Alzheimer’s Part-2

Alzheimer’s Part 2 Part 3


Conventional Treatment


Conventional Alzheimer’s treatment relies heavily on pharmacologic modulation and raising acetylcholine levels in the brain. There may be small symptomatic improvement initially, although the underlying process of the disease is unaffected.

The acetylcholinesterase inhibitors are typically the first line of drugs for mild to moderate. The drugs currently used are Aricept, Exelon, Razadyne (which is galantamine), and is also an over-the-counter nutritional. Although studies have repeatedly found that these acetylcholinesterase inhibitors reduce Alzheimer’s symptoms at first, they do not halt or reverse the underlying disease. The next group are the NMDA receptor blockers, which is Namenda, an N-methyl-D-aspartate receptor antagonist.

How do therapies treat the underlying disease:

The homework abnormality in Alzheimer’s is the accumulation of beta amyloid plaque and neurofibrillary tangles in the brain. In healthy brains, a significant amount of plaque does not occur. This plaque is formed from a specific protein called amyloid precursor protein (APP). But, the protein does not do the manufacturing on its own.

It relies on the action of two main enzymes: One is called beta secretase, and the other is gamma secretase.

There is also an alpha secretase, which make an alpha amyloid protein, which is turned into excitable, harmless proteins, which do not change normal brain function.

My goal is to stimulate the good enzymes that turn APP into harmless protein and inhibit the beta amyloid protein. It is also now known, that in an Alzheimer’s brain there are also neurofibrillary tangles.

In Alzheimer’s brain, the tau protein undergoes excessive phosphorylation, resulting in structural changes called cross-linking in tangles. The brain cell loses its structural integrity, almost like a building collapsing. There are many nutraceuticals that can influence Alzheimer’s in several ways.

We can effect less beta amyloid production as well as increase the clearing of the beta amyloid plaque and produce ewer neurofibrillary tangles.

Remember, the plaquing tangles cause trouble and are toxic to brain cells, literally killing them. Protecting our brain from plaque and tangles is accomplished first by reducing oxidation (free radicals) and glycation.

This in turn will reduce inflammation, improve insulin sensitivity, and improve energy production in the mitochondria.


There are no fewer than 7 double-blind placebo-controlled clinical trials in Alzheimer’s patients which show that this supplement slows the decline on cognitive testing. There is also recent studies showing that it inhibits Alzheimer’s by reducing oxidative damage and production of beta amyloid plaque and the cleavage of pro-proteins, resulting in apoptosis, or cell death of abnormal cells.

Alpha-lipoic Acid (LA):

Alpha-lipoic acid has been shown to improve cognitive function in groups of Alzheimer’s patients. Unfortunately, no significant trials followed because this is not patentable by the drug companies. Research does show that lipoic acid inhibits oxidation and the cellular toxicity of beta amyloids. It also increases glutathione, mitochondrial energy production, and increases mitochondrial number as well as increasing insulin sensitivity. It has consistently demonstrated the ability to dramatically slow progression of dementia.

Vitamins D3, B6, B12:


The benefits of certain B vitamins in the brain are several, but the most important is the control of homocystine. It is a toxic amino acid, and levels are easily measurable in the bloodstream. There is increased risk of Alzheimer’s, which is increased by 50% by every 5-unit rise in homocystine levels. A recent study showed that a level above 14 has an associated double-risk of Alzheimer’s. Homocystine is removed by the body by a process called methylation, and is important to be removed. I keep homocystine to the lower ends of normal range.

In an article published in July 2011 in Alzheimer’s and Dementia there was a clear association between homocystine and Alzheimer’s.

Vitamin D3:

Vitamin D3 works through a multitude of pathways and has been shown to decrease amyloid plaque as well as increase nerve growth factor and lower inflammation. Alzheimer’s patients have lower vitamin D levels than people without the disease.

Coffee, Caffeine:

Caffeine reduces the beta amyloid production, it appears to inhibit pathways that leads to tall fractionation, and exert an anti-inflammatory and antioxidant activity on the brain. Several studies have shown that a middle-aged person who trying 3 to 5 cups of coffee totaling about 300-500-mg of caffeine per day and had a 65% lower risk of developing Alzheimer’s later in life then those who did not drink coffee. My second given caffeine demonstrated significantly less beta amyloidotic in the hippocampus, the brain area related to memory.

