Tools for Natural Living

Alzheimer’s disease (AD) is a degenerative neurological disorder characterized by memory loss and general cognitive impairment. While many senior citizens may exhibit signs of moderate to severe dementia, AD is not a normal part of aging. Yet, more than half can attribute declining mental function to AD and not other factors, such as depression, stroke or Parkinson’s disease.

 

AD is not limited to the geriatric population. The term ‘early onset’ AD refers to an afflicted person who is under the age of 65 and it can occur in someone as young as 30 years of age. However, AD is always progressive and eventually fatal. In fact, AD is the seventh leading cause of death in the US, currently affecting more than 5,000,000 people. There is no cure at this time, so it is critical that proactive measures be taken at the first sign of symptoms, or if you are at high risk for developing AD.

 

What is Alzheimer’s disease?

 

This disorder gets its name from the German physician, Alois Alzheimer, who first identified its symptoms in the early 1900s. Since that time, researchers have learned that AD interferes with normal cognitive functioning by disrupting certain metabolic processes in brain cells, causing them to eventually die.

 

The two primary mechanisms by which this self-destruction takes place are the formation of amyloid paques and neurofibrillary tangles in the brain. Plaques are formed when deposits of a fibrous protein known as beta-amyloid become trapped between nerve cells and in parts of damaged neurons. Tangles are formed from bundles of another protein fiber called tau (pronounced ‘wow’), which take up residence inside dying brain cells.

 

Both of these events disrupt metabolic processes necessary to nourish cells and keep them alive. In effect, cellular food supply is cut off and the cells simply starve to death. Since these cells cease functioning, neurotransmission between cells is also cut off, resulting in impaired thinking, recall and even loss of speech or movement.

 

Risk Factors

 

AD is still a relatively poorly understood disease and researchers cannot say for certain what specifically causes brain cell network collapse. However, certain factors have been associated with the risk of developing this disease.

 

Age

The risk of developing AD increases with age, doubling for every five years reached after the age of 65. The chance of developing AD after age 85 increases 50 percent.

 

Family History

The likelihood of developing AD increases when one or more family members have been diagnosed with AD. In fact, AD tends to run in families. Researchers believe that this is due to genetic factors and have identified the suspect gene labeled as APOE, the type of gene responsible for transporting cholesterol to the brain. While everyone inherits some form of this gene from each parent, variations of this gene--APOE-e2, APOE-e3 or APOE-e4—suggest a higher risk of developing AD at some point in life. The presence of APOE-e4, however, often indicates the potential for early onset AD.

 

Obviously, the above risk factors are beyond the control of any individual. However, other risk factors can be avoid, such as:

 

Head Injury

There is a correlation between head trauma and the risk of developing AD. Therefore, it would be prudent to take precautions to avoid head injuries by wearing a helmet or other protective gear when participating in sports or riding a bike.

 

Heart Health

There is also an associated risk of AD occurring and conditions that damage heart muscle and tissue, such as high blood pressure, elevated cholesterol, and diabetes.

 

 

Symptoms and Diagnosis

 

Memory Loss

Forgetting the name of an acquaintance or failing to keep an appointment is normal. However, difficulty recalling well-known information is one of the first signs of AD.

 

Impaired Abstract Thinking

This includes difficulty processing information, such as how to add numbers or following a set of instructions.

 

Personality Changes

Mood swings, anxiety, confusion and/or paranoia may be exhibited.

 

Difficulty Carrying Out Daily Tasks

The AD person may stop suddenly in the middle of performing a simple task, forgetting what to do next. In addition, the person may display poor judgment, such as dressing inappropriately for the weather (i.e., putting on a winter coat in summer).

 

Language Difficulties

The AD afflicted person may not be able to name common objects and forget simple words.

 

Disorientation

People with AD frequently ‘take off’ on their own, forgetting where they are going or how to return home, even when in familiar surroundings.

 

Diagnosis

Early detection is important. While AD cannot be cured, it may be possible to delay its progression. In addition, identifying AD early allows the individual and family to plan appropriately for the future.

 

Currently, there are no medical specialists designated that focus entirely on treating AD. However, initial screening from a primary health care provider may result in a referral to a psychologist or neurologist.

 

The first step to diagnosis begins with a complete review of the medical history of the patient, followed by a physical exam and dementia screening tests. The standard screening test is the MMSE (min-mental screening examination) in which the practitioner will test a variety of mental functions by asking the subject to perform certain tasks, such as repeating a series of words of phrases, or copying a picture.

 

If initial screening warrants further examination, the patient may then undergo neurological testing and, possibly, brain imaging by means of an MRI (magnetic resonance imaging) or a PET (positron emission tomography).

 

 

Recommended Supplements in the Prevention and Treatment of Alzheimer’s Disease

 

Vitamin B12 (Cobalamin)

A deficiency in this vitamin is commonly seen in AD patients. In fact, researchers have found that the greater the deficiency, the more deterioration of cognitive functioning is experienced.

 

In a three-year population study involving 370 non-dementia Swedish adults over 75 years of age, it was determined that those who had low levels of vitamin B had twice the risk of developing AD.

 

Folate (Folic Acid)

The same risk for declining mental function due to vitamin B deficiency is also associated with those with folate levels. Folic acid is necessary in order for the body to synthesize S-adenosylmethionine (SAMe), which is needed for proper neurotransmission in the brain.

 

Omega-3

Fish oils contain fatty acids that impact neurological function, namely the omega-3 oils eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). DHA alone represents up to 50% of the total fatty acid content in the brain and its primary functions are to provide cellular energy and to regulate beta-amyloid release. A 10-year study that followed more than 1,000 geriatric subjects revealed that those deficient in DHA were 67% more likely to develop AD.

