Next month, we’ll get back to the brain and schools. But, during June and July we focus on your personal world. Last month, we focused on “7 Things You Can Do to Prevent Cancer”. This month, we’ll focus on how to prevent or reduce the effects of cognitive decline. This issue may apply to a family member or even yourself. After all, every 68 seconds, another American is diagnosed with Alzheimer’s disease and it’s a cold, cruel way to die.
When our thinking and memory capacity becomes diminished (by a stroke, trauma, aging or Alzheimer’s) we begin to lose our sense of self and we frustrate those around us. The good news is that there are some well-researched approaches that can make dramatic differences in brain health. The first thing you can do is….
1. Protect your brain
Make your brain work hard with new learning 3-5 times a week. Upgrade your reading from the “brain-dead” ones to some that are more challenging. Sitting around is a risk factor, learning new and challenging things is better for the brain. Here is a website to take your parents to where they can build their cognitive capacity or at least delay onset of Alzheimer’s symptoms.
2. Stay Active
Get physical: Find ways to stay active (walks, swimming and yoga are the best). Worry less about WHAT you do for activity and more that you do SOMETHING at all daily.
3. Foods to Eat
Protective foods typically reduce inflammation in the brain. Olive oil works well to fight inflammation and it’s perfect to cook with. A glass of red wine a day is okay, and other alcohol may be consumed, but sparingly. Cold water fish is good (such as salmon, mackerel, sardines, cod). All are a good sources of choline, along with whole-grain cereals, legumes, eggs, meat, and royal jelly (all of which contain both vitamin B5, omega 3s and choline). Turmeric, the bright yellow spice that is a primary ingredient in curry powder, shows great promise against Alzheimer’s disease (29 peer-reviewed studies), due to a variety of actions, including its ability to inhibit and even reverse beta-amyloids. Curry and ginger are both anti-inflammatory brain protective spices.
4. Keep sugars low
Choose greens and proteins over carbs and sugars. Cut your carbohydrate consumption in HALF. The key scientific principle, which forms the basis for these diets, is the relationship between consumption of carbohydrates and the subsequent effect on blood sugar (i.e. blood glucose) and specific hormones. Blood sugar levels in the human body must be maintained in a fairly narrow range to maintain health.
5. Stay up on the research
Even though this BrightBrain Bulletin comes out monthly, it only discusses Alzheimer’s once a year. Medicine is not our primary focus. Keep up on the latest discoveries. You might bookmark sites you like on this topic including:
a) Omega-3 fatty acids are neuroprotective during development and aging. With Omega 3 supplements (186 studies), positive effects were observed in some studies with very mild AD, especially for early onset conditions. Get it as fish oil (capsules or liquid). This non-prescriptive product (fish oil) may be purchased at a health food store. Get it fresh, the type that smells good and tastes good. Available in no-smell fish oil capsules at health food stores.
b) Lipoic acid (available in health food stores) is a naturally occurring co-factor for the mitochondrial enzymes. It has properties which can interfere with the pathogenesis or progression of Alzheimer’s (Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA, Münch G. 2008).
c) Small does of lithium (283 studies found at last count) suggest it may be a neuroprotective agent (it’s available in tablet form at health food stores) and have been shown to reduce the rate of dementia and AD (Wada A, Yokoo H, Yanagita T, Kobayashi H. 2005).
d) CoQ10 is widely available and very well tolerated with minimal adverse effects, making it an attractive potential therapy. Phase III trials of high-dose CoQ10 in large sample sizes are needed to further ascertain or confirm the effects of CoQ10 in neurodegenerative diseases, but early indications look promising (Spindler M, Beal MF, Henchcliffe C. 2009). It’s available in health food stores.
e) The hormone melatonin (available in tablet form at health food stores) may be effective against the famous and pesky plaques found in AD patients. Melatonin interacts with amyloyd beta and inhibits its aggregation (Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O’Leary OF, Castre, E, & Maffei L., 2008). This hormone (which also regulates sleep) is protective against Alzheimer’s.
f) The next intervention is galantamine (683 peer-reviewed studies). Galantamine, a natural substance found in certain flowers, has also shown promise in delaying the progression of Alzheimer’s by protecting and enhancing cholinergic function. Although this intervention is available as an FDA-approved prescription drug for the treatment of mild to moderate Alzheimer’s disease, it is also available as the original nutritional supplement that it has been LONG BEFORE a drug company made a prescription out of it and the FDA declared it a “drug.”
