What is Alzheimer’s disease?
The most common types of dementia are Alzheimer’s disease, vascular dementia, Parkinson’s disease, dementia with Lewy bodies, fronto-temporal dementia, Huntington’s disease, alcohol-related dementia, and Creutzfeldt-Jacob disease.
Alzheimer’s disease is a neurodegenerative form of dementia that causes diffuse neuronal death throughout the brain, culminating in severe brain dysfunction and death. Alzheimer’s disease accounts for 60–80% of all cases of dementia, and includes all cases of dementia with cortical atrophy, neurofibrillary tangles, and senile plaques, irrespective of age of onset. The plaques consist of a protein called amyloid-beta and occur between dying brain cells. The tangles are due to disintegration of the protein tau and occur within the brain neurons.
All types of dementia are caused by brain cell death. Alzheimer’s is a neurodegenerative disease, which means there is progressive brain cell death over time, which leads to brain shrinkage with fewer nerve cells and neural connections.
Twenty-one genes have been found to be associated with Alzheimer’s, enabling doctors to test whether a person has any of the genes that pinpoint higher risk.
Genetics are behind early-onset familial Alzheimer’s disease, which presents typically during the period 30–60 years of age and affects people who have a family history. Only 5% of all Alzheimer’s cases are early-onset, but this type can be the most frustrating because physicians tend not to suspect Alzheimer’s when a person is less than 60 years of age.
Conventional medical treatment for Alzheimer’s disease
The most appropriate treatment for a person with Alzheimer’s disease depends of a number of factors:
- Individual’s age, overall health, and medical history
- Disease progression
- Person’s tolerance for specific medicines and therapies
- Expectations for the course of the disease.
Within the brain, neurons connect and communicate at synapses, where tiny bursts of chemicals called neurotransmitters carry information from one neurone to the next. Alzheimer’s disease disrupts this process, and eventually destroys synapses and neurons, rendering the brain’s communication network ineffective. While these drugs help mask the symptoms of Alzheimer’s, they do not treat the underlying disease.
The medications used to treat Alzheimer’s aim to reduce cognitive symptoms, such as memory loss, confusion, and problems with thinking and reasoning. As Alzheimer’s progresses, brain cells die and neural connections are lost, causing cognitive symptoms to worsen.
A specialist, such as neurologist, geriatrician or psychiatrist, will usually be involved in obtaining an accurate diagnosis, assessing disease stage, and prescribing the most appropriate medication.
While medications cannot prevent damage to brain cells, they may lessen symptoms by affecting neurotransmitters, the chemicals responsible for transmitting messages in the brain. On average, Alzheimer’s drugs are effective for about six to 12 months in approximately half of the individuals who take them.
Cholinergic treatments (Aricept, Cognex, Exelon, Razadyne) curb the breakdown of acetylcholine, an important neurotransmitter for memory and learning. Acetylcholinesterase inhibitors work by blocking the actions of an enzyme called acetylcholinesterase, which destroys acetylcholine.
Certain acetylcholinesterase inhibitors are approved for use for people with mild to moderate Alzheimer’s disease and a number of them are available as subsidised medicines under the Australian Pharmaceutical Benefits Scheme.
Memantine (Namenda) is an NMDA (N-methyl-D-aspartate) receptor inhibitor, which regulates glutamate activity, a chemical messenger involved in learning and memory. Memantine protects brain cells against excess glutamate, a chemical messenger released in large amounts by cells damaged by Alzheimer’s disease and other neurological disorders. Memantine has been shown to improve mental function, and may enable a person to better cope with day-to-day activities.
In Australia, Memantine is currently approved for treatment when a person has moderately severe to severe Alzheimer’s disease. Memantine is available at subsidised rates under the Pharmaceutical Benefits Schedule for those who meet the necessary diagnostic criteria and disease stage.
Oestrogen has a number of beneficial effects on the brain and may protect the brain from deterioration in several ways. According to some researchers, oestrogen replacement therapy for postmenopausal women may delay the onset or even prevent Alzheimer’s disease, reducing a woman’s likelihood of developing the disease by as much as 30%.
Researchers have been working on a vaccine for Alzheimer’s disease for almost a decade. The strategy behind the immunotherapy approach is to use the body’s own immune system to destroy the amyloid plaques that block communication between brain cells.
Nutritional medicine treatment for Alzheimer’s disease?
From a nutritional perspective, the practitioner should attempt to identify all antecedents, trigger factors and mediators that are active in each patient and apply appropriate corrective treatment, if possible.
As with all chronic, multifactorial disease, emphasis is placed on identification of dietary and environmental factors that may be responsible for enhancing immune system activity (food allergens, gluten reactivity, heavy metal toxicity) or exacerbating inflammatory cytokine and eicosanoid production (essential fatty acid imbalance, antioxidant depletion).
Dietary-nutrient prescription is dependent on a thorough assessment of the patient’s individual nutritional status, genetic susceptibility, specific nutrient requirements, and social and environmental habitat.
