Several attempts have been made to treat or prevent AD using drugs that inhibit either β-secretase or γ-secretase, but many of these drugs have proved to be highly toxic or unsafe in humans, likely because β-secretase and γ-secretase are required to cleave additional proteins in the brain and other organs. Some of these fragments, such as Aβ42, are particularly prone to forming plaques, and their production is elevated in patients with mutations predisposing them to early-onset AD.
![plaque in the brain plaque in the brain](https://images.newscientist.com/wp-content/uploads/2016/11/02131929/m1080332-alzheimer_s_brain.jpg)
These peptides are generated by enzymes called β-secretase and γ-secretase, which sequentially cleave a protein called amyloid precursor protein on the surfaces of neurons to release Aβ fragments of varying lengths. “Our findings suggest a potential therapy that might prevent one of the key elements of AD.”Īmyloid plaques are composed of small protein fragments called amyloid beta (Aβ) peptides. Wagner, PhD, professor in the Department of Neurosciences at UC San Diego School of Medicine. “Alzheimer’s disease is an extraordinarily complex and multi-faceted condition that has, so far, defied effective treatment, let alone prevention,” said senior author Steven L.
![plaque in the brain plaque in the brain](https://previews.agefotostock.com/previewimage/medibigoff/006cd601f4eba0578bd0dcb866168b00/esy-043351593.jpg)
In studies using rodents and monkeys, the researchers report the drug was found to be safe and effective, paving the way for possible clinical trials in humans. In a new study, published Main the Journal of Experimental Medicine (JEM), researchers at University of California San Diego School of Medicine, Massachusetts General Hospital and elsewhere have identified a new drug that could prevent AD by modulating, rather than inhibiting, a key enzyme involved in forming amyloid plaques. Photo credit: National Institute of AgingĪmyloid plaques are pathological hallmarks of Alzheimer’s disease (AD) - clumps of misfolded proteins that accumulate in the brain, disrupting and killing neurons and resulting in the progressive cognitive impairment that is characteristic of the widespread neurological disorder. These aggregates of misfolded proteins disrupt and kill brain cells, and are a hallmark of Alzheimer’s disease.
![plaque in the brain plaque in the brain](https://images.newscientist.com/wp-content/uploads/2013/09/dn24221-1_800.jpg)
In this artist’s rendering, amyloid plaques are interspersed among neurons.