Alzheimers..Possible change of name?
Alzheimer’s disease is a very hard disease to cope with. It not only affects the bearer of the disease, but the families as well. A person diagnosed with AD, is unwillingly entered into a death sentence of forgetfulness. The research conducted by Eric Steen, et al. investigated the characteristics of Alzheimer’s disease with any abnormal patterns related to insulin and gene expression. They hypothesized that the insulin and the insulin like growth factor expression in Alzheimer’s disease would be significantly lower than in the normal aged adult.
Eric Steen et al. received their samples from various blood banks located nationally. There samples consisted of brain tissue obtained from the brain banks. They received twenty eight Alzheimer disease brain tissue, and twenty six normal aging brain tissue. Eric Steen et. Al. determined if the brain tissues were from the “normal” aging process by reviewing the medical case studies of the “normal” aged brain tissue donors. They used various methods to measure the chemical affects of insulin and other receptors. They measured by using real time quantitative RT-PCR (reverse transcription-polymerase chain reaction). This is a great method of measuring for it can detect mRNA levels in a small sample size. They used the western blot analysis to review the amount of Akt. They used immunoprecipitation to study the “interactions between the p85 subunit of PI3 kinase and insulin receptor substrate types 1 and 2.”(E.Steen et al. pg.65).
When E.Steen et al. used the western blot analysis they found “significantly reduced mean levels of phospho-AKT “(E.Steen et al. Pg.73) this could help validate the study that is being done because AKT is involved in cell increase, programmed cell death, and diabetes. AKT was found in large numbers in the hippocampal tissue of AD Brain tissue. This research has found that insulin, and the insulin like growth factors originate from problems linked to impaired CNS growth factor production. The neurons are expressing the growth factor genes. This “raises questions and concerns about the potential benefits of peripherally administered replacement therapy.”(E.Steen et al. Pg.77) The downfall with this finding is that peripherally administered replacement therapy is the best way to administer medications without the complications of the blood brain barrier. In AD brain tissue the IGF-II expression was higher in the hippocampus area of the brain. In the control group, insulin and IGF-1 receptors were expressed at significantly greater amounts than the AD brain tissue. “In AD, insulin gene expression in the hippocampus and hypothalamus was significantly reduced relative to control (insulin gene expression was not detected in the frontal cortex.”(E.Steen et al. pg.68) This shows that AD brain tissue has a lower amount of gene expression in the areas where short term memory is stored. The human growth factor and the receptor expression were found to have significance at the .01 level when insulin was concerned. This research suggests that if AD could somehow be treated with
ligands that can increase insulin and the growth factor signaler, it can increase the life and purpose of certain neuronal cells that are at a high risk of developing AD.
My summary is from research conducted by:
“Impaired Insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease- is this type 3 diabetes?” Eric Steen, Benjamin M. Terry, Enrique J. Riviera, Jennifer L. Cannon, Thomas R. Neely, Rose Tavares, X. Julia Xu, Jack R. Wands and Suzanne M. de la Monte. Journal of Alzheimer’s Disease vol. 7 (2005).
Eric Steen et al. received their samples from various blood banks located nationally. There samples consisted of brain tissue obtained from the brain banks. They received twenty eight Alzheimer disease brain tissue, and twenty six normal aging brain tissue. Eric Steen et. Al. determined if the brain tissues were from the “normal” aging process by reviewing the medical case studies of the “normal” aged brain tissue donors. They used various methods to measure the chemical affects of insulin and other receptors. They measured by using real time quantitative RT-PCR (reverse transcription-polymerase chain reaction). This is a great method of measuring for it can detect mRNA levels in a small sample size. They used the western blot analysis to review the amount of Akt. They used immunoprecipitation to study the “interactions between the p85 subunit of PI3 kinase and insulin receptor substrate types 1 and 2.”(E.Steen et al. pg.65).
When E.Steen et al. used the western blot analysis they found “significantly reduced mean levels of phospho-AKT “(E.Steen et al. Pg.73) this could help validate the study that is being done because AKT is involved in cell increase, programmed cell death, and diabetes. AKT was found in large numbers in the hippocampal tissue of AD Brain tissue. This research has found that insulin, and the insulin like growth factors originate from problems linked to impaired CNS growth factor production. The neurons are expressing the growth factor genes. This “raises questions and concerns about the potential benefits of peripherally administered replacement therapy.”(E.Steen et al. Pg.77) The downfall with this finding is that peripherally administered replacement therapy is the best way to administer medications without the complications of the blood brain barrier. In AD brain tissue the IGF-II expression was higher in the hippocampus area of the brain. In the control group, insulin and IGF-1 receptors were expressed at significantly greater amounts than the AD brain tissue. “In AD, insulin gene expression in the hippocampus and hypothalamus was significantly reduced relative to control (insulin gene expression was not detected in the frontal cortex.”(E.Steen et al. pg.68) This shows that AD brain tissue has a lower amount of gene expression in the areas where short term memory is stored. The human growth factor and the receptor expression were found to have significance at the .01 level when insulin was concerned. This research suggests that if AD could somehow be treated with
ligands that can increase insulin and the growth factor signaler, it can increase the life and purpose of certain neuronal cells that are at a high risk of developing AD.
My summary is from research conducted by:
“Impaired Insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease- is this type 3 diabetes?” Eric Steen, Benjamin M. Terry, Enrique J. Riviera, Jennifer L. Cannon, Thomas R. Neely, Rose Tavares, X. Julia Xu, Jack R. Wands and Suzanne M. de la Monte. Journal of Alzheimer’s Disease vol. 7 (2005).
