Barron's Medical Journal reporting from National Institution Of Health ( NIH ) Bethesda, Maryland USA Reporting B.Bobby Graham .
Bethesda ( AP ) --- President Obama legacy is helping millions of people live 23% longer. An example of The American People living longer is happening in Genomics and Alzheimer's
While scientists know Alzheimer's disease involves progressive brain cell failure, the science world has discovered two important genes. APOE-e4 
and TREM2 are game changers. Like other chronic conditions, experts believe that Alzheimer's develops as a complex result of multiple factors rather than any one overriding cause. Both age and genetics have been identified as risk factors, The discovery of additional risk factors has deepen our understanding of why Alzheimer's develops in some people and not others.
Apolipoprotein E-e4 (APOE4), discovered in 1993, is the first gene variation found to increase risk of Alzheimer's and remains the risk gene with the greatest known impact. Having this mutation, however, does not mean that a person will develop the disease. APOE-e4 is the first risk gene identified, and remains the gene with strongest impact on risk. APOE-e4 is one of three common forms of the APOE gene; the others are APOE-e2 and APOE-e3.
“It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.”
Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients.
Science in the next four years. Ms Conrad says a great example of the power of genomics was publicized in the New England Journal Of Medicine on November 14, 2012. The Gene TREM2. The TREM2 gene provides instructions for making a protein called triggering receptor expressed on myeloid cells 2. As its name suggests, this protein is made in myeloid cells, which are cells produced in bone marrow. The TREM2 protein is found on the cell surface, where it interacts with the protein produced from the TYROBP gene. The TREM2 and TYROBP proteins form a complex that transmits chemical signals to activate the cell. When the gene is not mutated, white blood cells in the brain spring into action, gobbling up and eliminating the plaque-forming toxic protein, beta amyloid. As a result, Alzheimer’s can be staved off or averted. But when the gene is mutated, the
brain’s white blood cells are hobbled, making them less effective in their attack on beta amyloid. People with the mutated gene have a threefold to five fold increase in the likelihood of developing Alzheimer’s disease in old age. Conrad says If The Mom And The Dad Has Gene Trem2 ....The Child has a 89% Chance Of Getting Alzheimer's
Alzheimer’s
disease (AD) is the most common form of dementia in the elderly. The genetic basis of lateonset AD (LOAD) is not well known. However, since 1993 the relationship with APOE gene is known, recently it has established a new relationship with the TREM2 gene. This review aims to show the implications of mutations in TREM2 gene in AD. Background: Mutations in TREM2 have been involved in Nasu-Hakola disease that causes frontotemporal dementia like (FTD-like) phenotype. Recently it has been involved in AD with an odds ratio as strong as previously reported with APOEε4. Methods and results: We review relevant papers concerning to TREM2 gene, not only its implication in neurodegenerative disease, but also those focused on Alzheimer´s Disease. Conclusion: There is an increased frequency of rare heterozygous TREM2 variations in AD and FTD, and TREM2 variants may play a role in neurodegenerative diseases in general. However, the relationship between TREM2 gene and neurodegenerative diseases is complex and ambiguous results. Surely the TREM2 variants have great interest in future research of neurodegenerative diseases.
President Obama Genomics is leading the way in a new discovery TREM2 Triggering receptor expressed on myeloid cells 2 is a protein that in humans is encoded by the TREM2 gene. The New Leading Technology To Cure Breast Cancer is also here according to Rose Conrad Ph.D. CEO GenNxeix Inc Nanoparticles 
and Semi Conductors GenNxeix Biotech Conrad explains: Quantum dots (QDs), also known as semiconducting nanoparticles, are promising zero‐dimensional advanced materials because of their nanoscale size and because they can be engineered to suit particular applications such as nonlinear optical devices (NLO), electro‐optical devices, and computing applications. QDs can be joined to polymers in order to produce nanocomposites which can be considered a scientific revolution of the 21st century. One of the fastest moving and most exciting interfaces of nanotechnology is the use of QDs in medicine, cell and molecular biology.
Recent advances in nanomaterials have produced a new class of markers and probes by conjugating semiconductor QDs with biomolecules that have affinities for binding with selected biological structures. The nanoscale of QDs ensures that they do not scatter light at visible or longer wavelengths, which is important in order to minimize optical losses in practical applications. Moreover, at this scale, quantum confinement and surface effects become very important and therefore manipulation of the dot diameter or modification of its surface allows the properties of the dot to be controlled. Quantum confinement affects the absorption and emission of photons from the dot. Thus, the absorption edge of a material can be tuned by control of the particle size. Nanocomposite systems for nanomedicine and bioengineering applications Nanoparticles has the potential to enable breast cancer research and improve molecular imaging, early detection, prevention, and treatment of breast cancer. GenNxeix scientist say photoluminescent nanoparticles will allow oncologists to discriminate between cancerous cells and healthy cells.
Proteomics and bioinformatics will enable researchers to identify markers of Breast cancer susceptibility and precancerous lesions Numerous investigations have shown that both tissue and cell distribution profiles of anticancer drugs can be controlled by their entrapment in submicronic colloidal systems (nanoparticles). The rationale behind this approach is to increase antitumor efficacy, while reducing systemic side-effects. This review provides an update of tumor targeting with conventional or long-circulating nanoparticles. The in vivo f
The discovery, said Dr. Sam Gandy of the Icahn School of Medicine at Mount Sinai in New York, is “a real game changer” and “a paradigm shifter.” He added, “I’m really enthusiastic to take a crack at this in my lab.”
Karen Duff, an Alzheimer’s researcher at Columbia University, while praising the work as “a tour de force,” cautioned that once Alzheimer’s starts, tangles can take off on their own and may need to be attacked by drugs that strike them specifically in order to stop devastation in the brain.
Dr. Tanzi is now starting an ambitious project to test 1,200 drugs on the market and 5,000 experimental ones that have finished the first phase of clinical testing — a project that is impossible with mice, for which each drug test takes a year. With their petri dish system, Dr. Tanzi said, “we can test hundreds of thousands of drugs in a matter of months.”
He already has used his system to look at drugs designed to prevent the formation of amyloid, the protein that clumps into plaques. The drugs, he reports, prevented both plaques and tangles in the petri dishes. Some are in clinical trials, and it is not known if they work in people. One was tested in patients and failed because it was too toxic. One hope is to find drugs for other diseases that are known to be safe and work on Alzheimer’s in the petri dish.
He also found an enzyme needed to make tangles after plaques are present. When he blocked that enzyme, plaques formed but not tangles. The enzyme is another potential drug target, he said.
Dr. Gandy wants to use the system to study the effects of genes that predispose someone to have Alzheimer’s, especially the most powerful one, ApoE4, which contributes to about half of all Alzheimer’s cases. No one really knows how or why it is linked to the disease, Dr. Gandy said.
“I think I would go after that to begin with,” he said.
Dr. Tanzi said that once his group had gotten the idea of growing neurons in a gel, setting up Alzheimer’s in a dish system had been straightforward. Group members used human embryonic stem cells — those cells that can become any cell of the body — and grew them with a mixture of chemicals that made them turn into neurons. They gave those neurons Alzheimer’s genes and grew them in wells in petri dishes that were lined with a commercially available gel.
Again genomics science is amazing.
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