Alzheimer'e Dementia is characterised by a loss of cognitive function. This can include disrupted thinking, memory, reasoning, communication, personality and cognitive speed. It is degenerative in nature, with cognitive abilities decreasing over time either slowly or more quickly depending on the cause of the dementia and the individual. Dementia is due to disease or injury in the brain, and is traditionally believed to be irreversible in the latter stages. Recent nutritional research suggests that it may be able to be stopped in very early stages (when it is known as Primary Degenerative Dementia).
The symptoms of dementia depend on the areas of the brain that are affected by disease, and therefore vary depending on the type of dementia that is present. However, memory problems are often the first indication of disease. Mild Cognitive Impairment refers to a condition that presents with disrupted memory without impairment in other areas of function. This particular symptomatology might indicate the initial stages of Alzheimer’s disease.
The more common types of dementia include Alzheimer’s Disease, vascular or multi-infarct dementia, Lewy Body Dementia and Parkinson’s disease. Dementia can also be caused by infectious diseases such as AIDS, or hereditary diseases such as Huntington's disease. Alcoholism and drug abuse may also result in some type of dementia.
Alzheimer's disease (AD) is the most common form of dementia. It is a progressive, degenerative disease of the brain, affecting up to 5% of people aged 71-79, increasing to up to 37% of people aged over 90 years.
The main features of AD are the amyloid plaques and tangled neuronal fibres that disrupt the normal organisation and function of the brain. These initially appear in the temporal lobe of the brain, the area that is responsible for memory and language. Thus, memory problems are often the first indicator of AD.
Because the presence of plaques and fibrillary tangles cannot be determined until autopsy, diagnosis is typically made based on behavioural changes, memory tests, cognitive questionnaires and elimination of other possible causes. Therefore, diagnosis is generally given as ‘dementia of the Alzheimer’s type’ or ‘probable Alzheimer’s Disease’. However, QEEG technology may be able to provide a more conclusive diagnosis, particularly in the early stages which can start some 12 years before full blown dementia. In those early stages the symptoms are referred to as Primary Degenerative Dementia.
Depression and Primary Degenerative Dementia have very similar overlapping symptoms making it difficult to differentiate between them on the basis of memory tests and depression questionnaires. However, QEEG is able to differentiate with a high degree of specificity between depression and Primary Degenerative Dementia. This enables more effective treatment addressing the root causes of either disorders . QEEG differential diagnosis was developed by Dr. Leslie Prichep and Dr. E. Roy John from the Brain research Laboratory of New York University Medical Centre and is available at the Behavioural Neurotherapy Clinic. Treatment of Primary Degenerative Dementia is possible using specific nutrients and Neurotherapy.
Although some cognitive decline is expected with normal ageing, AD should not be considered a normal part of ageing, since it represents a pathological state. In AD, dementia progresses at a rate of around 10–15% per year compared with healthy people whose decline progresses at around 1–2% / year 
There is no single known cause of AD, however there are a number of factors that may contribute to an increased likelihood of developing this disease. The presence of the apolipoprotein E variation (APOE-4) is a genetic factor associated with greater incidence of the disease. History of head injury or depression and lower levels of education may contribute to higher incidence. Scientific studies have also associated a number of nutritional factors with AD. For example, people suffering from AD are more likely to have a poor nutritional status and be deficient in vitamin B12 and folate. This might be due to the increased levels of homocysteine that results from deficiency in these B-group vitamins. Homocysteine causes damage to the blood vessels in the brain and may damage the hippocampus, a region of the brain used for memory . Another nutritional factor relates to antioxidants. Oxidative stress (damage from free radicals) may significantly contribute to the pathology of AD. Patients with AD are more likely to be deficient in the antioxidant vitamins C and E, or to have a lower dietary intake of these vitamins.
At present there is no cure for AD. Slowing cognitive decline and postponing functional and behavioural impairment is important [Gauthier]. Currently the main drug treatment is Donepezil, which may be able to slow the progression of dementia. However, this delay may be only for as long as 6 months to one year. Evidence suggests that early treatment with this drug provides greater benefits over the long term [Winblad, 2003].
Treating dietary and nutritional deficiencies many years before dementia provide the opportunity for better results. Reducing the impact of causative factors such as increased homocysteine and oxidative stress, particularly in groups that are at risk, may delay onset or decrease the likelihood of developing AD. Scientific studies have demonstrated that improving nutritional status via supplementation can improve cognition in older adults [Harris, 2005].
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