Alzheimer’s

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What Is?

What is Alzheimer’s

How to Treat Alzheimer's

Natural Treatments for Alzheimer's

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.

What are the symptoms of Alzheimer’s disease?

Alzheimer’s disease is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. In the early stages a person exhibits only mild symptoms, but symptoms always worsen. Disturbance of higher cortical function occurs first, followed several years later by features of subcortical dysfunction, as the disease progresses.

The most common symptom characteristic of Alzheimer’s dementia is prominent memory loss, especially learning and recalling new information. But the first presenting symptom can also be struggling to find the right words when speaking. Dementia affects cognitive function or thinking, the way a person behaves, and a person’s ability to complete everyday tasks. With dementia brain function is affected enough to interfere with completing daily personal care, and social or work activities.

A person with prominent visuospatial deficits has difficulty recognizing objects and faces, comprehending separate parts of a scene at once (simultanagnosia), and difficulty with reading text (alexia). The deficits that charactise ‘executive dysfunction’ include problems with reasoning, judgment, and problem solving.

Signs and symptoms for Alzheimer’s:

Memory and language impairment
Fall in vocal output, which increases in severity as the disease progresses
Visuospatial difficulties
General cognitive impairment
Psychiatric problems are common – depression and anxiety
Delusions (15% cases) and hallucinations
Seizures – late in the disease
Myoclonus (brief involuntary twitching)

The progression of Alzheimer’s can be broken down into three stages:

Preclinical (no signs or symptoms yet)
Mild cognitive impairment
Dementia.

The clinical definition of Alzheimer’s disease

In order to diagnose Alzheimer’s a doctor must first establish a person has dementia. A patient will demonstrate a decline in cognitive or behavioural function that prevents them from functioning properly at work or at usual activities.

A decline in at least two of these five symptoms must be evident.

Worsened ability to take in and remember new information:

Repetitive questions or conversations
Misplacing personal belongings
Forgetting events or appointments
Getting lost on a familiar route.

Impairments to reasoning, complex tasking, exercising judgment:

Poor understanding of safety risks
Inability to manage finances
Poor decision-making ability
Inability to plan complex or sequential activities.

Impaired visuospatial abilities:

Inability to recognize faces or common objects or to find objects in direct view
Inability to operate simple implements, or orient clothing to the body.

Impaired speaking, reading and writing:

Difficulty thinking of common words while speaking, hesitations
Errors in speech, spelling, and writing.
Changes in personality and behaviour, including
Out-of-character mood changes, including agitation, apathy, social withdrawal, less interest, motivation or initiative
Loss of empathy
Compulsive, obsessive, or socially unacceptable behaviour.

A diagnosis of Alzheimer’s is based on atypical or insidious onset, which means symptoms develop gradually over months to years rather than hours to days, and a marked worsening of the individual person’s normal level of cognition in particular areas, through observation or personal report.

For a person who meets the core clinical criteria for probable Alzheimer’s, evidence of a causative genetic mutation (in APP, PSEN1, or PSEN2), increases the certainty that the condition is caused by Alzheimer’s pathology. Less than 5% of cases are true ‘familial Alzheimer’s’ when the disease runs in families. Having a parent or sibling with Alzheimer’s means a person has a higher chance of getting Alzheimer’s. While genetic risk cannot be changed, some risk factors can be modified to compensate.

The biomarkers for brain amyloid-beta protein deposition are low cerebro-spinal fluid Aβ42 and positive PET amyloid imaging.

The diagnosis of probable Alzheimer’s dementia should not be applied when there is evidence of:

Substantial concomitant cerebrovascular disease, defined by a history of a stroke temporally related to the onset or worsening of cognitive impairment, or the presence of multiple or extensive infarcts, or severe white matter hyperintensity burden
Core features of dementia with Lewy bodies other than dementia itself
Prominent features of behavioural variant frontotemporal dementia
Prominent features of primary progressive aphasia (difficulty talking)
Evidence of another concurrent, active neurological disease, or a non-neurological medical comorbidity, or use of medication that could have a substantial effect on cognition.

Jointly developed by the National Institute on Aging and the Alzheimer’s Association.

Alzheimer’s Disease is not a normal part of aging. Although most people with Alzheimer’s Disease are over 65 years of age, and the risk of developing AD doubles every five years over 65 years of age, nearly half of 85-year-olds do not get AD.
A rare inherited form, symptoms start as early as 30–60 years of age.

What are common risk factors for Alzheimer’s disease?

Unavoidable risk factors

Age is the highest risk factor. Alzheimer’s is more likely in older people. More people more that 85 years of have have the disease compared with people more than 65 years of age. However, patients as young as 30 years of age can get the disease.

