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Scientists are conducting experiments to create a human/pig chimera to grasp a better understanding of diseases and drug treatments as seeing early human development. Regenerative medicine can be perfected with the research of this chimera because scientists will be able to see how human cells may grow and differentiate/specialize to create a whole new body. Currently, the only successful chimera was that of a mouse and a rat, from which rat cells were introduced into a mouse embryo and were allowed to mature.  Izispua Belmonte, a researcher from the Salk Institute of Biological Studies, used genome editing to direct the rat cells to the places where they needed to grow. CRISPR was used to delete a gene critical for the growth of an organ, and then allowed the rat cells into the niche to see if it fill the gap. Rat cells were also grown to create a gall bladder in the mouse, despite rats not being able to develop gall bladders as it was deemed vestigial and useless for their body for over 18 million years. This proves that the rat is still able to develop a gall bladder, but the genetic coding to do so is hidden by a specific genetic code, which remains unknown. A problem with this experiment however, is that the researchers do not want the pig/human chimera to become too human. They specifically avoided using human cells to create a brain inside the pig, and did so by using CRISPR to edit the pig’s genome. The work is currently still in progress, but may contribute greatly to science if the results come forward.

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Research led by Wellcome Trust Sanger Institute has discovered a new biological target for drugs to reduce the spread of tumors in cancer patients. The research data shows that targeting a Spns2 gene led to a three- quarters reduction in tumor spread. Removal of the spns2 gene caused the largest change, reducing spread of tumors to the lungs by approximately 4 times. Research Dr. David Adams said "Loss of the spns2 gene causes the greatest reduction in the formation of tumor colonies and represents a novel therapeutic target."

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Angelica: Genome engineering paves way for sickle cell cure

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Angelica: Genome engineering paves way for sickle cell cure

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https://www.sciencedaily.com/releases/2016/10/161012160205.htm
Sickle cells primarily afflicts those of African descent which leads to anemia or early death. Researchers want to re-infuse patients with edited stem cells. They began testing genetically modified stem cells on mice. They corrected the disease to cause a mutation in hematopoietic stem cells.

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In all organism, there's a microbiome that call our guts home. They provide multiple services that benefits us. Like providing us with nutrient processing, immune system development and maintenance.  Now scientist from the University of Wisconsin-Madison have uncover that the bacteria in our stomach chemically communicate with our cells far beyond the colon. They also uncovered that a plant based diet can boost communications between the microbiome and cells.
https://www.sciencedaily.com/releases/2016/11/161123124256.htm

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Researchers at North Carolina State University are using light-activated molecules to turn gene expression on and off. They are inhabiting an analogy allowing young scientists and students to understand that being able to control genetic expression is like flipping a light switch. Studying gene function can help regarding diseases like cancer.

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Level of Gene alters risk of Alzheimer’s disease, researchers find
Using new tech like sophisticated techniques that scan genomes of patients, and that a gene appears to either help depending on the level of gene in the brain. The scientists found strong evidence for the role of the gene, insulin-degrading enzyme (IDE). IDE is know to break apart amyloid beta, the protein that clumps together in the brains of Alzheimer’s patients. Genes by looking to see if patients had different variation is genes from non-patients that increased the risk for disease development Apo lipoprotein E-4 (APOE -4) the only major Alzheimer disease. Expression level of 12 gene in an unaffected area of the brain in 200 people with Alzheimer by this group and others in the literature. To read more https://www.sciencedaily.com/releases/2010/03/100315144820.htm

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Anti-CRISPR Gene Editing

Scientists have developed a way to inhibit the CRISPR-Cas9 activity. Using the proteins used y viruses against bacteria, the proteins latch on to the Cas9 and nullify its affects. This extends the control scientists have over CRISPR and prevents any unwanted changes. Developed jointly by the University of Toronto and Massachusetts Medical School.

Link: https://www.sciencedaily.com/releases/2016/12/161208143535.htm

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In Alzheimer's, excess tau protein damages brain's GPS

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.

