Alzheimer’s Disease Research

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.

Most citations used are taken from the NLM data base and are in the public domain.

THE COMPLEXITY OF NEURONS DEGENERATION IN DS

FAULTY DNA METHYLATION AND ALZHEIMERS DISEASE IN DS

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3965623/

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

http://www.tandfonline.com/doi/abs/10.1179/0001551213Z.0000000006?journalCode=yacb20

All untreated persons with DS develop Alzheimer’s disease pathology by age 40. A major goal of TNI is prevention.

http://www.ncbi.nlm.nih.gov/pubmed/25151119

http://www.ncbi.nlm.nih.gov/pubmed/24675226

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.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066992/

NGF in AD DS. This is corrected by TNI

http://www.ncbi.nlm.nih.gov/pubmed/24962069

Hippocampal cholinergic pathways AD DS. Corrected by TNI

http://www.ncbi.nlm.nih.gov/pubmed/25031177

Oxidation and DS and AZ. Corrected by TNI

http://www.biomed.cas.cz/physiolres/pdf/prepress/932722.pdf

Lipid peroxidation. Corrected by TNI

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4042144/

Metals and AD This responds to detox. See article on the Glymphatic System on site menu

http://www.ncbi.nlm.nih.gov/pubmed/2073062

Therapy strategy – The rationale of targeting