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"Pruning synapses" and other strides in Alzheimer's research

To date, Alzheimer's disease research has largely focused on controlling the brain plaque amyloid beta. But an article in today's San Francisco Chronicle suggests that this focus may be too narrow. As Erin Allday writes:

First, amyloid beta is probably just one piece of a long chain of events that go wrong in the brains of people with Alzheimer's. And second, that plaque buildup likely has been going on for years, even decades, before people are symptomatic. By the time doctors introduce a drug to attack amyloid beta, the disease has already progressed to the point that almost any treatment is bound to fail, scientists now believe.

The piece spotlights work being done on synapses - connections in the brain that facilitate communication between neurons - in the Stanford labs of neurobiologists Carla Shatz, PhD, and Ben Barres, MD, PhD. It also explains why scientists are working so hard to come up with answers:

The pressure to find treatments and preventions for Alzheimer's disease has been building steadily over the past decade, and it's becoming critical as the United States prepares for the crush of Baby Boomers who are approaching their 70s, when the disease is most likely to strike.

Aside from the personal losses to individuals and families, the needs of those patients will be an enormous burden on the nation's health care system, doctors say. In California alone, almost half a million people are living with Alzheimer's now, and that number is expected to climb to 660,000 by 2025, according to the Alzheimer's Association.

Previously: How villainous substance starts wrecking synapses long before clumping into Alzheimer’s plaquesProtein known for initiating immune response may set our brains up for neurodegenerative disorders, Malfunctioning glia – brain cells that aren’t nerve cells – may contribute big time to ALS and other neurological disorders and Stanford neurologist discusses promising advancements in Alzheimer’s research

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