Apparently, caffeine and habits beta amyloid plaque by inhibiting the activity of the activity of the harmful enzymes, beta and gamma secretase.


Curcumin binds copper and iron to prevent the oxidative and beta amyloid-producing effects of these metals, and it also appears to interfere with the formation of amyloid plaques once beta amyloid has been created. Other studies had shown that with curcumin there was increase in clearing of the beta amyloid plaque. It stimulates BDNF TO GROW NEW STEM CELLS.

GPC (glycerylphosphorylcholine, phosphatidylcholine, and glutathione):

These drugs not only our a powerful antioxidants, but they can also increase acetylcholine levels. There are many articles in GPC showing how it can significantly benefit dementia patient’s, some of them double-blind proceed vocal controls.


MCT is found in coconut oil and appears to be useful in appears to be useful in improving cognition in Alzheimer’s. In fact, there is now a prescription version called Axona, which is now available, but in my opinion, these are over-priced and totally unnecessary.

Coconut oil and MCT oil are widely available over-the-counter, and did not need a prescription. The benefits of MCT appears to be the ability of these fats to produce elevation of ketones bodies in the bladder and brain, and these ketones act as an alternative two glucose for fueling brain cells.

Brain imaging and basic science studies revealed a glucose metabolism is impaired and Alzheimer’s patient’s, and some referred to it as the third diabetes. These ketones provide an effective fuel for the brain. Ketones have been shown to block the detrimental effects of low oxygen and improving oxygen delivery to the brain.

Ketones increase blood flow to the brain by 39%. Multiple studies have shown that ketones protect the brain from damage caused by interruption of oxygen delivery to the brain. In tissue cultures, ketones have been shown to increase survival in motor neurons.

Ketones significantly reduced the amount of amyloid plaques that develops in mouths in dog models in Alzheimer’s.

The ketones improved daytime activity, increased performance of visual-spatial memory tests, and increased learning. Ketones improve the activity of neurotrophic factors, small proteins that nourish the neurons and let them make neurotransmitters and other chemical signals. The ketones also supply the lipid-building blocks for neurons and essentially new cells. They are a high-energy source that can be used by every organ in the body except the liver.

They protect the brain, reduce formation of free radicals, protect against chemical toxins, and protect against seizure disorders and epilepsy. They have also been found to reduce the liver’s output of glucose, and lower blood sugars in diabetics, as well as protecting against cancer, and improve heart function. Medium-chain triglycerides in coconut oil are an important part of my protocol.

N-acetylcysteine (NAC):

N-acetylcysteine, Omega-3 fatty acids with DHA, phosphatidylserine, glutathione, resveratrol, vitamin C, vitamin E, and beta carotene all have studies showing improvement in memory loss.

Additionally, carnosine and PQQ can regenerate mitochondria as well as improve the outcome of Alzheimer’s. Protein-rich polypeptides (PRP) were also used for amyloid plaque prevention as well as Huperzine A and Bacopa.

There are many other nutraceuticals that are used in my office to improve the outcomes of Alzheimer’s. Anyone reading this with memory loss or Alzheimer’s who is not suffering from known heart disease, in my opinion should stop their ‘statins.

Please refer to other areas of this site concerning ‘statins.

The angiotensin-converting ACE inhibitors as well as angiotensin-receptor blockers are frequently used in the treatment of high blood pressure. Some of the older drugs do not cross the blood-brain barrier. In one study, researchers found that for every year that a person takes essentially active drugs, the rate of cognition decline was reduced by 65%.

In contrast, the incidence of dementia was increased to 20% in those taking the ones that did not enter the brain.

A recent study in 2010, published in the British Medical Journal demonstrated that was taking the angiotensin-receptor blockers had a 19% lower rate of Alzheimer’s than those taking the older ACE inhibitors. I, myself, and taking and ARB that crosses the blood-brain barrier, and I make similar recommendations for my patient’s.

For those without high blood pressure, but at increased risk of dementia or Alzheimer’s, he may discuss with your doctor using a low-dose ARB in hopes of preventing further damage.

Proline-Rich Polypeptides: PRP Complex

Prolene-rich polypeptide complexes, highly stabilized, have been isolated from colostrum. They appear to be highly effective, and in vitro demonstrates they may offer neuro-protection including anti-inflammatory and antioxidant activity, and support mitochondrial function.