In fact, Galantamine studies, in quality controlled randomized trials, have documented a consistent, albeit sometimes modest, effect on cognition, behavioral symptoms and activities of daily living (ADLs). Although minor adverse effects are commonly reported, the products are generally well tolerated and have a favorable safety profile. This does NOT cure AD, but a modest effect may make a big difference, especially when it’s a loved one’s mind or even your own. One reputable company that sells Galantamine capsules online without a prescription is Life Enhancement http://www.life-enhancement.com
7. FDA Approved Drug Approved (sort of…)
Last August I said, “I want you to drop any delusions that drug companies can guarantee any quick, safe and effective treatments for Alzheimer’s. Almost all of them are going at the problem(s) the wrong way.” I might have been dead wrong (or, almost). Have you been waiting for a drug, tested by the FDA to reduce or eliminate the symptoms of Alzheimer’s? A new study shows it might already exist. Here’s what the actual study said:
“The Beta-amyloyd plaque area was reduced more than 50% within just 72 hours. Furthermore, bexarotene (the intervention) stimulated the rapid reversal of cognitive, social, and olfactory deficits and improved neural circuit function.” (Cramer PE, Cirrito JR, Wesson DW, Lee CY, Karlo JC, Zinn AE, Casali BT, Restivo JL, Goebel WD, James MJ, Brunden KR, Wilson DA, & Landreth GE., 2012).
“We have successfully reversed all of the known pathological features and behavioral deficits found in mouse models of Alzheimer’s disease. Never before has anyone observed clearance of amyloyd plaques with such speed in mouse models.” – Gary Landreth, lead author of study.
So why isn’t the drug out yet? It is. The drug is called bexarotene in a pill form under the trade name Targretin. Today, it is an FDA-approved treatment for certain lymphoma cancers that attacks the body’s immune system. Bexarotene is also commonly used “off label” to treat other (use your imagination, “wink..nod”) illnesses.
But this new development has three problems:
1) The FDA has NOT approved this drug for Alzheimer’s, since no one has done the clinical trials for it. Some people suffering from Alzheimer’s’ are already trying it “off label”, but no doctor or company can legally or ethically promote it as a treatment for Alzheimer’s until the human studies are done.
2) There are side effects. Earlier, I said I might have been “dead wrong” about a drug for Alzheimer’s. What I also said was, “Those that do make it to the marketplace are fraught with side effects.” While the FDA approved bexarotene for cancer, when they also approve a drug, they take into consideration the “risk/reward ratios” which have different standards for different drugs. In short, the FDA might approve a drug for one purpose, but not for another.
3) The new study mentioned above was on mice, not humans. It’s a long and bumpy road from animal studies to Stage III human study success. Having said that, professor Landreth is so excited about the animal studies so far, he’s got the patent and started up a company called ReXceptor to produce the drug if it gets cleared.
To read more articles about this promising approach, Go to: “Scientific American, bexarotene” or “ScienceNews, bexarotene”.
First, I’m not a medical doctor (and if I was, I might be too worried about lawsuits to suggest alternative interventions anyway). That means I am not qualified, nor can I diagnose, prescribe or suggest any specific treatment. Do not take anything based on this newsletter, rather allow it to inform your decisions based on a wide range of qualified advice.
Having said that, I am qualified to share the science and let you make your own decisions. These are some positive choices to prevent, delay or even reverse Alzheimer’s.
Best to you.
CEO, Jensen Learning
Ago Y. Beneficial effect of galantamine on sensory information-processing deficits. Yakugaku Zasshi 2010 Oct;130(10):1305-10.
Caller TA, Doolin JW, Haney JF, Murby AJ, West KG, Farrar HE, Ball A, Harris BT, Stommel EW. (2009) A cluster of amyotrophic lateral sclerosis in New Hampshire: a possible role for toxic cyanobacteria blooms. Amyotroph Lateral Scler.10 Suppl 2:101-8.
