Dementia is the umbrella term used tocharacterise a loss of cognitive function. Dementia can present as disrupted thinking, memory, reasoning, communication, personality, and cognitive speed. Dementia 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 itwas initially thought to be irreversible in the later stages. However recentresearch, in the field of nutrition, suggests thatDementia can be stopped in its early stages (Primary Degenerative Dementia).
The symptoms of Dementia depend on the affected brain areas, and therefore will vary on the type of dementia present. However, memory problems are always the first indicator. Mild Cognitive Impairment refers to disrupted memory, without impairment to other functional areas. Mild Cognitive Impairment often signalsthe initial stages of Alzheimer’s Disease (AD). AD typically progresses slowly through three general stages — mild (early stage), moderate (middle stage), and severe (late stage). WhileDementia used to be regarded as an ‘old person's disease’, it has become more common in young people aged 30 and above.
Common Dementias 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 are also risk factors for the development of Dementia.
Alzheimer's Disease (AD) is the most common form of Dementia. AD is a progressive, degenerative disease of the brain, which affects up to 5% of people aged 71-79, increasing to up to 37% of people aged 90 and above.
The main features of AD are the amyloid plaques and tangled neuronal fibres that disrupt the normalorganisation, and healthy function, of the human brain. These plaques and fibresinitiallydevelop in the brain’s temporal lobe – the area responsible for memory and language. For this reason, memory problems are often the first indicator of AD.
The presence of plaques and fibrillary tangles cannot be determined until autopsy. Considering this, AD diagnosis is typically based on behavioural changes, memory tests, cognitive questionnaires, and the elimination of other causes. Due to this uncertainty, AD is diagnosed – in life – as ‘Dementia of the Alzheimer’s Type’ or ‘Probable Alzheimer’s Disease’. Promisingly, it appears that QEEG technology canprovide a more conclusive diagnosis, particularly in the early stages of AD (~12 years before Dementia). These early stages, and accompanying symptoms, are referred to as Primary Degenerative Dementia.
Depression and Primary Degenerative Dementia have similar symptoms, making it difficult to differentiate between them based on memory tests and depression questionnaires. However, QEEG can differentiate between both with a high degree of specificity. In identifying the root cause of the symptoms (Depression vs. Dementia), QEEG can direct the most appropriate therapy. QEEG differential diagnosis was first developed by Dr. Leslie Prichep and Dr. E. Roy John, from the Brain Research Laboratory atthe New York University Medical Centre, and is now available at the Behavioural Neurotherapy Clinic. At BNC, we believe that the treatment of Primary Degenerative Dementia is possible with the help of specific (targeted) nutrients and Neurotherapy.
Although a degree of cognitive decline is expected with normal ageing, AD should not be considered normal, since it represents a pathological state. In AD, Dementia progresses at a rate of around 10–15% per year. This rate is only1–2% per year in healthy people.
Causes of Dementia
There is no known cause of AD, however there are severalrisk factors that contribute to its likelihood. The genetic presence of the apolipoprotein E variation (APOE-4) is associated with greater incidence of AD. In addition, a history of head injury, depression, and lower levels of education, contribute to higher incidence of AD. Nutritionalso plays a role. Peoplewith AD are more likely to have poor nutritional status andbe deficient in vitamin B12 and folate. High levels of homocysteine may result from a deficiency in these B-group vitamins. Homocysteine causes damage to the blood vessels in the brain,which may damage the hippocampus – the brain region used for memory . Another nutritional factor are antioxidants. Oxidative stress (damage from free radicals) is correlated with AD pathology. Those AD are more likely to be deficient in the antioxidantvitamins C and E or have lower dietary intake of them.
Nutritional Therapy for Dementia
There is no cure for AD. However, slowing down the rate of cognitive decline and delaying functional and behavioural impairment is important [Gauthier]. Currently, Donepezil is commonly prescribed, which may slow the progression of Dementia. However, the delay this drug offers may only be 6 months to a year. Regardless, early treatment with Donepezil will provide greater benefitsin the long term [Winblad, 2003].
At BNC, we believe that treating dietary and nutritional deficiencies, years before late-stage Dementia,provides the best results. Reducing ADrisk factors (increased homocysteine and oxidative stress), particularly in high-risk populations, may prevent, delay onset, or decrease the likelihood of its development. Improving brain health via nutritional supplementation improves cognition in older adults [Harris, 2005].
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Course for Parents & Therapists
Intensive Courses based on Pivotal Response Treatment (PRT)are designed train parents and caregivers, since they spend around 14 hours a day with their child. Take a course in PRT to learn how every moment can promote functional behaviours and compliance.
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