Alzheimer’s Treatment Protocol Released This Week!

I’ve written several times in recent months about my and Dr. Daley’s upcoming book: Alzheimer’s, Memory Loss and MCI: The Latest Science for Prevention and Treatment. We finally launched the book on Amazon.com and it is now available. Here is the link: http://www.amazon.com/Alzheimers-Memory-Science-Prevention-Treatment/dp/1470030470/ref=sr_1_1?s=books&ie=UTF8&qid=1343166651&sr=1-1&keywords=Alzheimer%27s%2C+Memory+Loss%2C+and+MCI+The+Latest+Science+for+Prevention+and+Treatment

We believe the program described in our book offers true hope for many of the 5.4 million Americans currently suffering from Alzheimer’s (AD) and millions more who would like to prevent it. Here’s why:

We spent an entire year researching the scientific literature for six prime components:

1.      The mechanisms underlying the accumulation of beta amyloid plaques and neurofibrillary tangles

2.      The enzyme systems and other biochemistry behind both of these pathologic structures

3.      What factors were instrumental in propelling these enzyme systems forward

4.      What factors, alone or in combination, were shown effective at mitigating those processes

5.      The role these two pathologic structures play in the destruction of brain cells

6.      Other accompanying processes that also contribute to brain cell loss: oxidative stress, glycation and inflammation

We identified nine biochemical avenues, seven of which are destructive to brain cells and two of which are nurturing or protective.

We identified 33 elements among lifestyle change, nutritional supplements, crucial bioidentical hormone replacement and a few highly effective prescription medications (none of which are FDA approved for Alzheimer’s!), all of which influence one or more of these nine avenues – either to inhibit the destructive avenues or promote and support those nurturing avenues.  

Each of these elements, by itself, has proven efficacy. Some, when used in combination, have demonstrated additive value. Yet, remarkably, no one has ever assembled all 33 elements into one comprehensive treatment program. In this book, we describe such a program and reduce it to six steps that can be taken by a motivated Alzheimer’s (AD) or MCI (mild cognitive impairment or pre-Alzheimer’s) patient or anyone who would like to prevent AD.

Our book describes in great detail exactly what to do to put these 33 elements to use for healing. This program puts the patient back in the driver’s seat – in control of the most effective modalities available today that we believe can slow, very possibly arrest and even possibly reverse Alzheimer’s, particularly if begun in the early stages of the disease.

What choice do AD victims and their families have today? They can rally around the cause, read books of touching stories and articles about the hope of new research and look to the community for palliative support. Or they can DO SOMETHING:  apply themselves to a science-backed comprehensive program with a goal of actually impacting their disease and enhancing their lives. We feel very strongly about our book and implore you to use it, teach it and let others know about it. May you know success.

David Leonardi, M.D. CNS, ABAAM

For Alzheimer's - something to DO, NOW...

There are a number of supplements with activity directly against the pathology in the Alzheimer’s brain. Here is just one, along with the published evidence (see references below).

Acetyl-L-Carnitine (ALCAR) is a nutritional supplement long known to have beneficial effects on the brain. In fact, more recent studies in animal models of AD showing that ALCAR inhibits several key pathways in the development of AD, including oxidative damage, the production of beta-amyloid protein, the cleavage of tau protein, apoptosis (cell self-destruction), and cellular stress intolerance.^1-8

In addition, no fewer than seven double-blind placebo-controlled human trials of ALCAR in AD patients, using from 1.2 to 3 grams daily, have shown that this supplement may slow the decline in or improve performance on cognitive function tests.^9-15

If anyone’s interested in a potential real solution to AD now, we’ve assembled approximately thirty elements backed by similar data that can be done now to slow progress, possibly arrest and potentially even reverse AD. We assembled them into a 6-step program in our upcoming book: Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment. We hope to have it on Amazon by the 2^nd week of June.

1.         H. M. Abdul et al., Acetyl-L-Carnitine-Induced Up-Regulation of Heat Shock Proteins Protects Cortical Neurons against Amyloid-Beta Peptide 1-42-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s Disease,” Journal of Neuroscience Research 84, no. 2 (2006): 398–408.