Cramer PE, Cirrito JR, Wesson DW, Lee CY, Karlo JC, Zinn AE, Casali BT, Restivo JL, Goebel WD, James MJ, Brunden KR, Wilson DA, Landreth GE. (2012) ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models. Science. Mar 23;335(6075):1503-6.
Crunkhorn S. (2012) Neurodegenerative disease: RXR agonist reverses Alzheimer’s disease. Nat Rev Drug Discov. Mar 30;11(4):271.
Ehninger D, Li W, Fox K, Stryker MP, Silva AJ (2008) Reversing neurodevelopmental disorders in adults. Neuron 60:950 –960.
Fan LY, Chiu MJ. (2010) Pharmacological treatment for Alzheimer’s disease: current approaches and future strategies. Acta Neurol Taiwan. Dec;19(4):228-45.
Greer PL, Greenberg ME (2008) From synapse to nucleus: calcium- dependent gene transcription in the control of synapse development and function. Neuron 59:846 – 860.
Giunta et al. (2010) Fish oil enhances anti-amyloidogenic properties of green tea EGCG in Tg2576 mice. Neurosci Lett 8(471):134-8.
He HY, Ray B, Dennis K,Quinlan EM (2007) Experience-dependent recovery of vision following chronic deprivation amblyopia. Nat Neurosci 10:1134 –1136.
Kavanagh, S, Howe I, Brashear HR, Wang D, Baelen BV, Todd M, Schwalen S. (2011) Long-term response to galantamine in relation to short-term efficacy data: pooled analysis in patients with mild to moderate Alzheimer’s disease. Curr Alzheimer Res Jan 11.
Keller C, Kadir A, Forsberg A, Porras O, Nordberg A. (2010) Long-term effects of galantamine treatment on brain functional activities as measured by PET in Alzheimer’s disease patients. J Alzheimers Dis. Dec 14.
Koepsell TD, Kurland BF, Harel O, Johnson EA, Zhou XH, Kukull WA. (2008) Education, cognitive function, and severity of neuropathology in Alzheimer disease. Neurology. May 6;70(19 Pt 2):1732-1739.
Lahiri DK, Chen DM, Lahiri P, Bondy S, Greig NH (November 2005). “Amyloid, cholinesterase, melatonin, and metals and their roles in aging and neurodegenerative diseases”. Ann. N. Y. Acad. Sci. 1056: 430–4.
Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O’Leary OF, Castre, E, Maffei L (2008) The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science 320:385–388.
Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA,
Münch G. (2008) Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer’s disease. Adv Drug Deliv Rev. Oct-Nov;60(13-14):1463-70.
Redolat R, Mesa-Gresa P. (2011) Potential Benefits and Limitations of Enriched
Environments and Cognitive Activity on Age-Related Behavioural Decline. Curr Top Behav Neurosci. Jun 4.
Spindler M, Beal MF, Henchcliffe C. Coenzyme Q10 effects in neurodegenerative disease. Neuropsychiatr Dis Treat. 2009;5:597-610.
Suzuki A, Stern SA, Bozdagi O, Huntley GW, Walker RH, Magistretti PJ, Alberini CM (2011) Astrocyte-neuron lactate transport is required for long-term memory formation. Cell. 2011 Mar 4; 144(5):810-23.
Van Puyvelde K, Mets T. (2011) Galantamine (Reminyl) once daily outcome and satisfaction survey (RODOS) in mild to moderate Alzheimer’s disease: A study in a real life population. Geriatr Gerontol Int Jan 4. doi: 10.1111/j.1447-0594.2010.00674.
Wada A, Yokoo H, Yanagita T, Kobayashi H. (2005) Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases. J. Pharmacol Sci. 2005 Dec;99(4):307-21.
Wang XC, Zhang YC, Chatterjie N, Grundke-Iqbal I, Iqbal K, Wang JZ (June 2008). “Effect of melatonin and melatonylvalpromide on beta-amyloid and neurofilaments in N2a cells”. Neurochem. Res. 33 (6): 1138–44.
Zhang C, Browne A, Child D, Tanzi RE. (2010) Curcumin decreases amyloid-beta peptide levels by attenuating the maturation of amyloid-beta precursor protein. J Biol Chem. Sep 10;285(37):28472-8.