Scientists at Mount Sinai worked with mice and discovered that the gene RTN1 produces the protein RNT1. Whenever the RTN1 gene is overexpressed, this causes high levels of the RNT1 protein. High levels of RNT1 protein causes kidney cells to self-destruct and induce Chronic Kidney Disease (CKD). CKD affects 10% of American adults and leads to renal disease, the need of dialysis, and even kidney transplants. After working with the mice kidneys, the Mt. Sinai scientists compared the RTN1 gene with a diseased human kidney and found the same results. They believe this can lead to more therapeutic options for those with CKD.

https://www.sciencedaily.com/releases/2015/12/151223221656.htm
Researchers at the Indiana University School of Medicine, linked atrophy to protein levels in blood. Although there is no cure for Alzheimer's disease their research provides a bio-marker blood test. Proteins produced by the genes in the blood are connected to brain atrophy. They used magnetic resonance imaging tools to measure brains. They found nine gene variations that are related to Alzheimer's disease. ABCA7 and MA4A6A are gene expressions that are related to memory . 

https://www.sciencedaily.com/releases/2016/12/161215143358.htm

Researchers have correlated the build up of plague in the brain with inflammation and deficiencies of certain cell types. Micrologia, a cell type that "eats" the protein plagues that cause Alzheimer's, were found deficient, as were Oligodendrocytes, which produce mylein sheathes around neurons. The study examined the brains of both people who died while suffering from Alzheimer's and those who died before they displayed symptoms of Alzheimer's. Researchers found this correlation by analyzing both the genes of the patient and the proteins found in their brain. The protein analysis is referred to as "Proteomic Analysis," and the genetic analysis is referred to as "genetic analysis." This study helps us understand how Alzheimer's develops and how we could possibly detect Alzheimer's. For instance, we can know if a patient is predisposed to developing alzheimer's later in life if they have a high concentration of amaloid plague associated proteins within their blood.

https://www.sciencedaily.com/releases/2016/08/160810142807.htm

Scientists discovered a gene signature in healthy brains that makes them more vulnerable to develop Alzheimer's once they're older. This is because the body's defense against the proteins responsible for the disease are weaker in these areas. Likewise, when people are young their bodies have defense mechanisms against the proteins but those defenses get weaker with age allowing the proteins to form and then build up more. Lastly, these findings may help researchers find out how Alzheimer's originates and could create preventative treatments. 

AML is a forceful blood growth that creates in bone marrow cells. Not long ago, the group announced there are 11 sorts of AML, each with particular hereditary components. Presently they report how a patient's individual hereditary points of interest can be joined into foreseeing the result and treatment decision for that patient. They manufactured a learning bank utilizing information from patients with AML in Germany and Austria. These results helped the research group built a tool to demonstrate how the knowledge bank could be utilized to give customised data about the best treatment alternatives for another patient. There are two alternatives for young patients with AML: a stem cell transplant or chemotherapy. The group assesses that up to one in three patients would be recommended an alternate treatment regimen utilizing the instrument contrasted and current practice. In the long haul they trust the apparatus could save one in ten youthful AML patients from a transplant while keeping up general survival rates.

In this article from the Columbia Medical Center, researchers have figured that the "Tau Proteins" which are proteins that stabilize micro-tubules might be causing disorientation which lead to Alzheimer disease. 

They have developed a solution to solve this problem which is by deep-brain stimulation or light-based therapy.