Particular parts of the brain structure
A new study which could lead to new techniques to block or slow down the memory-destroying disease, researchers said.
For the analysis, the researchers examined brain samples from patients in memory clinics and discovered that the existence of healthful dendritic spines (connections between nerves) offer protection against Alzheimer’s in individuals whose brains possess proteins linked to the disease.
The findings, published recently in the Annals of Neurology, would be the first of their type, the study authors stated.
“Among the precursors of Alzheimer’s is that the growth in the mind of proteins called amyloid and tau, which we refer to as the pathology of Alzheimer’s disease,” said the study’s lead author, Jeremy Herskowitzsaid
He is an assistant professor with the University of Alabama in Birmingham School of Medicine’s division of neurology.
“But about 30 percent of the aging people possess amyloid and tau buildup but not develop dementia. Our analysis revealed that these folks had bigger, more varied dendritic spines compared to people who have dementia, suggesting that backbone health plays a important part in the beginning of illness,” Herskowitz said in a university news release.
Neurons, that are brain cells, which are constantly sending out dendritic spines in search of different neurons. When they link, a synapse — a market of advice — happens between nerves. This is the foundation for learning and memory, the investigators explained.
“One clear culprit in Alzheimer’s disease is that the reduction of dendritic spines and therefore the reduction of synapses,” Herskowitz said.
“This could impair the capacity to believe, so the premise was that people without dementia had wholesome [dendritic] spines and people with dementia didn’t. But nobody had gone in to see if this was accurate,” he noticed.
Healthy dendritic spines may be hereditary, or the consequence of healthful lifestyle habits — like good diet and exercise — that are proven to decrease the risk of dementia, Herskowitz said.
The newest findings give “a target for medication which would be made to encourage and preserve dendritic spine wellbeing in a bid to reconstruct neurons or stop their loss,” he added.
“This information indicates that rebuilding volunteers is potential. And as we’re better able to spot the gain of both amyloid and tau early in the development of this disease, even before symptoms appear, we may be able to one day provide a medicine which could lead to preserving healthful dendritic spines in people who have the Alzheimer’s pathology,” he concluded.