In a series of experiments, researchers found that RPR completely abolished amyloid plaque formation, and in a longer study, it was shown that the friables were much shorter and less dense.

There was also noted to be a down-regulation in inflammatory pathways such as the interleukin 1 and tumor necrosis family, and down-regulation in expression associated with amyloid plaque formation.

How Hormones Affect Alzheimer’s:

Is it a coincidence that hormone levels decline with age, or is that alzheimer’s disease increases without age? I think not. As our bodies age from oxidative stress, glycation, inflammation, sleep deprivation, chronic stress, and lifestyle errors, our endocrine glands age too.

Hormones began to decline in his early is age 30. For example, around that age testosterone levels beginning to decline by an average of 1% per year. DHEA drops twice as fast, by 2% per year. Melatonin drops by about 80%, sometime between its peak at age 13 and age 35. Estradiol and progesterone undergo a gradual decline in women.

Hormones are essential for brain health.


Testosterone benefits memory loss in Alzheimer’s in several ways. It reduces beta amyloid production, enhances beta amyloid breakdown and removal, protects brain from beta amyloid already there, and reduces the cleavage of tau to prevent neurofibrillary tangles.

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

Testosterone replacement in normal-aged men experience improvement in both verbal and spatial memory. These studies showed benefit when the testosterone was replaced to the upper limits of normal.

Testosterone influences brain level to beta amyloid through two other hormones:

Dihydrotesterone, and estradiol.

These two hormones stimulate activity of an enzyme called neprilysin, which cleaves beta amyloid into smaller and more soluble components that can be removed by the brain.

Testosterone has been shown to increase the production of alpha amyloid at the expense of beta amyloid production.

To put it simply, testosterone reduces the production of beta amyloid plaque in the brain.

Testosterone also blocks calpain, inhibiting neurofibrillary tangles formation. This reduction in tangles by testosterone was further confirmed to improve brain cell survival. Finally, testosterone has been shown to protect brain cells from the toxicity of beta amyloid by increasing the production of brain-protective protein called HS protein 70.


Estradiol in addition to testosterone, increases the production of alpha amyloid, reducing beta amyloid production. It also increases, like DHT neprilysin, helping break down and remove beta amyloids in the brain.

Estradiol also increases insulin-degrading enzyme, (IDE) and transthyretin, and like testosterone, estradiol boosts production of HSP70, protecting brain cells from amyloid plaque already there.

Of interest to note is postmenopausal women with Alzheimer’s had lower levels of estradiol in the spinal fluid than women without Alzheimer’s, and cognitive tests were higher in women with higher estradiol levels, and women with Alzheimer’s improved when treated with bio-identical estrogen.


When progesterone was administered, it also was shown to slow the production of beta amyloid plaque.

There was an increase in brain levels of BDNF, the important protein that stimulates development of new brain cells, and helps establish connection between brain cells. There was also slowing of the degeneration of tau protein, which begins to process the development of neurofibrillary tangles. Progesterone augments testosterone and estrogen use.

Even though progesterone is a female hormone, I, myself, as well as my male patients, use progesterone to slow the Alzheimer’s process, and for prostate and heart protection.


The benefits of DHEA are many. There is a direct inhibition of the activity of beta secretase, inhibiting beta amyloid formation.

Studies have shown that Alzheimer’s victims have lower DHEA-S levels than matched controls, in the volume of their hippocampus, the memory area of the brain.

The brain shrinks as DHEA-S levels decline. Incubating brain cells with DHEA also lowered interleukin 2, which accelerates the Alzheimer’s process.

A study performed in 2010 on adult mice showed that beta amyloid protein works against the survival of new brain cells that were forming, but that with treatment with DHEA aided both the survival and growth of young brain cells. One of the ways beta amyloid protein kills brain is by opening up calcium channels, and the calcium kills the cell. DHEA has been shown to decrease the calcium influx into the cells by beta amyloid.

A protein called VEGF promotes the delivery of new blood vessels into the brain, and this was increased by DHEA. Other levels showed that low DHEA levels correlated with higher phos relation of tau proteins and beta amyloid relation.


Melatonin has been shown to prevent cell damage induced by beta amyloid in the hippocampus of the brain. This is the primary memory region. Melatonin was shown to greatly reduce oxidation in the brain and improve mitochondrial function.





Ask dr silver if you are a candidate for stem cells!!


Dean Silver, M.D.