A recent research conducted at Tufts University School of Medicine (TUSM) by analyzing post mortem samples of brains affected with Alzheimer disease says that a moderate to severe traumatic brain injury could result in regulation of BACE1 enzyme. The BACE1 enzyme elevates the levels of amyloid-beta, a brain peptide which is a leading cause of Alzheimer disease. “A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for 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,” said Kendall Walker, doctor associate in the neuroscience department, Tufts University School of Medicine (TUSM). The brain post-mortem study says that the reduced levels of two intracellular trafficking proteins GGA1 and GGA3 were responsible for the rise in BACE1 enzyme levels and hence the sustained amyloid-beta production was observed in the brains after 7 days of injury. When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes and facilitating their transport to lysosomes within brain cells, an area of the cell that breaks down and removes excess cellular material. BACE1 enzyme levels may be stabilized when levels of the two proteins are low, likely caused by an interruption in the natural disposal process of the enzyme. 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, said Tesco, assistant professor of neuroscience department, Tufts University School of Medicine (TUSM).