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https://www.sciencedaily.com/releases/2012/05/120510114107.htm
Researchers at North Carolina State University have been using light activated molecules such as Triplex-forming oligonucleotides (TFOs) which are commonly used molecules that can prevent gene transcription by binding to double-stranded DNA. To find a way to more precisely control TFOs, and the transcription of certain genes so the researchers attached a light-activated "cage" to a TFO. When exposed to ultraviolet (UV) light, the cage is removed, and the TFO is free to bind with DNA, inhibiting transcription of the gene of interest.
Doing this can be used as a targeted therapy to combat diseases like cancer

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https://www.sciencedaily.com/releases/2016/11/161109175141.htm
In a new study, researchers have explored that the purpose of mitochondria in Alzheimer's diseases and also on how the mitochondria uses its energy centers for cells and why they are important in health. Meanwhile, the study grows on as developments regarding gene mutations are affecting mitochondrial function which is effective to the diseases.

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'Mysterious non-protein-coding RNAs play important roles in gene expression

eRNAs, a mysterious subset of non-coding RNAs, are transcribed from enhancer sequences and play a key role in gene expression. Researchers have found that an activator enzyme, CBP, binds to eRNAs and controls patterns of gene expression. This leads researches to ask themselves why are non-coding regions transcribed if they have “no” function. Such information is useful to those studying cancer because it has recently been found that cancer mutations occur in enhancer regions of the genome rather than in protein-coding regions.

Source: https://www.sciencedaily.com/releases/2017/01/170112141331.htm

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Neurodegeneration 'switched off' in mice- Saige Cade

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Neurodegeneration 'switched off' in mice- Saige Cade

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https://www.sciencedaily.com/releases/2012/05/120510141401.htm
Researcher at Medical Research Council (MRC) Toxicology Unit at the University of Leicester have found a way to block the pathway that causes brain cell death in mice with neurodegenerative disease. Some of the dieseases labeled as neurodegenerative diseases include Alzheimer's, Parkinson's and prion disease. The mice with prion disease where a build up of mis-shapen proteins is linked with brain cell death. Due to this build up of proteins, cells switch off the production of proteins as a defense mechanism. Since there is no protein production due to the build up, cell death occurs. By injecting a protein that blocks the 'off' switch of the pathway, the scientist are able to restore protein production which halts the neurodegeneration.

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"Best treatment option written in cancer's genetic script."

https://www.sciencedaily.com/releases/2017/01/170116121804.htm

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.

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Discovery of neurotransmission gene may permit early detection of Alzheimer's disease. Translational Psychiatry, 2016 

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Discovery of neurotransmission gene may permit early detection of Alzheimer's disease. Translational Psychiatry, 2016 

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https://www.sciencedaily.com/releases/2016/11/161116123440.htm
Dr. David Gurwitz of the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University’s Sackler School of Medicine and Professor Illana Gozes, Head of the Elton Laboratory for Molecular Neuroendocrinology at TAU’s Sagol School of Neuroscience led research on possible signs and triggers for Alzheimer’s Disease. This was the first research project of its kind, as the gene Regulator of Protein Signaling 2 (RGS2) had never been studied as a suspect of the progression of Alzheimer’s. “The researchers report that lower RGS2 expression in AD patient cells increases their sensitivity to toxic effects of amyloid-β.” They began their study with the knowledge that of two specific characteristics of Alzheimer’s- dregs of “misfolded amyloid-β (Aβ) peptide plaques, and phosphorylated tau protein neurofibrillary tangles found in diseased brains”- one, Aβ peptides, are also found in healthy brains. This realization led to the query of the significance of these peptides in the configuration of Alzheimer’s disease. Through further investigation, the researchers discovered a negative correlation between the expression of RGS2 and the progression of Alzheimer’s disease in an individual. “The new TAU study furthermore proposes that reduced RGS2 expression increases the susceptibility of brain neurons to the potentially damaging effects of Aβ.” They found, similarly, that reduced expression of the RGS2 was correlated with an increased neurotoxicity of Aβ. "The next step will be to design early blood diagnostics and novel therapeutics to offset the negative effects of reduced expression of the RGS2 protein in the brain,” concluded Dr. Gurwitz.