2.         G. Traina et al., “In the Rat Brain Acetyl-L-Carnitine Treatment Modulates the Expression of Genes Involved in Neuronal Ceroid Lipofuscinosis,” Molecular Neurobiology 38, no. 2 (2008): 146–52.

3.         G. Traina, G. Federighi, and M. Brunelli, “Up-Regulation of Kinesin Light-Chain 1 Gene Expression by Acetyl-L-Carnitine: Therapeutic Possibility in Alzheimer’s Disease,” Neurochemistry International 53, no. 6–8 (2008): 244–7.

4.         R. Epis et al., “Modulatory Effect of Acetyl-L-Carnitine on Amyloid Precursor Protein Metabolism in Hippocampal Neurons,” European Journal of Pharmacology 597, no. 1–3 (2008): 51–6.

5.         J. Suchy, A. Chan, and T. B. Shea, “Dietary Supplementation with a Combination of Alpha-Lipoic Acid, Acetyl-L-Carnitine, Glycerophosphocoline, Docosahexaenoic Acid, and Phosphatidylserine Reduces Oxidative Damage to Murine Brain and Improves Cognitive Performance,” Nutrition Research 29, no. 1 (2009): 70–4.

6.         G. Traina et al., “Cytoprotective Effect of Acetyl-L-Carnitine Evidenced by Analysis of Gene Expression in the Rat Brain,” Molecular Neurobiology 39, no. 2 (2009): 101–6.

7.         J. C. Shenk et al., “The Effect of Acetyl-L-Carnitine and R-Alpha-Lipoic Acid Treatment in ApoE4 Mouse as a Model of Human Alzheimer’s Disease,” Journal of the Neurological Sciences 283, no. 1–2 (2009): 199–206.

8.         Y. Y. Yin et al., “Acetyl-L-Carnitine Attenuates Okadaic Acid Induced Tau Hyperphosphorylation and Spatial Memory Impairment in Rats,” Journal of Alzheimer’s Disease 19, no. 2 (2010): 735–46.

9.         L. J. Thal et al., “A 1-Year Multicenter Placebo-Controlled Study of Acetyl-L-Carnitine in Patients with Alzheimer’s Disease,” Neurology 47, no. 3 (1996): 705–11.

10.       J. O. Brooks et al., “Acetyl L-Carnitine Slows Decline in Younger Patients with Alzheimer’s Disease: A Reanalysis of a Double-Blind, Placebo-Controlled Study Using the Trilinear Approach,” International Psychogeriatrics 10, no. 2 (1998): 193–203.

11.       G. Salvioli and M. Neri. “L-Acetylcarnitine Treatment of Mental Decline in the Elderly,” Drugs Under Experimental and Clinical Research 20, no. 4 (1994): 169–76.

12.       M. Sano et al., “Double-Blind Parallel Design Pilot Study of Acetyl Levocarnitine in Patients with Alzheimer’s Disease,” Archives of Neurology 49, no. 11 (1992): 1137–41.

13.       A. Spagnoli et al., “Long-Term Acetyl-L-Carnitine Treatment in Alzheimer’s Disease,” Neurology 41, no. 11 (1991): 1726–32.

14.       C. Cipolli and G. Chiari, [“Effects of L-Acetylcarnitine on Mental Deterioration in the Aged: Initial Results,”]. La Clinica Terapeutica 132, no. 6 Suppl. (1990): 479–510. [in Italian].

15.       W. M. Herrmann, B. Dietrich, and R. Hiersemenzel. “Pharmaco-Electroencephalographic and Clinical Effects of the Cholinergic Substance—Acetyl-L-Carnitine—in Patients with Organic Brain Syndrome,” International Journal of Clinical Pharmacology Research 10, 1–2 (1990): 81–4.

Beyond Palliation. Something to do NOW.

There are a number of supplements with activity directly against the pathology in the Alzheimer’s brain. Here is just one, along with the published evidence (see references below).