 

Coenzyme Q10 (CoQ10)

Research has found that CoQ10 plays a role in mitochondrial function and beta-amyloid production, thereby helping to inhibit the formation of amyloid plaques.

 

Acetyl-L-carnitine (ACL)

This antioxidant is also involved in mitochondria function and offers protection of neurons from beta-amyloid secretion. ACL arginate is a form of carnitine that actually stimulates growth of neurons more than 19% than nerve growth factor, a protein necessary for neuron function and endurance.

 

 

Beneficial Herbs in the Treatment and Prevention of Alzheimer’s Disease

 

Turmeric

This relative of ginger is rich in the antioxidant and anti-inflammatory agent, curcumin. A 2004 study involving mice demonstrated that curcumin reduced beta amyloid accumulation in the brain and, according to the researchers, more effectively than any other drugs being studied for the treatment of AD. A clinical trial to determine the efficacy of curcumin on human subjects was conducted at the UCLA Alzheimer's Disease Center, with results indicating that curcumin reduces amyloid plaques in the human brain.

 

Ginkgo biloba

Ginkgo biloba is valued for many properties, including its antioxidant and anti-inflammatory qualities. This herb is also considered to be a mild vasodilator, neurotransmitter regulator and antiplatelet agent. Studies involving AD patients consistently show an improvement of cognitive function with the introduction of ginkgo extracts. Researchers suspect this is due to the botanical’s ability to reduce brain cholesterol levels and beta-amyloid production and release.

 

Green Tea

Accumulated levels of metals, such as aluminum and iron, have been linked to AD. In excess, these metals promote the production of free radicals. However, the introduction of a chelating agent that will bind with these metals is one way to counteract this mechanism. Green tea contains a high content of catechins, bioflavonoids that exhibit powerful chelating properties as well as antioxidant effects. The green tea catechin of special interest is epigallocatechin gallate (EGCG), which is known to deter beta-amyloid release.

 

Resveratrol

Resveratrol refers to a group of polyphenols found in grapes and red wine. The March 2008 issue of the Journal of Nutrition published the results of a study that found that these polyphenols offered protection from neurologic deterioration following induced stroke in rats. Further, the researchers noted that red wine polyphenol compounds may not only minimize neurological damage after stroke, but there is evidence that these compounds may even be helpful in preventing stroke from occurring.

 

 

Safety Precautions

 

Vitamin B12

Do not supplement with this vitamin if you have Leber's optic atrophy.

 

Folic acid

Supplementation should be supervised if you have a vitamin B-12 deficiency since folic acid can escalate neurological damage caused by low levels of B-12.

 

Omega-3 (EPA/DHA)

Supplementation with omega-3 fatty acids may increase the risk of bleeding in conjunction with taking warfarin (Coumadin). This supplement should be avoided two weeks before and after surgery.

 

Coenzyme Q10

Supplementation should be supervised if you are diabetic, or taking statin drugs.

 

Curcumin (Tumeric)

Curcumin can stimulate bile production and should be avoided if there is a history of gallstones, peptic ulcers, gastroesophageal reflux disease, or if you are taking warfarin or antiplatelet medications.

 

Gingko biloba

Should not be taken together with NSAIDS, blood thinners, diuretics, or SSRI’s.

 

Green Tea

May increase the risk of bleeding if taken with warfarin or aspirin.

Should be avoided two weeks before and after surgery.

 

 

References

 

1. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 2004 Dec;1030:434-41.

 

2. Ringman JM, Frautschy SA, et al. A potential role of the curry spice curcumin in Alzheimer's disease. Curr Alzheimer Res. 2005 Apr;2(2):131-6.

 

3. Yang F, Lim GP, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005 Feb 18;280(7):5892-901.

 

4. Baum L, Ng A. Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer's disease animal models. J Alzheimers Dis. 2004 Aug;6(4):367-77.

 

5. Engelborghs S, Vloeberghs E, et al. Correlations between cognitive, behavioural and

psychological findings and levels of vitamin B12 and folate in patients with dementia. Int J Geriatr Psychiatry. 2004;19(4):365-70.

 

6. Kado DM, Karlamangla AS, et al. Homocysteine versus the vitamins folate, B6, and B12 as predictors of cognitive function and decline in older high-functioning adults: MacArthur Studies of Successful Aging. Am J Med. 2005 Feb;118(2):161-7.

 

7. Wang HX, Wahlin A, et al. Vitamin B(12) and folate in relation to the development of Alzheimer's disease. Neurology. 2001 May 8;56(9):1188-94.

 

8. Ames BN, Liu J. Delaying the mitochondrial decay of aging with acetylcarnitine. Ann N Y Acad Sci. 2004 Nov;1033:108-16.

 

9. Tchantchou F, Graves M, et al. N-acetyl cysteine alleviates oxidative damage to central nervous system of ApoE-deficient mice following folate and vitamin E-deficiency. J Alzheimers Dis. 2005 Apr;7(2):135-8.

 

10. Dhitavat S, Ortiz D, et al. Folate, vitamin E, and acetyl-L-carnitine provide synergistic protection against oxidative stress resulting from exposure of human neuroblastoma cells to amyloid-beta. Brain Res. 2005 Nov 9;1061(2):114-7.

 

11. Dhanasekaran M, Ren J. The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus. Curr Neurovasc Res. 2005 Dec;2(5):447-59.

 

12. Moreira PI, Santos MS, et al. CoQ10 therapy attenuates amyloid beta-peptide toxicity in brain mitochondria isolated from aged diabetic rats. Exp Neurol. 2005 Nov;196(1):112-9.

 

13. Ono K, Hasegawa K, et al. Preformed beta-amyloid fibrils are destabilized by coenzyme Q10 in vitro. Biochem Biophys Res Commun. 2005 Apr 29;330(1):111-6.