How resilient are your brain connections?
The conclusion of a new study suggests possible new ways to prevent or slow the memory-destroying disease, Alzheimer’s, researchers said.
For the study, the researchers analyzed brain samples from patients at memory clinics and found that the presence of healthy dendritic spines (connections between neurons) provide protection against Alzheimer’s in people whose brains have proteins associated with the disease.
The findings, published recently in the Annals of Neurology, are the first of their kind, the study authors said.
“One of the precursors of Alzheimer’s is the development in the brain of proteins called amyloid and tau, which we refer to as the pathology of Alzheimer’s,” said the study’s lead author, Jeremy Herskowitz.
He’s an assistant professor with the University of Alabama at Birmingham School of Medicine’s department of neurology.
“However, about 30 percent of the aging population have amyloid and tau buildup but never develop dementia. Our study showed that these individuals had larger, more numerous dendritic spines than those with dementia, indicating that spine health plays a major role in the onset of disease,” Herskowitz said in a university news release.
Neurons, which are brain cells, are constantly sending out dendritic spines in search of other neurons. When they connect, a synapse—an exchange of information—occurs between neurons. This is the basis for memory and learning, the researchers explained.
“One obvious culprit in Alzheimer’s disease is the loss of dendritic spines and thus the loss of synapses,” Herskowitz said.
“This would impair the ability to think, so the assumption has been that those without dementia had healthy (dendritic) spines and those with dementia did not. But no one had gone in to see if that was true,” he noted.
Healthy dendritic spines could be genetic, or the result of beneficial lifestyle habits—such as good diet and exercise—which are known to reduce the risk of dementia, Herskowitz said.
The new findings provide “a target for drugs that would be designed to support and maintain dendritic spine health in an effort to rebuild neurons or prevent their loss,” he added.
“This data suggests that rebuilding neurons is possible. And as we are better able to identify the increase of amyloid and tau early in the progression of the disease, even before symptoms arise, we might be able to one day offer a medication that can contribute to maintaining healthy dendritic spines in those with the Alzheimer’s pathology,” he concluded.
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