Acetyl-L-Carnitine (ALCAR) is a nutritional supplement long known to have beneficial effects on the brain. In fact, more recent studies in animal models of AD showing that ALCAR inhibits several key pathways in the development of AD, including oxidative damage, the production of beta-amyloid protein, the cleavage of tau protein, apoptosis (cell self-destruction), and cellular stress intolerance.1-5

In addition, no fewer than seven double-blind placebo-controlled human trials of ALCAR in AD patients, using from 1.2 to 3 grams daily, have shown that this supplement may slow the decline in or improve performance on cognitive function tests.6-13

If anyone’s interested in a potential real solution to AD now, we’ve assembled approximately thirty elements backed by similar data that can be done now to slow progress, possibly arrest and potentially even reverse AD. We assembled them into a 6-step program in our upcoming book: Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment. We hope to have it on Amazon by the 2nd week of June.

1.         H. M. Abdul et al., Acetyl-L-Carnitine-Induced Up-Regulation of Heat Shock Proteins Protects Cortical Neurons against Amyloid-Beta Peptide 1-42-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s Disease,” Journal of Neuroscience Research 84, no. 2 (2006): 398–408.

2.         G. Traina et al., “In the Rat Brain Acetyl-L-Carnitine Treatment Modulates the Expression of Genes Involved in Neuronal Ceroid Lipofuscinosis,” Molecular Neurobiology 38, no. 2 (2008): 146–52.

3.         G. Traina, G. Federighi, and M. Brunelli, “Up-Regulation of Kinesin Light-Chain 1 Gene Expression by Acetyl-L-Carnitine: Therapeutic Possibility in Alzheimer’s Disease,” Neurochemistry International 53, no. 6–8 (2008): 244–7.

4.         R. Epis et al., “Modulatory Effect of Acetyl-L-Carnitine on Amyloid Precursor Protein Metabolism in Hippocampal Neurons,” European Journal of Pharmacology 597, no. 1–3 (2008): 51–6.

5.         J. Suchy, A. Chan, and T. B. Shea, “Dietary Supplementation with a Combination of Alpha-Lipoic Acid, Acetyl-L-Carnitine, Glycerophosphocoline, Docosahexaenoic Acid, and Phosphatidylserine Reduces Oxidative Damage to Murine Brain and Improves Cognitive Performance,” Nutrition Research 29, no. 1 (2009): 70–4.

6.         Y. Y. Yin et al., “Acetyl-L-Carnitine Attenuates Okadaic Acid Induced Tau Hyperphosphorylation and Spatial Memory Impairment in Rats,” Journal of Alzheimer’s Disease 19, no. 2 (2010): 735–46.

7.         L. J. Thal et al., “A 1-Year Multicenter Placebo-Controlled Study of Acetyl-L-Carnitine in Patients with Alzheimer’s Disease,” Neurology 47, no. 3 (1996): 705–11.

8.         J. O. Brooks et al., “Acetyl L-Carnitine Slows Decline in Younger Patients with Alzheimer’s Disease: A Reanalysis of a Double-Blind, Placebo-Controlled Study Using the Trilinear Approach,” International Psychogeriatrics 10, no. 2 (1998): 193–203.

9.         G. Salvioli and M. Neri. “L-Acetylcarnitine Treatment of Mental Decline in the Elderly,” Drugs Under Experimental and Clinical Research 20, no. 4 (1994): 169–76.

10.       M. Sano et al., “Double-Blind Parallel Design Pilot Study of Acetyl Levocarnitine in Patients with Alzheimer’s Disease,” Archives of Neurology 49, no. 11 (1992): 1137–41.

11.       A. Spagnoli et al., “Long-Term Acetyl-L-Carnitine Treatment in Alzheimer’s Disease,” Neurology 41, no. 11 (1991): 1726–32.

Hormone Depletion and Risk of Alzheimer’s Disease

Hormone Depletion and Risk of Alzheimer’s Disease

It is estimated that nearly 500,000 cases of Alzheimer’s (AD) will be diagnosed this year, approximately one every 69 seconds. As we all know, AD preferentially attacks older folks. Fourteen percent of all people aged 71 and older have dementia. But 71 is not very old these days. So many people in their 70s and even 80s are active physically and mentally and are enjoying life with family and leisure activities. Yet one in six women and one in ten men aged 55 and older will be demented at some time in their life.

