Researchers at the University of Florida in the United States have uncovered the mechanism by which anti-inflammatory processes could trigger Alzheimer’s  Disease.

The link between inflammation and the disease has long been known but the new work suggests that simply reducing inflammation might not be the best way forward. According to the team, the anti-inflammatory process might actually trigger the build-up of sticky clumps of protein that form the plaques that block brain cells’ ability to communicate,  a well-known characteristic of the illness.

The findings suggests that Alzheimer’s treatments need to hone in on which forms of Apolipoprotein E, a major risk factor for Alzheimer’s disease, patients carry in their genes. The researchers say that the anti-inflammatory protein interleukin 10, or IL-10, can  increase the amount of apolipoprotein E, or APOE, protein, and thereby plaque, in the brain. In the 1990s, researchers theorised that nonsteroidal anti-inflammatory drugs, or NSAIDs, might protect people from the onset of Alzheimer’s by dampening inflammation that released harmful proteins. Though NSAIDs were effective in some studies, other research did not show any clear protective benefit.

Todd Golde, M.D., Ph.D., director of the Center for Translational Research in Neurodegenerative Disease and the lead author on the new paper about the Florida study, said: “There are many different kinds of NSAIDs. Not all NSAIDs are equal and it wasn’t clear what else they were doing when they were addressing their intended target.” Previously, researchers had hypothesised that a flood of proteins, called cytokines, involved in promoting inflammation in the brain contributed to the formation of plaque in Alzheimer’s disease. However, the new study suggests that anti-inflammatory stimuli may increase plaque instead. Paramita Chakrabarty, Ph.D., a member of the UF Center for Translational Research in Neurodegenerative Disease, an assistant professor in the UF College of Medicine department of neuroscience and the paper’s co-author, said: “This is another piece of evidence that overturns the long-held hypothesis that a ‘cytokine storm’ creates a self-reinforcing, neurotoxic feedback loop that promotes amyloid-beta plaque deposition.”

Therapy takes big step forward

Neurocrine Biosciences has been granted orphan drug status by the United States Food and Drug Administration for NBI-77860, a corticotropin-releasing factor 1 receptor antagonist used to treat congenital adrenal hyperplasia (CAH), which affects 30,000 people in the United States. Malcolm Lloyd-Smith, Chief Regulatory Officer of Neurocrine Biosciences, said: “This status represents a significant regulatory milestone for the CAH programme and underscores the importance of bringing a safe and effective CAH therapy to market.” Further studies into the therapy are under way.

Companies sign agreement

Swiss firm Novartis has signed collaboration and licensing agreements with Intellia Therapeutics to support the development of new medicines. The work will use CRISPR genome-editing technology to develop drug discovery tools and involve experts at Intellia and Caribou Biosciences, two of the leading biotechnology companies developing the technology. CRISPR allows scientists to precisely edit the genes of targeted cells and is used to create very specific models of disease for use in drug discovery.

Japan the target for drug programme

HUYA Bioscience International, which helps to develop biopharmaceutical products originating in China, is pressing ahead with plans to use the cancer drug HBI-8000 for the treatment of adult T-cell leukemia/lymphoma (ATL) and peripheral T-cell lymphoma in Japan. The company says that there is an unmet medical need in Japan where ATRL is responsible for 700-1,000 deaths per year. HTLV-1, the virus that causes ATL, infects more than a million people in Japan.  Worldwide, the figure is more than ten million.