Amyloid protein content material in the brain linked to Alzheimer’s disease risk Experts from the Flanders Interuniversity Institute for Biotechnology linked to the University of Antwerp will be the first to show that the number of amyloid proteins in brain cells is a significant risk aspect for Alzheimer’s disease. Amyloid protein was already known to become the primary element of the senile plaques in the brains of sufferers pharmacy journal . The new discovery demonstrates that the greater the amount of the protein that is produced, younger the dementia individual is certainly. Alzheimer’s disease Alzheimer’s disease is a storage disorder that affects up to 70 percent of most dementia individuals. In Belgium, about 100,000 people suffer from this disease. The condition gradually destroys mind cells in the deep areas of the brain that are in charge of memory and knowledge. Since the disease was initially reported by Alois Alzheimer – 100 years ago now – researchers have been looking diligently for methods to treat it. Amyloid plaque formation plays a key role Genetic study has previously proven a primary connection between amyloid proteins and the development of senile plaques and lack of cells. Amyloid proteins originates when it’s slice by enzymes from a more substantial precursor protein. In very rare cases , mutations appear in that amyloid precursor protein, causing it to change shape and become cut differently. The amyloid protein that’s formed has different features, causing it to begin to stick and precipitate as amyloid plaques together. The development of amyloid plaques in the brain tissue of Alzheimer sufferers is a central element in the visit a therapy for Alzheimer’s disease. A lot or very little of the amyloid precursor protein is a risk factor The fact that patients with Down syndrome get Alzheimer’s disease shows that the amount of the amyloid precursor proteins contributes to the disease: actually, patients with Down syndrome possess 3 copies of the gene for the amyloid precursor protein and for that reason produce 150 percent instead of 100 percent of the protein. Related StoriesEight myths and truths about Alzheimer's diseaseResearchers successfully restoration nerve cell harm in Alzheimer's dementiaRice scientists solve long-standing mystery regarding hemophilia proteinSo, Jessie Theuns and her co-workers, under the direction of Christine Van Broeckhoven, hypothesized that the number of amyloid precursor protein might also are likely involved in Alzheimer’s disease. The geneticists from Antwerp systematically studied the hereditary code that’s responsible for controlling the expression of the gene . Biological processes in our body are regulated strictly, primarily by controlling the quantity of each protein that’s produced closely. The promoter of a gene has the most significant control function in this process. In youthful Belgian and Dutch Alzheimer’s patients , the experts found genetic variants in the promoter that improved the gene expression and therefore the forming of the amyloid precursor protein. These variants in the promoter that boost expression occur up to 20 times more often compared to the mutations in the precursor protein that change the form. Furthermore, there exists a connection with the age of which the symptoms are 1st detected: the higher the expression , the younger the patient . Thus, the quantity of amyloid precursor proteins is usually a genetic risk element for Alzheimer’s disease in the ageing process. Potential customers for tests and remedies These new findings result in a new understanding: specifically, that the number of the amyloid precursor protein, and thus of the amyloid protein, in brain cells contributes significantly to the risk of contracting Alzheimer’s. This discovery will have to be taken into account in diagnostic checks and in the seek out new medicines.
Amino acid arginine improves treatment for type 2 diabetes More than 371 million people worldwide suffer from diabetes, of whom 90 percent are affected by lifestyle-related diabetes mellitus type 2 . In new experiments, experts from the University of Copenhagen working in collaboration with a extensive analysis group at the University of Cincinnati, USA, possess demonstrated that the amino acid arginine improves glucose metabolism considerably in both lean and obese mice. ‘Actually, the amino acid is just as effective as several well-established medicines for type 2 diabetics,’ says postdoc Christoffer Clemmensen. He has conducted the new experiments structured at Faculty of Health and Medical Sciences, University of Copenhagen. He’s currently conducting analysis at the Institute for Obesity and Diabetes at Helmholtz Zentrum M-nchen, the German Research Center for Environmental Wellness in Munich. To test the result of the amino acid arginine, researchers subjected lean and obese animal versions to a so-called glucose tolerance test, which measures the physical body;s capability to remove glucose from the bloodstream over time. ‘We’ve demonstrated that both lean and extra fat laboratory mice benefit substantially from arginine supplements. Actually, we improved glucose rate of metabolism by as much as 40 percent in both groups. We are able to also discover that arginine increases the body's creation of glucagon-like peptide-1 , an intestinal hormone which plays a significant role in regulating hunger and glucose metabolism, and which is used in numerous drugs for treating type 2 diabetes therefore,’ says Christoffer Clemmensen, and continues: ‘You cannot, of course, cure diabetes by eating unlimited levels of arginine-wealthy hazelnuts and almonds. However, our results indicate that diet-centered interventions with arginine-comprising foods can have a positive influence on how the body processes the food we eat.’ Related StoriesMayo Clinic investigators discover novel mechanism linked to diabetes riskStudy suggests need for specific treatment plans for adolescents with onset type 2 diabetesNew Cleveland Clinic study displays bariatric surgery is secure choice for managing type 2 diabetes in obese or mildly obese patients The research findings were recently published in the American scientific journal Endocrinology under the heading Oral l-arginine Stimulates GLP-1 Secretion to boost Glucose Tolerance in Male Mice. Hormone plays essential role Experts have known for many years that the amino acid arginine is usually very important to the body's ability to secrete insulin. However, the most recent findings show that it is an indirect process. The process is actually controlled by arginine's ability to secrete the intestinal hormone GLP-1, which affects insulin secretion subsequently. ‘Mice without GLP-1 receptors are not affected to the same level by arginine. There is absolutely no perceptible improvement in glucose rate of metabolism or insulin secretion, confirming our hypothesis of a close biological connection between arginine and GLP-1,’ says Christoffer Clemmensen, who carried out the biological experiments in the USA using a special pet model where the receptor for GLP-1 is normally genetically inactivated. The new findings provide optimism for better and more targeted drugs for treating type 2 diabetes; the outlook is long-term, but promising. ‘This interesting result has raised several new questions which we want to investigate. Can other proteins do what arginine will? Which intestinal mechanisms 'measure' business lead and arginine to the launch of GLP-1? Finally, there may be the more long-term perspective – the issue of if the findings can be transferred from mice to humans and be used to create drugs which will benefit diabetes patients,’ says Professor Hans Br-uner-Osborne, who is continuing work on the task in the study group at the Division of Drug Design and Pharmacology at the University of Copenhagen.