It’s not a coincidence that Alzheimer’s risk increases with age while hormone levels decline with age. Is there a link? The biochemistry behind the development of AD certainly supports a very strong and direct link. Testosterone, estradiol, progesterone, DHEA and melatonin are all hormones that decline with age, yet play a critical part in protecting the brain from the ravages of memory loss, brain cell loss and the pathologic processes of AD itself. I don’t have time to cover all these today but I can start with testosterone and try to cover the others soon.

Testosterone is, of course, designated a male hormone but plays a crucial role in life for women as well. Women have only about 10% as much testosterone as men but that 10% is important for many functions, including brain power! Here are just a few pieces of evidence.

In population studies of normal men, those with higher testosterone levels were shown to have better cognitive function than those with lower levels.^1,2

In clinical trials of testosterone replacement, normal aging men with testosterone levels at the lower end of the normal range experienced improvements in both verbal and spatial memory when the level was raised to the upper normal range.³

But how about men with Alzheimer’s? Well, testosterone replacement was also very effective in improving both verbal and spatial memory in a study of men with either Alzheimer’s or mild cognitive impairment (pre-Alzheimer’s).⁴

One of the two hallmarks of AD is the accumulation of beta amyloid protein, forming plaques in the AD brain.

Testosterone influences brain levels of beta amyloid through two other hormones: dihydrotestosterone (DHT) and estradiol (a female hormone). Some of the testosterone in both men and women is converted by the body into these other two hormones. So the more testosterone we have, the more DHT and estradiol our bodies can make. Both DHT and estradiol influence brain beta amyloid by stimulating the activity of an enzyme called neprilysin.^5,6 Neprilysin cleaves beta amyloid into smaller, more soluble components that can be removed from the brain. Estradiol also eliminates beta amyloid by multiple mechanisms that I can discuss in a later blog.

Beta amyloid (the harmful protein) comes from the cleavage of amyloid precursor protein (APP) by the enzyme beta secretase. When APP is cleaved by an enzyme called alpha secretase, a harmless soluble form of amyloid—alpha amyloid—is made. Testosterone has been shown to increase the production of alpha amyloid at the expense of production of beta amyloid.⁸ To put it simply, testosterone reduces the production of beta amyloid in the brain!

It’s important to realize also, why beta amyloid is associated with AD – because it is directly toxic to brain cells. It suppresses their activity to the point that they eventually just die. In addition to reducing beta amyloid production and enhancing its removal, testosterone has been shown to directly protect brain cells from the toxicity of beta amyloid. It does so by increasing the production of a brain-protective protein called HS Protein 70.¹⁰

The second hallmark of AD is the formation of neurofibrillary tangles (NFTs) from the collapse of a protein in brain cells called tau. Tau supports the brain cell structurally, somewhat like the steel frame inside a commercial building. When the tau collapses, the brain cell dies because it looses it’s important structural integrity. Tau collapses and forms NFTs  because it is cleaved by destructive enzymes. One of these bad enzymes that cleaves the tau protein is called calpain. Testosterone actually blocks the calpain enzyme, inhibiting NFT formation.⁹ In an extension of this finding, the reduction in NFT formation by testosterone was further confirmed to improve brain-cell survival.⁹

I’ve got to get back to my day job, now but I can tell you that the evidence for protecting the brain from deterioration is no less impressive for estradiol, progesterone, DHEA and melatonin. I’ll try to fill you in on these later. The important point is that hormone depletion is related epidemiologically and biochemically to AD. When those two types of evidence are combined the point is very difficult to deny. Hormone replacement (HRT), then, becomes a very promising technique for protecting the brain – something we’ve known at the Leonardi Institute for some time now. And I can tell you our bioidentical HRT patients are thriving physically and mentally, on par with people twenty to thirty years their junior! All this and much more about AD is revealed in my and Dr. Nathan Daley’s upcoming book: Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment, which should be released sometime in May. More soon, I hope and a great day to all!

Dr. Dave Leonardi

References:

1.         1. Yaffe, K., L. Y. Lui, J. Zmuda, and J. Cauley. 2002. Sex hormones and cognitive function in older men. Journal of the American Geriatrics Society 50 (4): 707–12.

