One example this morning: The government is launching a new plan to attack Alzheimer’s. ”More than 5 million Americans are living with Alzheimer’s disease. On Tuesday, the Obama Administration announced the launch of the National Alzheimer’s Plan, with the goal of finding effective ways to prevent and treat the devastating effects of dementia by 2025.” Time Magazine
Two years ago the Mayo clinic released a study showing a direct tie between endothelial nitric oxide and Alzheimer’s. Essentially, nitric oxide protects the endothelium (thin layer of cells that protects the interior of all blood vessels.) The food we eat plays a major role in the health of that lining.
“If you look at any risk factor for cardiovascular disease – the standard risk factors like high cholesterol, diabetes, hypertension, smoking, sedentary lifestyle, aging – all of these have been associated with loss of nitric oxide in the endothelium (the linings of blood vessels), a condition known as endothelial dysfunction.” -Zvonimir S. Katusic, M.D., Ph.D., senior author and professor at the Mayo Clinic.
“Once you lose that [baseline of] nitric oxide, you see the increases in APP (amyloid precursor protein) and BACE1 (an enzyme that together with APP helps to create Alzheimer plaques), and the increase in amyloid beta generation.” -Susan Austin, PhD., first author of the study, and a research fellow at the Mayo Clinic
“For years we’ve been hearing that there is a connection between heart health and brain health. “What’s good for the heart is good for the brain” — namely, don’t smoke, get lots of exercise, eat lots of beans & green leafy vegetables, and cut out the fat.
Cardiovascular diseases and Alzheimer/brain diseases share similar blood vessel pathologies, but as Dr. Randolph Schiffer, the head of the Cleveland Clinic’s Ruvo Center for Brain Health said last May, “We lack the exact kind of science we’d like to have concerning this connection.”
Thanks to three researchers at the Mayo Clinic (Susan A. Austin, Ph.D., Anantha V. Santhanam, Ph.D., & Zvonimir S. Katusic, MD, Ph.D.) we may finally have that connection between heart & brain health: Nitric Oxide.
Here’s why I’m so excited. If the loss of nitric oxide in the blood vessels of the brain is the culprit behind Alzheimer’s & dementia, we’ve got a fixable problem. But, here’s the catch. You can’t wait too long to start fixing this problem. And, you have to be willing to change your lifestyle.
If you wait until your baseline nitric oxide supply gets too low, it may be too late.
- Preserving healthy blood vessel walls is important to preventing cognitive impairment and ultimately Alzheimer’s disease. And a hefty supply of nitric oxide is the key.
- As Dr. Caldwell Esselstyn (www.heartattackproof.com) has shown with hundreds of heart disease patients, you can preserve or repair your blood vessel walls by eating a plant-based diet that’s high in the building blocks of nitric oxide: leafy greens, legumes, oats & beans.
- Exercise also stimulates the endothelium (blood vessel linings) to produce more nitric oxide.
- According to Esselstyn’s research, just 3-4 weeks on a plant-based diet that’s high in greens, without meat, dairy, added fat or oil, is all it takes to start the healing process in (coronary) blood vessels, and put the nitric oxide factory back into business. Let’s hope it’s true for the blood vessels in the brain, as well.”
Circ Res. 2010 Dec 10;107(12):1498-502. Epub 2010 Dec 2.
Endothelial nitric oxide modulates expression and processing of amyloid precursor protein.
Departments of Anesthesiology and Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic College of Medicine, Rochester, Minn., 55905, USA.
the exact etiology of sporadic Alzheimer disease (AD) is unclear, but it is interesting that several cardiovascular risk factors are associated with higher incidence of AD. The link between these risk factors and AD has yet to be identified; however, a common feature is endothelial dysfunction, specifically, decreased bioavailability of nitric oxide (NO).
to determine the relationship between endothelial derived NO and the expression and processing of amyloid precursor protein (APP).
METHODS AND RESULTS:
we used human brain microvascular endothelial cells to examine the role of NO in modulating APP expression and processing in vitro. Inhibition of endothelial nitric oxide synthase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1 (β-site APP-cleaving enzyme1) protein levels, as well as increased secretion of the amyloidogenic peptide amyloid β (Aβ) (control 10.93 ± 0.70 pg/mL; L-NAME 168.21 ± 27.38 pg/mL; P<0.001). To examine the role of NO in modulation of APP expression and processing in vivo, we used brain and cerebral microvessels from eNOS-deficient (eNOS(-/-)) mice. Brain tissue from eNOS(-/-) mice had statistically higher APP and BACE1 protein levels, as well as increased BACE1 enzyme activity and Aβ (Aβ(1)(-)(42) wild-type control, 0.737 pg/mg; eNOS(-/-), 1.475 pg/mg; P<0.05), compared with wild-type controls (n=6 to 8 animals per background). Brain microvessels from eNOS(-/-) mice also showed statistically higher BACE1 protein levels as compared with wild-type control.
Our data suggest that endothelial Nitric Oxide plays an important role in modulating APP expression and processing within the brain and cerebrovasculature. The NO/cGMP pathway may be an important therapeutic target in preventing and treating mild cognitive impairment, as well as Alzheimers Disease.