A genetic (family) history of Alzheimer’s is the second highest risk factor

Having a certain gene called APO-E4 is a significant risk factor – three to eight times more risk than a person without the gene

Gender – being female is a risk factor because more women than men are affected

Trisomy 21 (Down’s syndrome) patients may develop histopathological brain changes indistinguishable from Alzheimer’s disease in their third and fourth decade, attributable to an extra copy of the APP gene.

Potentially avoidable or modifiable factors

Major head injury and recurrent head injury are significant risk factors and the risk increases with the severity of trauma
Mineral toxicity (lead, mercury and aluminium) appears to increase the risk of Alzheimer’s but the exact role isn’t clear
Progressive oxidative damage appears to increase risk and is associated with brain tissue accumulation of amyloid-beta proteins
Dyslipidaemia, hypertension, excess cytokine production, and insulin resistance are also implicated as causal factors
Compromised microvascular circulation with accompanying impaired nutrient delivery and secondary cellular hypometabolism may be the basic causal mechanism for development of Alzheimer’s disease
Factors that increase vascular risk increase risk of Alzheimer’s, including diabetes, high cholesterol and high blood pressure
Low educational and occupational attainment
Sleep disorders, such as sleep apnoea
Oestrogen hormone replacement therapy.

Researchers at Rutgers-Robert Wood Johnson Medical School, New Jersey, found that people with Alzheimer’s disease had four times higher levels of a DDT byproduct in their blood stream compared with control subjects. DDT is an organochloride pesticide used to control malaria and typhus during World War II and in general agriculture. When the environmental and health dangers of DDT were realised, the chemical was banned.

DDT appears to promote the development of amyloid plaques, which clog the neurons and could be the cause of Alzheimer’s disease. The pesticide also might further increase the risk for people who already have a genetic predisposition toward developing Alzheimer’s.

How is Alzheimer’s disease diagnosed?

An accurate diagnosis is critical for any disease that affects the brain. Consult a doctor early if you suspect you or someone you know has dementia, in order to obtain an early stage a diagnosis. A complete medical and psychological assessment may identify a treatable condition or confirm dementia, which will require further assessment and treatment.

When a doctor suspects that a person has Alzheimer’s he or she will perform a thorough examination to assess:

Detailed medical history – to establish whether there is a slow or sudden onset of symptoms and the progress of symptoms
Thorough physical and neurological examination
Laboratory tests – blood and urine tests called a dementia screen to rule out other illnesses
Neuropsychological testing to assess comprehension, insight, and judgement
Diagnostic tests such as a chest x-ray, ECG, or brain CT
Mental status testing to assess memory, reading ability, writing and mental arithmetic
Psychiatric assessment to identify treatable disorders that can mimic dementia, such as depression and anxiety, and also to manage

psychiatric symptoms, which may occur alongside dementia.
Based on content from the Fight Dementia Campaign website

Abnormal protein clumps in the brain tissue are characteristic of the disease. However, researchers and physicians believe that there could be another underlying process that is actually causing Alzheimer’s disease.

How does a doctor diagnose Alzheimer’s disease?

Alzheimer’s begins with memory loss, but as the disease progresses other mental, emotional, and physical issues become evident.

A person with Alzheimer’s is prone to agitation and aggression or may easily become anxious or upset. He or she might fidget, shout, throw things, or attempt to hit carers and family. Creating a quiet, stable environment can help calm a person and reduce these episodes.

A person with Alzheimer’s is prone to bladder and bowel control problems, in particular in late stage disease. Planning for these difficulties and anticipating needs can make a difference to coping for patients and carers.

Many people with Alzheimer’s disease become depressed in the early stages of the disease, as they come to terms with how much their lives will change. Antidepressant drugs may help a person to cope with this realisaiton. Taking regular exercise, spending time around other people, and keeping busy with hobbies and activities will help elevate mood.

People with Alzheimer’s can lose their balance and take nasty tumbles, which can cause serious harm. To help prevent falls and injuries, encourage regular exercise to keep the musculoskeletal system strong and improve balance. Creating a safer environment at home will help.

Remove any obstacles that someone could trip on or bump into, install at least one handrail in stairways, use non-skid strips in the shower, bathtub, and along slippery surfaces. Install night-lights to improve visability and stick easy-to-see motifs on large windows and glass doors.

Many people with Alzheimer’s disease die from complications such as falls and infections, including bladder infections, flu, and pneumonia. Be vigilant for a fever or sudden changes in symptoms or behaviours, which could indicate an infection.