2.         2. Barrett-Connor, E., D. Goodman-Gruen, and B. Patay. 1999. Endogenous sex hormones and cognitive function in older men. The Journal of Clinical Endocrinology and Metabolism 84 (10): 3681–5.

3.        3. Cherrier, M. M., A. M. Matsumoto, J. K. Amory, M. Johnson, S. Craft, E. R. Peskind, and M. A. Raskind. 2007. Characterization of verbal and spatial memory changes from moderate to supraphysiological increases in serum testosterone in healthy older men. Psychoneuroendocrinology 32 (1): 72–9.

4.         4. Cherrier, M. M., A. M. Matsumoto, J. K. Amory, S. Asthana, W. Bremner, E. R. Peskind, M. A. Raskind, and S. Craft. 2005. Testosterone improves spatial memory in men with Alzheimer disease and mild cognitive impairment. Neurology 64 (12): 2063–8.

5.         5. Yao, M., T. V. Nguyen, E. R. Rosario, M. Ramsden, and C. J. Pike. 2008. Androgens regulate neprilysin expression: Role in reducing beta-amyloid levels. Journal of Neurochemistry 105 (6): 2477–88.

6.         6. Yang, H. Q., Z. K. Sun, Q. H. Jiang, Q. Shang, and J. Xu. 2009. [Effect of estrogen-depletion and 17beta-estradiol replacement therapy upon rat hippocampus beta-amyloid generation]. Zhonghua Yi Xue Za Zhi 89 (37): 2658–61. [in Chinese].

7.         7. Gouras, G. K., H. Xu, R. S. Gross, J. P. Greenfield, B. Hai, R. Wang, and P. Greengard. 2000. Testosterone reduces neuronal secretion of Alzheimer’s beta-amyloid peptides. Proceedings of the National Academy of Sciences of the United States of America 97 (3): 1202–5.

8.         8. Park, S. Y., C. Tournell, R. C. Sinjoanu, and A. Ferreira. 2007. Caspase-3- and calpain-mediated tau cleavage are differentially prevented by estrogen and testosterone in beta-amyloid-treated hippocampal neurons. Neuroscience 144 (1): 119–27.

9.         9. Zhang, Y., N. Champagne, L. K. Beitel, C. G. Goodyer, M. Trifiro, and A. LeBlanc. 2004. Estrogen and androgen protection of human neurons against intracellular amyloid beta1-42 toxicity through heat shock protein 70. The Journal of Neuroscience 24 (23): 5315–21.

How Did I Get Alzheimer's?

I can imagine being officially diagnosed with Alzheimer's disease (AD). My first thought would be "No, this can't be!"

My second would be "How did this happen?"

The etiology of AD is multifactorial and a bit complex. But by gaining some understanding of those multiple causes we open up opportunities to prevent and even treat the disease.  

To get AD, one must have the genetic disposition to be susceptible. Then the factors of aging play a role in actually getting the disease to develop. By genetic disposition I don't mean having "the Alzheimer's gene". Very few AD victims have genetically transmitted AD. What I mean by being genetically susceptible is that one does not have the genetics to be particularly protected from the disease. This is true for most of us. So we're all at risk. In fact, AD is now the 6th leading cause of death worldwide.

So given that nearly all of us have the genetic capability to develop AD, what specifically is going on to cause the disease? And, more importantly, is there anything I can do to prevent or treat the disease if I’m already diagnosed?

As I mentioned, AD is multifactorial in its causation. The brain is being attacked along seven different avenues, much like a city under siege by an enemy approaching from seven different directions. Here are the seven avenues of attack:

1.     Oxidative Stress

2.     Glycation

3.     Inflammation

4.     Production of beta amyloid protein

5.     Reduced elimination of beta amyloid protein

6.     Brain cell destruction by beta amyloid protein

7.     Development of abnormal tau protein

Please don’t let the medical terminology discourage you. I can simplify these terms for you, albeit not in this blog alone. It will take a number of sessions to get all this on the table. For now, it’s important to understand that all seven of these “attacks” can be defended. And doing so can be very worthwhile. In fact the first three are related directly to aging itself and to our most destructive age-related diseases. For today, let’s just look at number one: oxidative stress.

