Alzheimer s Disease is a devastating type of dementia, accounting for 60 to 80 percent of dementia cases, and currently affecting over 5 million Americans. According to the Alzheimer s Association, it is the 6th leading cause of death in the United States, and someone in the U.S. develops the disease every 66 seconds. By 2050, the number of cases is projected to reach 13.8 million.Scientists and researchers have grappled with understanding the disease in a search for a cure since 1906, when German neurologist Dr. Alois Alzheimer discovered the plaques and tangles in the brain of a woman who had died of an unknown mental illness with symptoms of memory loss, difficulty with language, and erratic behavior. Over the progression of the disease, amyloid plaque deposits and neurofibrillary tangles build up in the brain, disrupting connections between nerve cells and ultimately death of nerve cells and brain’tissue.A recent study led by scientists from the University of Glasgow in Scotland and Hong Kong University of Science and Technology has produced a potential breakthrough in Alzheimer s disease treatment.In mice with a progressive disease similar to Alzheimer s, the researchers injected a protein called IL-33. Within a week, the memory and cognitive functions of the affected mice improved to normal levels.  The daily protein injections cleared out existing amyloid plaque in the brain of mice and stopped its development. The results have yet to be tested in humans, with no guarantee the protein will have similar results in human trials. A 2014 study estimated positive results from experiments on mice translate to success in humans at a rate of 8 percent.Nonetheless, the’study is promising as no cure or treatment is currently available for Alzheimer s disease. Alzheimer s care and other forms of dementia are estimated to cost the United States $236 billion in 2016.Working with the mice, the Scottish and Chinese researchers found the protein, IL-33, promotes the development of microglia, immune cells in the brain, and direct them towards the plaque formed by Alzheimer s disease. The relevance of this finding to human Alzheimer s is at present unclear. But there are encouraging hints,  said Professor Eddy Liew, a leading researcher of the’study from the University of Glasgow, in a press release.  For example, previous genetic studies have shown an association between IL-33 mutations and Alzheimer s disease in European and Chinese populations. Furthermore, the brain of patients with Alzheimer s disease contains less IL-33 than the brain from non-Alzheimer s patients. There have been enough false  breakthroughs  in the medical field to caution us not to hold our breath until rigorous clinical trials have been done. The researchers will soon begin the first phase of clinical trials on humans to test the toxicity of the protein IL-33 at the doses used on mice, with the global medical community anticipating with hope for favorable results.Featured Image Courtesy of Flickr
Your task is to classify the provided input as real or fake news. Label 0 is meant for fake news, Label 1 is for real news. TEXT: Alzheimer s Disease is a devastating type of dementia, accounting for 60 to 80 percent of dementia cases, and currently affecting over 5 million Americans. According to the Alzheimer s Association, it is the 6th leading cause of death in the United States, and someone in the U.S. develops the disease every 66 seconds. By 2050, the number of cases is projected to reach 13.8 million.Scientists and researchers have grappled with understanding the disease in a search for a cure since 1906, when German neurologist Dr. Alois Alzheimer discovered the plaques and tangles in the brain of a woman who had died of an unknown mental illness with symptoms of memory loss, difficulty with language, and erratic behavior. Over the progression of the disease, amyloid plaque deposits and neurofibrillary tangles build up in the brain, disrupting connections between nerve cells and ultimately death of nerve cells and brain’tissue.A recent study led by scientists from the University of Glasgow in Scotland and Hong Kong University of Science and Technology has produced a potential breakthrough in Alzheimer s disease treatment.In mice with a progressive disease similar to Alzheimer s, the researchers injected a protein called IL-33. Within a week, the memory and cognitive functions of the affected mice improved to normal levels.  The daily protein injections cleared out existing amyloid plaque in the brain of mice and stopped its development. The results have yet to be tested in humans, with no guarantee the protein will have similar results in human trials. A 2014 study estimated positive results from experiments on mice translate to success in humans at a rate of 8 percent.Nonetheless, the’study is promising as no cure or treatment is currently available for Alzheimer s disease. Alzheimer s care and other forms of dementia are estimated to cost the United States $236 billion in 2016.Working with the mice, the Scottish and Chinese researchers found the protein, IL-33, promotes the development of microglia, immune cells in the brain, and direct them towards the plaque formed by Alzheimer s disease. The relevance of this finding to human Alzheimer s is at present unclear. But there are encouraging hints,  said Professor Eddy Liew, a leading researcher of the’study from the University of Glasgow, in a press release.  For example, previous genetic studies have shown an association between IL-33 mutations and Alzheimer s disease in European and Chinese populations. Furthermore, the brain of patients with Alzheimer s disease contains less IL-33 than the brain from non-Alzheimer s patients. There have been enough false  breakthroughs  in the medical field to caution us not to hold our breath until rigorous clinical trials have been done. The researchers will soon begin the first phase of clinical trials on humans to test the toxicity of the protein IL-33 at the doses used on mice, with the global medical community anticipating with hope for favorable results.Featured Image Courtesy of Flickr