Financial Times: New Alzheimer's drug a test for amyloid hypothesis
UC's Espay comments on lecanemab
Japanese company Eisai released preliminary trial data in September on experimental Alzheimer's drug lecanemab that showed it slowed the progression rate of the disease.
The drug is the latest in a series of drugs that stem from what's called the amyloid hypothesis that Alzheimer's is primarily caused by the build-up of amyloid plaques in the brain. Drugs like lecanemab aim to remove the plaques to slow the rate of decline.
The University of Cincinnati's Alberto Espay, MD, proposes an alternative theory that it is the loss of the normal amyloid protein, rather than the build-up of the abnormal amyloid plaques, that leads to degeneration.
Espay, professor of neurology in the UC College of Medicine, director and endowed chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders at the UC Gardner Neuroscience Institute and a UC Health physician, told the Financial Times that lecanemab increases levels of the normal protein in the brain in addition to removing plaques, which could be the cause of the benefits seen in the trial.
Read the Financial Times article. (Note: Account creation or subscription may be required to access article.)
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