If you remember from high school chemistry, an atom has a nucleus called a proton, which is orbited by electrons. Electrons like to travel in pairs. And if an electron is all by itself orbiting the proton, that atom is a free radical. That electron will do anything it can to get a mate, so what it typically does is jump ship to the next atom, knock an electron out of its orbit and take its mate. Then the atom that lost the electron becomes the free radical and it immediately goes to the next atom, knocks an electron out of its orbit and takes its mate and so on. What we end up with is a rapid fire transfer of electrons. This is called oxidative stress because every time there is an electron transfer, there is a potential structure change in a molecule. Most of the time it is of no consequence; it may simply be a skin cell ready to slough off anyway. But when brain cells are exposed to oxidative stress (electron transfers and structural changes) it often results in the death of the brain cell. Oxidative stress is one of the primary mechanisms by which we lose brain cells--as in Alzheimer’s, Parkinson’s and even normal brain ageing.

So, clearly, we would like to control oxidative stress if we could.  And the degree of oxidative stress that we undergo is related to the degree of pollution to which we are exposed. For example, when you’re driving in any degree of traffic, do you remember to use the recirc button in your car? That is the button that circulates cabin air around and around and prevents outside air from entering the car. If outside air is being sucked in from the outside, you’re breathing in carbon monoxide which is colorless, odorless and tasteless, so you can’t detect it, and you are also breathing in diesel particulates and other products of hydrocarbon combustion. These not only damage our lungs, but create a shower of free radicals in our bodies. So use your recirc button constantly until you’re completely out of traffic, and then open your vehicle to fresh air.

And what about your water source? Most drinking water is either carbon filtered or simply direct from the tap. Carbon filtration removes toxins and impurities but leaves the minerals in place. Some minerals (e.g. calcium, potassium and magnesium) are beneficial but many others (e.g. aluminum, mercury and, when in excess – even iron) are strong pro-oxidants. That means they promote free radicals and electron transfers and are toxic to brain cells. Reverse osmosis as well as distillation (another processing technique of boiling the water into vapor and recondensing) take out virtually all the impurities and minerals, both toxic and healthful. These are great systems for eliminating those pro-oxidant metals and protecting our brains but we should then be careful to supplement calcium, magnesium and potassium in some form.

Pesticides found in conventional produce also create free radicals. Pesticides are removed from our blood by the liver in a detoxification process. But in that process, a huge shower of free radicals is produced. Organic produce, containing little or no pesticide, doesn’t require hepatic detoxification, so no free radicals are produced in response to eating it.

 Eating produce itself, however, is important because fruits and non-starch vegetables are the very foods that contain antioxidants.  Antioxidants are molecules that can accept the free radical and neutralize it without creating another one, stopping the chain of electron transfers. They are able to do this just by their chemical structure.  Antioxidants are substances such as beta carotene, Vitamins C and E, selenium, alpha lipoic acid, Co Q10, N-Acetyl Cysteine and others. In addition to organic produce, it’s is good idea to take a broad spectrum of antioxidant supplement. Antioxidants work in different tissues by different mechanisms and they complement each other. Some actually help to regenerate others. For example, Vitamin C regenerates vitamin E in the body.

In summary, reducing oxidative stress is a good way to protect your brain and one of many steps we can take to combat AD. To do so, make your air and water as free as possible from free radical-generating pollutants, eat plenty of organic non-starch vegetables and fruits and take a reasonable broad spectrum antioxidant supplement.

But to have a substantial impact on AD, one must defend the brain against all seven of the avenues of attack. I’ll write more on the other six avenues in future blogs along with something about the two “supply avenues” to keep open: cognitive enhancers and brain plasticity. Sorry this is more complex than taking a pill once a day but until we have such a magic bullet, at least we have an effective means of combating this otherwise invariably fatal disease. If you want all the answers now, our book, “Alzheimer’s, Memory Loss, MCI: The Latest Science for Prevention and Treatment” will be published in early May, 2012. It was written by me and my associate, Nathan Daley, M.D.

