Researchers at the Columbia University Medical Center (CUMC) have identified a brain protein that may have a role in causing the dementia of Alzheimer’s disease.
The finding could allow scientists to develop more effective treatments.
Neurons are the wiring through which information, in the form of electricity, travels through the brain. For these electrical impulses to get where they’re going, they have to jump across the spaces between neurons. These spaces are called synapses, and a protein called caspase-2 usually maintains them. One of the early effects of Alzheimer’s, however, is a disruption of normal synapse function, which can lead to neuron death. Columbia researchers thought caspase-2 might play a role in that degeneration of synapses.
They tested that idea by specially breeding mice who had amyloid-beta plaques in their brains and lacked the caspase-2 brain protein. Buildups of amyloid-beta appear to be one of the main causes of Alzheimer’s symptoms, and mice with amyloid-beta plaques suffer memory losses like that of human Alzheimer’s sufferers.
The new mice, however, did not lose memory as they aged - in fact, it stayed the same as normal mice. This seems to indicate that when brains have amyloid-beta plaques, as they do in Alzheimer’s cases, the normal caspace-2 protein somehow causes memory loss.
The researchers think the amyloid-beta plaques in Alzheimer’s patients make caspace-2 and a few other proteins more active, damaging the way electrical signals travel through the brain.
This new knowledge about the activities of the caspace-2 protein may allow researchers to develop new medical therapies to treat Alzheimer’s.
Alzheimer's is a degenerative brain disorder that usually strikes older adults. As it progresses, the disease causes memory loss and behavior changes. It also affects thinking and language skills. Patients usually need extensive care from relatives or medical professionals for years, costing billions of dollars.
The U.S. Centers for Disease Control says around the world about 18 million people now have Alzheimer's - and the number is expected to rise to 34 million by 2025.
The finding could allow scientists to develop more effective treatments.
Neurons are the wiring through which information, in the form of electricity, travels through the brain. For these electrical impulses to get where they’re going, they have to jump across the spaces between neurons. These spaces are called synapses, and a protein called caspase-2 usually maintains them. One of the early effects of Alzheimer’s, however, is a disruption of normal synapse function, which can lead to neuron death. Columbia researchers thought caspase-2 might play a role in that degeneration of synapses.
They tested that idea by specially breeding mice who had amyloid-beta plaques in their brains and lacked the caspase-2 brain protein. Buildups of amyloid-beta appear to be one of the main causes of Alzheimer’s symptoms, and mice with amyloid-beta plaques suffer memory losses like that of human Alzheimer’s sufferers.
The new mice, however, did not lose memory as they aged - in fact, it stayed the same as normal mice. This seems to indicate that when brains have amyloid-beta plaques, as they do in Alzheimer’s cases, the normal caspace-2 protein somehow causes memory loss.
The researchers think the amyloid-beta plaques in Alzheimer’s patients make caspace-2 and a few other proteins more active, damaging the way electrical signals travel through the brain.
This new knowledge about the activities of the caspace-2 protein may allow researchers to develop new medical therapies to treat Alzheimer’s.
Alzheimer's is a degenerative brain disorder that usually strikes older adults. As it progresses, the disease causes memory loss and behavior changes. It also affects thinking and language skills. Patients usually need extensive care from relatives or medical professionals for years, costing billions of dollars.
The U.S. Centers for Disease Control says around the world about 18 million people now have Alzheimer's - and the number is expected to rise to 34 million by 2025.
