 Dilsher Dhoot,1,3 Michael D. Nyby,1 Michael L. Tuck,1 Sally A.
Frautschy,1,2,3 and Greg M. Cole1,2,3

Departments of 1Medicine and 2Neurology, University of California, Los
Angeles, California 90095, 3Geriatric Research, Education and Clinical
Center, Veterans Affairs, Greater Los Angeles Healthcare System, North
Hills, California 91343, and 4Department of Post-Genomics and
Diseases, Division of Psychiatry and Behavioral Proteomics, Osaka
University Graduate School of Medicine D3, Suita-shi, Osaka 565-0871,
Japan

Correspondence should be addressed to Greg M. Cole, Veterans Affairs,
Greater Los Angeles Healthcare System Research 151, Building 7, Room
A101, 16111 Plummer Street, North Hills, CA 91343. Email:
gmcole@ucla.edu

Environmental and genetic factors, notably ApoE4, contribute to the
etiology of late-onset Alzheimer's disease (LOAD). Reduced mRNA and
protein for an apolipoprotein E (ApoE) receptor family member, SorLA
(LR11) has been found in LOAD but not early-onset AD, suggesting that
LR11 loss is not secondary to pathology. LR11 is a neuronal sorting
protein that reduces amyloid precursor protein (APP) trafficking to
secretases that generate β-amyloid (Aβ). Genetic polymorphisms that
reduce LR11 expression are associated with increased AD risk. However
these polymorphisms account for only a fraction of cases with LR11
deficits, suggesting involvement of environmental factors. Because
lipoprotein receptors are typically lipid-regulated, we postulated
that LR11 is regulated by docosahexaenoic acid (DHA), an essential -3
fatty acid related to reduced AD risk and reduced Aβ accumulation. In
this study, we report that DHA significantly increases LR11 in
multiple systems, including primary rat neurons, aged non-Tg mice and
an aged DHA-depleted APPsw AD mouse model. DHA also increased LR11 in
a human neuronal line. In vivo elevation of LR11 was also observed
with dietary fish oil in young rats with insulin resistance, a model
for type II diabetes, another AD risk factor. These data argue that
DHA induction of LR11 does not require DHA-depleting diets and is not
age dependent. Because reduced LR11 is known to increase Aβ production
and may be a significant genetic cause of LOAD, our results indicate
that DHA increases in SorLA/LR11 levels may play an important role in
preventing LOAD.

Received Aug. 8, 2007; revised Oct. 10, 2007; accepted Oct. 30, 2007.

Correspondence should be addressed to Greg M. Cole, Veterans Affairs,
Greater Los Angeles Healthcare System Research 151, Building 7, Room
A101, 16111 Plummer Street, North Hills, CA 91343. Email:
gmcole@ucla.edu