Alzheimer's is Treatable

Chuck came to see me with a complaint of memory loss and becoming easily confused. Chuck was 79 and lived alone so had plenty of reason to be alarmed. We tested Chuck and found him to have early Alzheimer's disease (AD). Rather than advising him to get his affairs in order and schedule some custodial care, we invited Chuck to participate in our 6 Step Program for the treatment of Alzheimer's. Chuck readily agreed to do so and 6 months later had improved in 5 of 6 cognitive categories that typically deteriorate in Alzheimer's.  Everyone thinks that a diagnosis of Alzheimer's disease is a death sentence. Actually, if you're willing to do something about it, it may be just a wake-up call. Your brain is telling you that you've been living in a manner that doesn't provide it the environment it prefers. It's asking you to change that environment. If you do, chances are that you can reverse your disease. At least, Dr. Nathan Daley and I strongly believe that to be true and we're hell bent to prove it. Chuck is job one, with many more to follow. 

Nathan Daley, M.D. and I, David Leonardi, M.D. have devoted the better part of the last 18 months to the research of Alzheimer's disease. We're not new at this. I've been practicing Preventive Medicine for 13 years and Dr. Daley completed his residency in Preventive Medicine at U.C. San Diego in 2010 along with an Integrative Medicine Fellowship at the U. of Arizona the same year. We've just written a book about our findings that will be published in December of this year (2011). Unlike dozens of other books on the topic of Alzheimer’s disease, it's not about how to deal with the inevitable decline. It's about how to TREAT the disease with the intent of reversing it. I say intent because we've not proven it (yet). But we intend to. If you're interested, here's how. 

You see, there is no proven cure yet for Alzheimer's because the drug companies for decades have been looking for the magic bullet - a single drug to pop once a day and solve the problem, much like Lipitor for preventing heart attacks. Well, hold on. Sorry, but Alzheimer's is not that simple. Heart attacks aren't simple either, but not nearly as complex as Alzheimer's. We humans are all about biochemistry. In fact, we're just a big biochemistry set in action. And if you examine the biochemistry of Alzheimer's, you'll see it has dozens of components. There are dozens of chemical reactions that lead up to the loss of brain cells. These reactions can be divided into 9 categories that we call the nine avenues. Seven of the avenues are destructive and need to be defended. The other two are like supply avenues and need to be replenished. A single drug couldn't possibly have the capacity to function correctly along all nine avenues. If it aids with one avenue, the disease will march ahead along the other eight. That's why the current medications for Alzheimer's, which merely squeeze more acetylcholine out of our brain cells only temporarily improve or stabilize the patient. 

To actually improve the Alzheimer's brain, we have to function along all 9 avenues. This can only be done by a comprehensive approach - one that employs lifestyle change, specific nutritional supplements and even hormone replacement. Don't get discouraged. It's not that complicated. If Chuck can do it, so can you. It's all spelled out in our book, but I'll try to give you a sense of it here. The medical literature is replete with thousands of studies on Alzheimer's and the biochemistry behind it. And these brilliant scientists have not left out the studies on reversing that biochemistry. Clinical trials are being published on a daily basis.

The biochemical pathways by which Alzheimer's develops aren't perfectly understood but we know a LOT. Without driving you nuts with the science, let me just say that the biochemical culprits identified that kill brain cells are two proteins that accumulate in the Alzheimer's brain. These two toxic proteins are beta amyloid and tau. These proteins are actually normal ones and it is indeed normal to have these in your brain. We all do. The difference with Alzheimer's is that the beta amyloid protein accumulates in large quantities and the tau protein is disfigured. It all has to do with biochemical reactions occurring in the brain that have gone awry. And the reason they've gone awry is that the patient has first, a possible genetic predisposition to that abnormal biochemistry and second, has provided an environment for his or her brain cells to promote that biochemistry (lifestyle and other problems). But we believe that even those with a genetic predisposition to the disease can reverse it by altering that biochemistry. 