Alzheimer’s disease key facts and statistics

More than 332,000 Australians and some 44 million people worldwide suffer with dementia. In the absence of a medical breakthrough, the number of Australians with dementia is expected to reach 900,000 by 2050. Each week, at least 1,700 Australians are newly diagnosed with dementia.

Approximately 24,700 Australians have early-onset dementia, a type of dementia that develops between 30–60 years of age.

An estimated 1.2 million people are involved in the caring for Australians living with dementia, which is among the top five causes of death in Australia. Families notice the symptoms of dementia on average three years before a clinical diagnosis is confirmed.

Dementia is the greatest cause of disability in older Australians (>65 years of age) and the third leading cause of disability burden overall.

Glossary – Alzheimer's disease

Glossary

Acetylcholine – chemical in the brain (neurotransmitter) involved in learning and memory. Acetylcholine is greatly diminished in the brains of people with Alzheimer’s disease.

Alexia – difficulty with reading text

Alzheimer’s disease – progressive, fatal disease in which nerve cells in the brain degenerate and brain matter shrinks, resulting in impaired thinking, behaviour and memory

Ambulation – ability to walk and move about freely

Amino acids – basic building blocks of proteins. There are 20 amino acids necessary for human growth and function.

Amyloid – protein deposited in plaques in the brain of a person with Alzheimer’s.

Amyloid imaging – PET scan showing amyloid-beta proteins in the brain.

Amyloid plaque – abnormal clusters of dead and dying nerve cells, other brain cells, and amyloid protein fragments, evident when a person has Alzheimer’s

Antibodies – specialized proteins produced by the cells of the immune system that counteract specific foreign substances. Antibodies may also be produced outside the body and infused as a treatment for Alzheimer’s disease.

Anti-inflammatory drugs – reduce inflammation by modifying the body’s immune response.

Anxiety – feeling of apprehension, fear, nervousness or dread accompanied by restlessness or tension.

Apathy – a lack of interest, concern or emotion.

Aphasia – difficulty expressing oneself verbally.

Assessment – when a doctor or health professional evaluates a person’s mental, emotional and social capabilities.

Associated disorders – concurrent conditions that are present at the same time.

Asymptomatic - means no symptoms or no clear sign that disease is present.

Atrophic shrinking – describes the loss of brain tissue seen in Alzheimer’s disease on brain CT or during autopsy.

Autopsy – examination of a body’s tissues and organs after death.

Axon – part of a nerve cell that normally transmits outgoing signals from one cell to another.

Basal ganglia – part of the brain that controls movement, judgment, personality, and speech.

Behavioural symptoms – emotional symptoms, such as wandering, depression, anxiety, hostility and sleep disturbances.

Biomarker – indicate a specific disease. Alzheimer’s biomarkers are amyloid plaques and neurofibrillary tangles.

Blood-brain barrier – selective barrier that controls the entry of substances from the blood into the brain.

Calcium channel blocker – drug that blocks the entry of calcium into cells, thereby reducing activities that require calcium, such as the transmission of nerve impulses. Primarily used primarily to treat heart disease but may be potential treatments for Alzheimer’s disease.

Choline – neurotransmitter that enables cells to communicate.

Choline acetyltransferase (CAT)  An enzyme that controls the production of acetylcholine. CAT is depleted in the brains of individuals with Alzheimer’s disease.

Cholinergic system – system of nerve cells that uses acetylcholine as its neurotransmitter and is damaged in the brains of individual’s with Alzheimer’s disease.

Cholinesterase – an enzyme that breaks down acetylcholine, an important chemical for learning and memory, which is low in people with Alzheimer’s.

Cholinesterase inhibitors are used to stop the breakdown acetylcholine and increase levels in Alzheimer’s disease, and include the drugs Aricept, Cognex, Exelon, Razadyne.

Cognitive abilities – mental abilities, such as judgment, memory, learning, comprehension and reasoning.

Cognitive symptoms – symptoms that relate to loss of thought processes, such as learning, comprehension, memory, reasoning and judgment.

Deficits – physical or cognitive abilities that a person has lost, has difficulty with, or can no longer perform because of dementia.

Delusion – false idea that is firmly believed and strongly maintained in spite of proof or evidence to the contrary.

Dementia – irreversible disease characterised by severe loss of mental functions, including thinking, memory and reasoning that interferes with a person’s daily functioning.

Disease stage – disease progression defined by levels of severity: prodromal, early, mild, moderate, moderately severe, severe.

Dysphasia – inability to find the right word or understand the meaning of a word.

