IT'S more than a century since Alois Alzheimer first noticed and reported sticky plaques in the post-mortem brain of a patient with what we now know to be Alzheimer's disease, yet the jury is still out on whether the plaques actually cause the disease. We might soon have a better idea: a new drug appears to be the first to harmlessly switch off production of plaque in the human brain. Further trials due to end next year and beyond might show if that halts the disease. The role of plaque in the disease has been questioned following several high-profile failures of drugs that eliminate plaque that already exists in the brain or which seek to stop it being produced there. The only plaque-clearing drug to have shown any clinical promise so far – aducanumab also caused some quite severe side effects, such as brain swelling.
Now more than ever, Alzheimer's disease poses an enormous burden. The neurodegenerative disease afflicts more than five million Americans, robbing them of their memories and placing strain and heartache on their loved ones. This toll costs the U.S. economy hundreds of billions of dollars each year. But a new study of mice published in the Journal of Experimental Medicine suggests that by shutting off just one protein, future medications could potentially break up the sticky plaques associated with Alzheimer's. The protein in question, BACE1, plays a fundamental role in neural development.
Alzheimer's disease can be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer's disease, the protein goes haywire, clumping together to form twisted tangles and, it is thought, releasing toxic chemicals that harm the brain. Now Lars Ittner at the University of New South Wales, Australia, and his colleagues have pinpointed a crucial enzyme that controls how tau proteins behave in the brain.
Certain antibodies may be able to remove Alzheimer's plaques from the brain, according to new research carried about in mice. As much as 20 years before the symptoms of Alzheimer's set in, people with the disease begin to develop amyloid beta plaques that build up in the brain and, scientists believe, interfere with neural signals to cause cognitive and memory losses. But researchers at Washington University School of Medicine have developed an antibody that can remove the proteins these plaques are made of altogether, according to their new research. Several recent clinical trials have tried to use antibodies to target the plaques, but none have gotten past these trial phases, and many treatments have come with unsustainable side effects. The new approach may offer a way around these side effects and stop Alzheimer's plaques before its heart-breaking symptoms begin, the researchers hope.