In our research we identified over 30 elements that can reverse various aspects of that biochemistry. They all function along one or more of the 9 avenues I mentioned above. While each of these 30 elements has demonstrated benefits in studies published in peer-reviewed medical journals, not a single one by itself amounts to a cure (just like there is no single drug cure). But as we made discovery after impressive discovery in our literature search, we began to be overwhelmed by one central thought: If each of these elements has significant proven benefit along one or more biochemical avenues of Alzheimer's, why hasn't anyone assembled all of them into one comprehensive program? To provide you with an analogy, when Henry Ford was building his first automobile he needed a wheels, a motor, a drive train, a steering mechanism and brakes. Mr. Ford didn't look at any one of those single parts, such as the motor and say, "Well, I can see a benefit, but it won't get me across town, so forget it". Instead, he saw that the whole can be greater than the sum of the parts. So he assembled the parts and built himself a Ford. In the world of Alzheimer's research we're missing the forest for the trees. We have over 30 great trees but no one ever assembled them to create the forest. So, we did it. And Chuck is our first beneficiary. 

These 30-some elements are in the categories of lifestyle change, nutritional supplements and bioidentical hormones. Now, two of these 3 categories can be a bit frightening to some people. Nutritional supplements aren't too scary but lifestyle change might concern some people who prefer to be sedentary and eat junk food. And bioidentical hormone replacement likely sounds too complicated or controversial to others. Yet, if a drug company handed you a pill that promised to make you better, or even slow your brain deterioration you'd likely swallow it before they could hand you the invoice.  

As for lifestyle change, don't worry about a thing. We're just going to recommend the healthiest foods on the planet because they've been demonstrated in published trials to alter the Alzheimer's biochemistry. Then we'll suggest some physical activity that you can do within any limitations you may have. You need not become an Olympic athlete - just move to the best of your ability. Why? You got it - because that also alters the Alzheimer's biochemistry. 

Now, in terms of bioidentical hormone replacement, consider this. As we age, hormone levels decline significantly. As we age and hormone levels decline, Alzheimer's risk rises. Coincidence? Actually, no. Study after study shows how certain hormones are critically important for optimal brain function and more importantly, have a direct inhibitory effect on Alzheimer's biochemistry. Indeed, testosterone, the quintessential male hormone, plays a key role in combating the formation of beta amyloid protein in the brain. The same is true for the female hormones estradiol and progesterone. What's important is how they're administered and in what specific form. All the details appear in our book. But a healthy diet, exercise and the appropriate hormone replacement are not likely to provide the best possible benefit for Alzheimer's. In fact, that is very unlikely. These encompass only about 9 or 10 of our 30-some elements. For optimal benefit, these should be combined with the nutritional supplements we recommend in our book. 

If you've done the math, you may be coming to the realization that we recommend a large number of supplements. We do, only because each has very promising benefits according to clinical studies. Because taking the full complement of our recommendations would entail more pills than anyone would accept, we've combined the majority of these into a berry flavored powder for our patients that can be mixed with water or mixed into a smoothie, if preferred. So we've undertaken considerable effort to make this program as palatable as possible for people with Alzheimer's disease to follow. Before I finish this article, I'd like to just give you a flavor (no pun intended) about a couple of the elements we use and how they work. I'm hoping that will provide you with a sense of how powerful they can be when combined. That in turn, may provide you with hope and some level of confidence that your fate is far from sealed. 

I'll start with testosterone. Here are just a few of the facts we present in our book. In studies of normal men, higher testosterone levels are associated with better cognitive function. Furthermore, in men with levels of testosterone at the lower end of he normal range, raising their levels to upper normal resulted in improvements in both verbal and spatial memory. Let's go one step further. Testosterone has also been studied in actual patients with Alzheimer's disease and has been shown to improve verbal and spatial memory in these Alzheimer's patients as well. This is just a taste of the benefits seen with testosterone for Alzheimer's. In our book we actually cite 47 published studies on testosterone, Alzheimer's disease and cognition. Testosterone, again, is only one of over 30 elements in our program. 

Let's take a brief look at a nutritional supplement with which many people are familiar - curcumin. Curcumin is a component of the Indian spice, turmeric. It's been well shown to have anti-inflammatory, antioxidant and anti-cancer benefits. In terms of Alzheimer's disease, curcumin has been demonstrated to do all of the following: 

1. Help to bind pro-oxidative metals such as copper and iron that create excessive oxidation in the brain and damage brain cells.

2. Reduce the formation of beta amyloid protein in the brain. 

3. Increase the clearance of beta amyloid protein from the brain, something Alzheimer's patients do very poorly.