A-beta, a substance suspected as a prime culprit in Alzheimer’s disease, may start impairing learning and memory long before plaques form in the brain.
A new study led by investigators at the Stanford University School of Medicine has implicated the blocking of endocannabinoids — signaling substances that are the brain’s internal versions of the psychoactive chemicals in marijuana and hashish — in the early pathology of Alzheimer’s disease.
A substance called A-beta — strongly suspected to play a key role in Alzheimer’s because it’s the chief constituent of the hallmark clumps dotting the brains of people with Alzheimer’s — may, in the disease’s earliest stages, impair learning and memory by blocking the natural, beneficial action of endocannabinoids in the brain, the study demonstrates. The Stanford group is now trying to figure out the molecular details of how and where this interference occurs. Pinning down those details could pave the path to new drugs to stave off the defects in learning ability and memory that characterize Alzheimer’s.
In the study, published June 18 in Neuron, researchers analyzed A-beta’s effects on a brain structure known as the hippocampus. In all mammals, this midbrain structure serves as a combination GPS system and memory-filing assistant, along with other duties.
“The hippocampus tells us where we are in space at any given time,” said Daniel Madison, PhD, associate professor of molecular and cellular physiology and the study’s senior author. “It also processes new experiences so that our memories of them can be stored in other parts of the brain. It’s the filing secretary, not the filing cabinet.”
By Bruce Goldman
Read the full story at med.stanford.edu