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The most robust group of non-amyloid drugs are agents that targets tau, another protein that can form toxic aggregations in the brain. Two anti-tau monoclonal antibodies—ABBV-8E12 and RO7105705—are currently in phase 2 clinical trials, while a third BIIB092 will soon begin recruiting patients for a phase 2 trial. This class of medications has experienced its own share of failures, however; the anti-tau drug LMTM—a derivative of the chemical dye methylene blue—recently fizzled in a phase 3 study.
Among other classes of drugs, azeliragon, a small molecule that inhibits the receptor for advanced glycation end products (AGEs), is currently undergoing a phase 3 study. AGE receptors are involved in transporting amyloid beta fragments into brain cells but they are also associated with inflammation. Another agent in the pipeline is lumateperone, a molecule that targets several types of serotonin, dopamine, and glutamate receptors. Lumateperone is not a cognitive agent; rather it is being tested for the treatment of agitation in AD and other dementias.
In parallel with these trials, new tools are being developed to sharpen the picture of a brain with AD. Many recent trials rely on biomarkers from brain scans or cerebral spinal fluid samples to identify people with early stage AD; these approaches are effective but also expensive and invasive. A study published by researchers in Australia and Japan last week identified blood-based biomarkers that might identify people with prodromal AD, which could greatly speed up the recruiting process for clinical studies.
For related information, see the Psychiatric News article “Long-Term SSRI Use May Slow Progression to Alzheimer’s Dementia.”
(Image: iStock/shironosov)