Early-onset Alzheimer’s disease – Alzheimer’s disease in which individuals are diagnosed with the disease before age 65.

Enzyme – protein produced by living organisms that promotes or influences chemical reactions.

Oestrogen – sex hormone produced by the ovaries and testes, which stimulates secondary sexual characteristics and induces menstruation on women; important for maintaining normal brain function and development of nerve cells.

Familial Alzheimer’s – genetic form of Alzheimer’s disease that runs in families.

Fatty acids – acids derived from the breakdown of fats.

Free radicals – highly reactive molecules capable of causing damage in brain and other tissues. Free radicals are common by-products of normal chemical reactions occurring in cells.

Frontotemporal dementia – originally called Pick’s disease, caused by an accumulation of tau proteins in nerve cells. Results in dramatic changes to personality and social behaviour but typically does not affect memory until later in the disease.

Gait – an individual’s manner of walking. A person in the later stages of Alzheimer’s disease often can’t his or her feet as they walk known as a magnetic gait.

Genetic susceptibility – more likely than the average person to develop a disease as the result of genetics.

Hallucination – a person can see, hear, smell, taste or feel something that is not there.

Inflammatory response – immune system’s normal response to tissue injury or abnormal stimulation caused by a physical, chemical or biological substance.

Late-onset Alzheimer’s disease – most common form of Alzheimer’s disease, usually occurring after age 65.

Lewy body dementia – type of dementia characterised by protein deposits called Lewy bodies in the cortex of the brain.

Mitochondria components – found in cells; serve as primary energy sources for cellular functions.

Monoamine oxidase B (MAO-B) An enzyme that breaks down certain neurotransmitters, including dopamine, serotonin and noradrenaline.

Monoamine oxidase inhibitor (MAOI) A drug that interferes with the action of monoamine oxidase, slowing the breakdown of certain neurotransmitters; often used in treating depression.

N- acetylcysteine

Neurone – the basic working unit of the nervous system. The nerve cell comprises a cell body containing the nucleus, several short branches called dendrites, and one long arm called an the axon with short branches along its length and at its end. Neurones send signals that control the actions of other cells in the body, such as other nerve cells and muscle fibres.

Neurodegenerative disease – neurological disorder marked by the loss of nerve cells, such as Alzheimer’s disease and Parkinson’s disease.

Neurofibrillary tangle – accumulation of twisted protein (tau protein) fragments inside nerve cells. The two biomarkers characteristic of Alzheimer’s are amyloid plaques and neurofibrillary tangles.

Neurological disorder – disturbance in structure or function of the nervous system due to either developmental abnormality, disease, injury or chemical toxin.

Neurotransmission – passage of signals from one nerve cell to another through chemicals called neurotransmitters or electrical signals.

Neurotransmitter – chemical in the brain that is necessary for communication between nerve cells, such as acetylcholine, dopamine, norepinephrine and serotonin.

Parkinson’s disease – progressive, neurodegenerative disease with an unknown cause charactersed by the death of nerve cells in a specific area of the brain. A person with Parkinson’s disease lacks the neurotransmitter dopamine. Symptoms include tremors, speech impediments, and movement difficulties. Dementia is often occurs late in the disease.

Pick’s disease – frontotemporal dementia caused by an accumulation of tau proteins in nerve cells. Results in dramatic changes to personality and social behavior but typically does not affect memory until later in the disease.

Positron emission tomography (PET) scan – diagnostic imaging scan that measures functional activity of the brain and shows amyloid plaques

Prodromal Alzheimer’s disease – early stage disease characteristed by memory impairment and a biomarker (amyloid plaque or neurofibrillary tangles).

Proteases – enzymes that break down proteins in the body.

Protein metabolism – breakdown of proteins into amino acids, a process essential to human growth and metabolism.

Pseudodementia – severe form of depression resulting from a progressive brain disorder in which cognitive changes mimic those of dementia.

Psychosis – state of mind in which thinking becomes irrational or disturbed and refers to delusions, hallucinations, and other severe thought disturbances.

Receptor agonist – substance that mimics a specific neurotransmitter that is able to attach to that neurotransmitter’s receptor and produces the same action the neurotransmitter usually produces. Receptor agonists are used to treat diseases and disorders in which the original chemical substance is missing or depleted.

Risk factor – factor that increases a person’s likelihood of developing a disease or predisposes a person to a certain condition.

Simultanagnosia – rare neurological disorder characterized by an inability to perceive more than one object at a time.

Subcortical dementia – impairment of the lower part of the brain that affects the speed of motor and mental processes; associated with disease of the basal ganglia, such as Huntington’s disease.