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Bobak Torabi - Stem cell therapy reverses blindness in animals with end-stage retinal degeneration

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Bobak Torabi - Stem cell therapy reverses blindness in animals with end-stage retinal degeneration

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Link:https://www.sciencedaily.com/releases/2017/01/170110120709.htm

Scientists are attempting to reverse the permanent damager End-stage retinal degeneration has on elderly patients. (leading to blindness and other permanent damage) Scientists decided to turn to animals to see if sight can be restored using this method. They chose to convert mice skin cells into stem cells which were then specialized into retinal tissue, these new cells were found to have some response to light stimulation. Meaning that these stem cells are the first step to restoring eye sight in people who are permanently blind due to age.

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Gene signature in healthy brains pinpoints the origins of Alzheimer's disease

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.

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https://www.sciencedaily.com/releases/2016/10/161012132529.htm

In this article, they articulate on other diseases such as Parkinson's that could occur due to having a specific protein (amyloid beta) associated with having Alzheimer's disease. So in other words, patients who have Alzheimer's disease also have the possibility of having Parkinson's due to the specific protein (amyloid beta) being present from having Alzheimer's.

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Mouse models point of potential treatment for alzeimers

https://www.sciencedaily.com/releases/2017/01/170105100948.htm

Scientists at temple University, Philadelphia experimented on a mouse to see potential treatments of alzheimers. They placed an inhibitor called lipozygenase, an enzyme that can reverse cognitive decline in the mouse and studied its behavior . Which is a over a period of time if the results of alzheimers is negative, then it can be a breakthrough for future treatments.

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Researchers at the University of Cambridge discovered a gene signature in healthy brains that give off the same pattern which allows the spread of Alzheimer's. This discovery can help find the origins of the disease and help find treatments to prevent the disease for at-risk individuals. The gene signature found was located in a specific area of the brain where it is most vulnerable to the disease because the body's defensive mechanisms are weaker in this area. This shows that health individuals that have this gene signature have a greater risk at acquiring the disease later in life. They found out that their answer to their research was in the mechanism of control of amyloid-beta and tau. They concluded that there is a clear link between aggregation phenomenon and the order in which the effects of Alzheimer's disease are known to spread through the different regions of the brain.

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Alzheimer's: Proteomics gives clues toward alternatives to amyloid

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.

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Two Alzheimer's risk genes linked to brain atrophy, promise future blood markers

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 .

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https://www.sciencedaily.com/releases/2010/03/100315144820.htm
Scientists have found evidence that the role of the gene, insulin-degrading enzyme, influences the risk of Alzheimer's disease. IDE is known to break apart amyloid beta, and researchers suggested that little expression of the gene may promote the development of the disease and increased expression of IDE seems to protect against the disease. In their research, they measured mRNA expression levels of 12 genes in the brain with people who have Alzheimer's and then identified genetic variation within these genes. They concluded that "genetic variation in IDE can influence levels of this gene in the brain, thereby modulating development of Alzheimer's by modifying its efficiency in breaking apart amyloid beta."

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Researchers at Howard Hughes University have uncovered indication of the amyloid-b protein(APP's) that deposits to kill brain cells and lead to Alzheimer’s. The discovery reveals how the found APP’s are responsible for activation of gene transcription and uncovers the question: Could scientists find a better treatment for Alzheimer’s? Generally, if medicine could create a medication or procedure that puts these gene switching proteins to a halt, amyloid plaque could be halted, brain cells wouldn’t be killed, and Alzheimer’s disease could be further prevented. The researchers conducted studies to find the processes of amyloid b-proteins. They created a modified version of APP that was injected with one of two variables of DNA, either: DNA-binding proteins (Gal4) or (LexA) DNA  that switch on specific genes. These GMO’s were inserted in to APP’s and watched to see whether transcription of the amyloid plaque would occur. Although, they further injected the protein Fe65 and found that this is what triggers transcription. Furthermore, Alzheimer’s disease can be further regulated when detailed studies of this new discovery is tested and medication can develop.

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Key gene found to drive kidney disease severity. (2015)

https://www.sciencedaily.com/releases/2015/07/150731182847.htm

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.