![\"TAU_HIGH.JPG\"](\"https:\/\/blogs.nature.com\/spoonful\/files\/TAU_HIGH.JPG\")
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The main culprit behind Alzheimer\u2019s disease has long thought to be the toxic protein beta-amyloid, which forms diffuse plaques in the brain. As such, most researchers have assumed that the nerve cell-engulfing tangles caused by a second protein called tau were mere consequences of the amyloid plaques. But given the failure of current amyloid-targeting drugs to reverse the course of the devastating neurodegenerative disorder, the plaque theory has been waning<\/a>.<\/p>\n In its place, the focus is shifting over to blocking tau<\/a>. In a series of new studies reported yesterday at the International Conference on Alzheimer\u2019s Disease<\/a> in Honolulu, Hawaii, researchers reported four new experimental therapies that either target tau directly or mediate levels of both tau and beta-amyloid conjointly.<\/p>\n In one study, a team led by Kaj Blennow<\/a> of the University of Gothenburg in Sweden looked at the effects of an experimental drug called bapineuzumab, which had been designed to reduce clumps of amyloid-beta. Blennow\u2019s team analyzed spinal fluid samples<\/a> from two phase 2 clinical trials, and found that patients given bapineuzumab \u2014 which is being developed jointly by Pfizer, Elan Corp and Johnson & Johnson \u2014 had significantly lower levels of tau in their brain. These findings add to a small imaging study, published in April in Lancet Neurology<\/a>, showing that drug cut amyloid levels in the brain by 25%.<\/p>\n Independently, Delphine Boche<\/a> of the University of Southampton, UK and her colleagues investigated levels of tau in patients given a beta-amyloid immunotherapy as part of a phase 2 trial that had to be stopped early after a few participants developed serious brain inflammation. The researchers found that immunized Alzheimer\u2019s subjects had significantly less tau in their dendrites compared to unimmunized controls.<\/p>\n \u201cThe findings show that treatment aimed at beta amyloid may also modify tau changes in Alzheimer\u2019s,\u201d Boche said in a press release<\/a>.<\/p>\n Two research teams also reported findings from new rodent models of Alzheimer\u2019s. Allal Boutajangout<\/a> of the New York University School of Medicine treated diseased mice with a monoclonal antibody called PHF-1 and found that mice performed better than controls in a balance test and had 58% less tau pathology in the brain’s hippocampus. Meanwhile, Michal Novak<\/a> of the Slovak Academy of Sciences in Bratislava developed a new transgenic rat model of Alzheimer\u2019s rat that expresses non-mutated tau yet can generate Alzheimer’s tangles. Immunizing the rats with a mutated version of tau, Novak announced, prevented the tangle development and slowed the loss of learning behaviors.<\/p>\n \u201cIt is very important that we have a variety of therapeutic targets in the fight against Alzheimer’s disease,\u201d William Thies, chief medical and scientific officer at the Alzheimer’s Association, said in a press release<\/a>. \u201cThe more opportunities that we investigate to intervene and change the relentless and progressive course of Alzheimer’s, the better chance that we will find something that works.\u201d<\/p>\n Image of tau tangles via Wikimedia Commons<\/em><\/p>\n","protected":false},"excerpt":{"rendered":" The main culprit behind Alzheimer’s disease has long thought to be the toxic protein beta-amyloid, which forms diffuse plaques in the brain. As such, most researchers have assumed that the nerve cell-engulfing tangles caused by a second protein called tau were mere consequences of the amyloid plaques. But given the failure of current amyloid-targeting drugs to reverse the course of the devastating neurodegenerative disorder, the plaque theory has been waning. In its place, the focus is shifting over to blocking tau. In a series of new studies reported yesterday at the International Conference on Alzheimer’s Disease in Honolulu, Hawaii, researchers … Read more<\/a> Continue reading