Synapse – junction between neurones (brain cells) where a signal is transmitted from one nerve cell to another, usually by a chemical called a neurotransmitter.

Tau protein – protein that makes up neurofibrillary tangles found in degenerating nerve cells.

Vascular dementia or multi-infarct dementia

Wandering – when a person with dementia strays and becomes lost in familiar surroundings

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.

Treating the accompanying symptoms of Alzheimer’s

All types of dementia are accompanied by a number of behavioural and psychological symptoms, which can be distressing for both patients and care givers, including depression, anxiety, sleeplessness, delusions, hallucinations, ideas of persecution, inability to recognise relatives or places, agitation, and aggressive behaviour.

Major tranquillisers, also called antipsychotics or neurcoleptics, can help control agitation, aggressions, delusions, and hallucinations.

Depression is extremely common in people with Alzheimer’s and can be treated with antidepressants. Severe anxiety can be quite debilitating and cause considerable stress for the patient, family, and caregivers. Benzodiazepines can help reduce anxiety over short-term periods, but aren’t effective in the longer term.

Sleep disturbance is common in people with Alzheimer’s. Night-time wakening and wandering can also disturb the quality of sleep of those living with a person with Alzheimer’s. If too much sedation is administered during daytime, a person might have difficulties sleeping at night. Treating insomnia can be challenging and sleeping tablets are used as a last resort, because of the likelihood of dependency, rebound sleeplessness, and anxiety.

Currently no cure for Alzheimer’s disease is available. Symptoms are usually permanent, but they can vary in intensity. However, a number of treatments are available to ease symptoms and improve quality of life.

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:

Phosphatidylserine	300mg
L-acetylcarnitine	2000mg
Vitamin E (mixed tocopherol)	2000 IU
Gingko biloba	120mg
Vitamin B12	1000 mcg weekly IM injection
Coenzyme Q10	200mg
N-acetylcysteine	1000mg
Alpha lipoic acid	300–500mg
NADH	10mg
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.

The role of essential fatty acid imbalance in Alzheimer’s disease

In order to balance essential fatty acids, omega-6 fatty acid and saturated fat intake should be minimised, and omega-3 fatty acid intake should be optimised.

Omega-3 fatty acids are a type of polyunsaturated fatty acid. Research has linked certain types of omega-3 fatty acids — docosahexaneoic acid (DHA) and eicosapentaenoic acid (EPA) — to a reduced risk of cardiovascular disease.

Research has also linked high intake of omega-3 fatty acids to a reduced risk neurodegenerative change – the underlying cause of dementia and Alzheimer’s. The chief omega-3 in the brain is DHA, which is found in the fatty membranes that surround nerve cells, especially at the microscopic junctions where cells connect to one another.

Hypothesises about why omega-3s might influence dementia risk include their benefit for the heart and blood vessels, anti-inflammatory effects, and support and protection of nerve cell membranes.

Researchers believe supplemental DHA can promote the synthesis of synaptic membranes, which will elevate the levels of both the phosphatides and the specific pre- and post-synaptic proteins that characterise these membranes.

DHA also increases the numbers of dendritic spines and synapses on hippocampal neurons, the part of the brain responsible for learning, memory, and navigation. DHA could improve brain processes principally through promoting neurotransmission, by increasing the numbers of specific synapses.

The role of antioxidant depletion in Alzheimer’s disease

Increased oxidative stress is implicated in the pathogenesis of Alzheimer’s disease. Research suggests that mitochondrial dysfunction and increased reactive oxygen species occur prior to amyloid-beta deposition in the brain. The production of reactive oxygen species, which leads to oxidative stress, can occur very early; even before neurofibrillary tangles and senile plaques appear. Oxidative stress can lead to tissue damage through a number of different cellular molecular pathways.

Reactive oxygen species can damage intra-cellular substances, such as lipids, proteins, and nucleic acids, leading to cell death and weakened cellular antioxidant defence systems.

Antioxidant treatment may act to prevent the spread of tissue damage and improve neurological outcome. Several researchers hope to prove that dietary intake of several antioxidant vitamins might prevent or reduce the progression of Alzheimer’s disease.

The benefits of the antioxidants resveratrol (found in red grapes), vitamin E, vitamin C, Gingko biloba, and coenzyme Q10 have all been investigated for treating Alzheimer’s. An antioxidant-rich diet of fruits, vegetables, fish, and nuts will help protect brain cells from oxidative stress.

A growing number of nutritional supplements and ‘treatment foods’ are available as memory enhancers or treatments to delay or prevent Alzheimer’s and related dementias.