DOWN SYNDROME AND THE DEVELOPMENT OF ALZHIEMERS DISEASE
The greatest tragedy associated with Down syndrome is the development of Alzheimer’s pathology by age 40 followed by death by age 60, according to current research. One hundred percent of adults with Down syndrome will have detectable plaque by age 40 which has progressively been developing since childhood. Not all persons with Down syndrome will present with dementia. Alzheimer’s disease, even in the non DS population, begins with the formation of neuro fibrillation, with the noticeable effects increasing over time. Dementia does not occur swiftly. In the non DS patient, dementia may be far more noticeable than in a person with Down syndrome due to lack of verbal skills and existing cognitive disability in the latter population. Further, the life expectancy of persons with DS is only 50 to 60 years and many patients pass away long before actual dementia has been diagnosed.
Numerous differences in the brains of people with Down syndrome have been shown to contribute to the development of Alzheimer’s disease. Faulty DNA methylation being among them. In DS, methylation issues are primarily associated with the extra copy of a gene called CBS. Cystathionine beta synthase figures heavily in the methyl/folate cycle and because this gene is over expressed, it interferes with the body’s ability to metabolize folic acid. Folic acid is inactive when injested and must go through a process to be changed into methyltetrahydrofolate, which can then be utilized by the body for proper DNA methylation.
Both cognitive decline and the development of plaque is preventable. In Both Down syndrome and Alzheimer’s disease the pathology of plaque includes several proteins, including TAU, Amyloid proteins and a toxin, peroxynitrite. The absence of one may be enough to alter the course of this disease.
Each section of research on this site will deal with a separate aspect of Down syndrome.
Rationale for prevention of AD by Targeted Nutritional Intervention – the following issues involved in the development of Alzheimer’s disease have been addressed by Targeted Nutritional Intervention specific to their role in cognitive decline in DS
All untreated persons with DS develop Alzheimer’s disease pathology by age 40. A major goal of TNI is prevention.
Metal ions in Ad and DS. Note these may be related to vaccines or environmental exposure. It is possible, through TNI detox to reduce the level of heavy metal ions in the brain. See Article on the Glymphatic system.
NGF in AD DS. This is corrected by TNI
Hippocampal cholinergic pathways AD DS. Corrected by TNI
Oxidation and DS and AZ. Corrected by TNI
Lipid peroxidation. Corrected by TNI
Metals and AD This responds to detox. See article on the Glymphatic System on site menu
Therapy strategy – The rationale of targeting
Acetylcholine receptors. Targeted by TNI
NGF targeted by TNI
Mitochondria and ferritin. Targeted by TNI
DYRK1a over expression and AD. Targeted by TNI
Polymorphisms in BACE 2. Testing for SNPs can be important in treatment.
DNA methylation corrected by TNI
Diet low glycemic index. Monitoring of glycemic index a part of adult protocol
APP AD DS this gene is over expressed and targeted by TNI
Malabsorption corrected with this protocol
Glutathione corrected by TNI
Omega 3 fatty acids. Corrected through TNI
Nutrients and AD
Vitamin C deficiency in AD.
Three week supplements
Supplements reduced mortality in AD patients.
Supplements and AD a French Study
Safe natural way to prevent cognitive decline.
Vitamin DOUBLE BLIND.
Therapy for DS.
Green tea and AD.
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