Scientists have identified antibodies that stimulated bone marrow cells to differentiate into microglia-like cells and migrate to the brain, where they reduced the levels of amyloid plaque in mouse models of Alzheimer's disease.
Buoyed by strong scientific evidence and subtle hints of success in clinical trials, the search continues for disease-modifying therapies for Alzheimer's disease (AD) that target amyloid-beta.
Whether it's perseverance or perseveration remains to be seen. But between the strong scientific evidence implicating amyloid beta in Alzheimer's disease (AD) and evidence of some progress in clinical trials, neither industry nor academia is willing to call it quits on pursuing amyloid beta as a target.
When they are directed against the wrong targets, immunoglobulin gamma (IgG) antibodies are the drivers of many autoimmune disorders. But high-dose IgG antibodies are also used to resolve inflammation.
For science as a whole, 2017 was the best of times and the worst of times. The year saw the approval of three gene therapies, a clinical milestone that has its basis in modern molecular biology.
Experimental drugs are increasingly being tested in combinations from the early stages of drug development, with the rationale that such combination treatments provide added benefit over each single agent by interacting with each other.