Following careful assessment, synthesis and prescription of a dietary and nutrient supplement program should proceed systematically, correcting for disturbances of:
- Digestion – usually requires support to obviate food sensitivity reactions occurring secondary to maldigestion with oligopeptide stimulation of cytokine producing cells in the gut-associated lymphoid tissue (GALT)
- Diet – should be optimised to correct for insulin resistance and dyslipidaemia; remove reactive foods and maximise antioxidant intake
- EFA balance – omega-6 fatty acid and saturated fat intake should be minimised and omega-3 fatty acid intake optimised
- Antioxidant status – optimise intake of ascorbate, mixed tocopherols, tocotrienols, and flavonoid antioxidants
- Bowel flora dysbiosis – correct with probiotics and antifungal therapy, especially if evidence of immune system hyperactivity
- Specific disease treatment, including medical, nutritional, and phytonutrient therapy
- Liver detoxification problems – may be worth testing to ensure Phase 1 and Phase 2 detoxification is not dysregulated and contributing to cerebral toxicity or excessive free radical genesis
- Hormone adequacy – some evidence suggests that the anabolic hormone DHEA may be beneficial in preventing disease and retarding disease progression. Initial hopes that oestrogen therapy may also confer a beneficial preventive effect on disease incidence have not apparently been borne out by recent studies.
- Neurotransmitter balance – evidence indicates that improving acetylcholine status may be beneficial in improving cognitive function in early disease and delay disease progression (anticholinesterase drugs, phosphatidylcholine supplements, Niacin and NADH therapy).
Specific Nutrients reportedly beneficial in Alzheimer’s disease include:
|Vitamin E (mixed tocopherol)||2000 IU|
|Vitamin B12||1000 mcg weekly IM injection|
|Alpha lipoic acid||300–500mg|
|Vitamin D||400 IU|
Phosphatidylserine is the lipid (fat) in membranes that surround nerve cells. In Alzheimer’s disease and other neurodegenerative disorders, phosphatidylserine is believed to build up cell membranes and provide protection from degeneration. Supplements are derived from soya beans or cabbage. Soy lecithin is by far the best source. Other dietary sources include brain, kidney, liver, tuna, eel, Atlantic herring and mackerel, chicken heart, offal, and white beans.
L-acetylcarnitine contributes to movement of fatty acids and other vital fuels from the cell into mitochondria and is essential for brain health and efficiency. L-acetylcarnitine has been shown to reduce the build-up of amyloid-beta and tau proteins through improved clearance from brain cells.
Ginkgo biloba is a plant extract that has been shown to have antioxidant and anti-inflammatory effects on cells within the brain, through protection of cell membranes and regulation of neurotransmitter function.
Coenzyme Q10, a component of the mitochondrial electron transport chain, is a neuroprotective antioxidant required for normal cell reactions. Increased oxidative stress is implicated in the pathogenesis of Alzheimer’s disease. Mitochondrial dysfunction and increased reactive oxygen species are known to occur prior to amyloid plaque deposition in the brain. CoQ10 reduces oxidative stress and amyloid pathology and improves behavioural performance in laboratory experiments using mice. Coenzyme Q10 human trials including patients with neurodegerative Alzheimer’s, Parkinson’s, and Huntington’s diseases are underway.
Caprylic acid is a medium-chain triglyceride (fat) the body breaks down into ketone bodies, which may provide an alternative energy source for brain cells that have lost their ability to use glucose. Diagnostic brain imaging has shown that people with Alzheimer’s have reduced levels of brain glucose, the brain’s primary source of energy. Coconut oil and coconut water are cost-effective sources of caprylic acid, and there are anecdotal reports of MCT oil and coconut oil reversing early Alheimer’s Disease.
Nicotinamide adenine dinucleotide (NADH), the biologically active coenzyme form of vitamin B3 (Niacinamide), is an important coenzyme that occurs naturally in the body and plays a role in the chemical process to generate energy and sustain life. NADH is needed to oxidize sugars, fats, and proteins. NADH is important for ATP manufacture, an important substance for body and brain energy needs. The human brain produces and uses approximately 20% of ATP available for energy.
Animal proteins, such as beef, chicken, lamb, and fish, as well as yeast contain higher amounts of NADH, while vegetables and fruits have lower amounts of NADH. However, in reality we don’t get much NADH from food.
NADH therapy may increase natural dopamine production and spare tryptophan in the body from being used for NADH production. The increased available tryptophan levels may enhance levels of the neurotransmitter serotonin, which affects moods.
NADH treatment reportedly improves mental clarity, alertness, concentration, and memory, and may be beneficial in people with Alzheimer’s disease. NADH is also used to boost stamina, and treat depression, chronic fatigue syndrome, and Parkinson’s disease.
N-acetylcysteine treatment has been shown to improve many outcome indicators in people with Alzheimer’s. N-acetylcysteine is a component of the powerful antioxidant glutathione, which provides the brain tissue against cell death from oxidative stress – the uncontrolled oxidation of lipids in the cells. The brain is particularly vulnerable to oxidative stress because its blood supply is highly oxygenated and brain tissue is full of lipids.