Researchers from Tufts University School of Medicine (TUSM) found that a single episode of traumatic brain injury could result in elevation of the enzyme, BACE1 in the brain.
The enzyme causes elevated levels of amyloid-beta, a brain peptide whose build-up is associated with Alzheimer's disease.
"A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer's disease," Kendall Walker from department of neuroscience at the University, said.
In an analysis of post-mortem brain samples from patients with Alzheimer's disease, the researchers found that levels of two intracellular trafficking proteins GGA1 and GGA3 were reduced while BACE1 levels were elevated in the brains of Alzheimer's disease patients compared to the brains of people without Alzheimer's disease, suggesting a possible inverse association.
"When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes," Tesco, assistant professor of neuroscience from TUSM, said in a statement.
"We found that GGA1 and GGA3 act synergistically to regulate BACE1 post-injury. The identification of this interaction may provide a drug target to therapeutically regulate the BACE1 enzyme and reduce the deposition of amyloid-beta in Alzheimer's patients," she continued.
Moderate-to-severe traumatic brain injuries are caused most often by traumas, such as severe falls or motor vehicle accidents, but not all traumas to the head result in it.
The study was published in The Journal of Neuroscience.
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