Alzheimer's disease is on the rise and every 3 seconds, someone in the world seems to have been developing it. Since there is no cure yet to stop or slow down its progression, it can be wise to prevent it in the first place. Nowadays there are several genetic testing companies that can identify your risk for diseases like Alzheimer's. Here are a few ways that can help prevent Alzheimer's: Also, several autopsies have found that a majority of people with Alzheimer's disease also had cardiovascular diseases. It is assumed that plaques and tangles present in the brain can remain in the brain and not show any symptoms unless there is evidence of vascular diseases.
"In keeping with the tenets of personalized medicine, the introduced framework could lead to more effective medical care, decreased undesired secondary effects, and substantial reduction of pharmaceutical/clinical costs associated with clinical trials, thereby accelerating the creation-evaluation cycle of new therapeutic agents, says Iturria-Medina. "Our future work will focus on applying the pTIF to other neurological disorders, extensively validating it, and, importantly, making the resulting analytic tools available to the international community, via open-access platforms."
Brain cells are reshuffling their own DNA. The finding may explain how Alzheimer's disease develops and pave the way for new treatments using existing HIV drugs. Most drugs for treating Alzheimer's disease are designed to clear out clumps of beta-amyloid protein that build up in the brain of people with the condition. But they have had disappointing outcomes in clinical trials so far. While studying the gene responsible for making beta-amyloid – called APP – Jerold Chun at Sanford Burnham Prebys Medical Discovery Institute in California and his colleagues discovered something strange.
Two thin wires implanted in the brain may help treat Alzheimer's disease by delivering electrical current. In the first test of this technique in people, two out of the three people who received the treatment showed less of a decline in their mental abilities than people at a similar stage of the disease who didn't have the surgery. However, a larger randomised control trial is needed to know if the treatment really does work. The technique used is called deep brain stimulation, and is already used to treat the tremors and movement problems of some people with severe Parkinson's disease. As well as having wires surgically inserted into the brain, recipients also get a power supply for the wires implanted under the skin near their collar bones.
Last week, at the Sixth Annual Traumatic Brain Injury Conference in Arlington, Virginia, neurologist Samuel Gandy presented a former National Football League player's positron emission tomography (PET) scan as the "most dramatic" evidence yet of chronic traumatic encephalopathy (CTE) in a living person. "I've never seen anything like it," he said of the scan, which used a PET tracer called T807 to reveal deposits of a sticky, helical protein called tau in the player's brain. The announcement could represent a milestone for tau imaging, a promising but controversial strategy for diagnosing neurodegenerative diseases such as Alzheimer's in living patients. If the science pans out, it could also transform the medical and legal status of CTE, which at present can only be officially diagnosed after death, when a pathologist looks for tau in brain tissue.