Alzheimer`S Disease Ebooks

More than five million Americans today have Alzheimers. This debilitating disease is also one of the most heartbreaking, as loved ones slowly slip away and become. This course covers an overview of Alzheimers disease, the pathology of Alzheimers disease and the updated criteria and guidelines for the diagnosis of Alzheimer. Alzheimers treatment breakthrough British scientists pave way for simple pill to cure disease. Scientists have hailed an historic turning point in the search for a medicine that could beat Alzheimers disease, after a drug like compound was used to halt brain cell death in mice for the first time. Click image above to view graphic. Although the prospect of a pill for Alzheimers remains a long way off, the landmark British study provides a major new pathway for future drug treatments. The compound works by blocking a faulty signal in brains affected by neurodegenerative diseases, which shuts down the production of essential proteins, leading to brain cells being unprotected and dying off. It was tested in mice with prion disease the best animal model of human neurodegenerative disorders but scientists said they were confident the same principles would apply in a human brain with debilitating brain diseases such as Alzheimers or Parkinsons. The study, published today in the journal Science Translational Medicine, was carried out at the Medical Research Councils MRC Toxicology Unit at the University of Leicester. Its a real step forward, team leader Professor Giovanna Mallucci told The Independent. Its the first time a substance has been given to mice that prevents brain disease. The fact that this is a compound that can be given orally, that gets into the brain and prevents brain disease, is a first in itself We can go forward and develop better molecules and I cant see why preventing this process should only be restricted to mice. I think this probably will translate into other mammalian brains. In debilitating brain diseases like Alzheimers, the production of new proteins in the brain is shut down by a build up of misfolded proteins or amyloids. This build up leads to an over activation of a natural defence mechanism that stops essential proteins being produced. Without these proteins to protect them, brain cells die off leading to the symptoms of diseases like Alzheimers. The compound used in the study works by inhibiting an enzyme, known as PERK, which plays a key role in activating this defence mechanism. In mice with prions disease, it restored proteins to protect brain cells stopping the disease in its tracks, restoring some normal behaviours and preventing memory loss. Although the compound also produced significant side effects in mice, including weight loss and mild diabetes, which was caused by damage to the pancreas, Professor Mallucci said it would not be impossible to develop a drug that protected the brain without the side effects and that work towards doing so had been very promising. The breakthrough was greeted with excitement by scientists, who nonetheless cautioned that it remained a significant proof of principle and a possible basis for new treatments, rather than a guarantee of an Alzheimers cure in the near future. Computer graphic of a vertical coronal slice through the brain of an Alzheimer patient credit Science Photo LibraryProfessor Roger Morris, acting head Kings College Londons department of chemistry, said This is the first convincing report that a small drug, of the type most conveniently turned into medicines, stops the progressive death of neurons in the brain as found, for instance, in Alzheimers disease. A diagnosis of Alzheimers disease AD, sadly, has become a rite of passage in socalled developed countries. AD is considered the most common form of dementia. True, this study has been done in mice, not man and it is prion disease, not Alzheimers, that has been cured. However, there is considerable evidence that the way neurons die in both diseases is similar and lessons learned in mice from prion disease have proved accurate guides to attenuate the progress of Alzheimers disease in patients. From finding the first effective drug in a mouse, to having an effective medicine in man, usually takes decades to bring to fruition, in the very few cases in which it is successful. So, a cure for Alzheimers is not just around the corner. Family Fun Carton Wallet Template. However, the critical point of principle made by Professor Malluccis study is that a drug, given orally, can arrest neurodegeneration caused by amyloid in the brain. This finding, I suspect, will be judged by history as a turning point in the search for medicines to control and prevent Alzheimers disease. David Allsopp, professor of neuroscience at Lancaster University said that the study had thrown up very dramatic and highly encouraging results, but said that more research was needed to overcome the problematic side effects and to prove the technique would be effective against other disease like Alzheimers and Parkinsons. There are currently 8. UK with dementia and Alzheimers disease is the most common cause. The number of people living with the condition is set to break one million by 2. NHS and the social care system. Parkinsons affect 1 in 5. Dr Eric Karran, director of research at Alzheimers Research UK, said Targeting a mechanism relevant to a number of neurodegenerative diseases could yield a single drug with wide reaching benefits, but this compound is still at an early stage. It will be important for these findings to be repeated and tested in models of other neurodegenerative diseases, including Alzheimers disease. While Alzheimers is the most common form of dementia, other diseases that cause dementia are also characterised by the abnormal build up of proteins in the brain. If this process is also working overtime in these conditions too, targeting it could be a promising avenue for investigation. However, what is true in animals does not always hold true in people and the ultimate test for this compound will be to see whether it is safe and effective in people with these diseases.