Although it was discover in 1906 , Alzheimer ’s disease didn’treceivesignificant research attention until the 1970s . In 1984 , scientists identified the plaque - like buildup of amyloid beta protein in brainiac tissue that have nerve impairment and can conduct to symptom like memory loss , personality changes , and strong-arm infirmity .
Now , researchers are larn why amyloid genus Beta tends to collect in brain tissue like barnacles on a ship . It might not be mobilize expressly to cause hurt , but to protect the brain from another encroacher : the herpes virus simplex virus .
AsThe Atlanticrecentlynoted , a number of studies have strengthen the impression that amyloid beta activeness is work in response to herpes virus , the virus that journey along heart pathways and typically causes stale sores around the mouthpiece ( HSV-1 ) or genitals ( HSV-2 ) . In a study involve mouse , those engineered to bring on more amyloid beta were more resistant to the herpes virus than those who were not .
But when too much amyloid genus Beta is give rise to combat the virus , the protein can involve the mentality ’s neuron . And while herpes tends to target specific nerve pathway in the trunk that result in extraneous sores , it ’s potential that the virus might act other than in an older population that is susceptible to more widespread infection . Roughlyhalfof adult under years 50 in the U.S. are infected with HSV-1 and 12 percent with HSV-2 , which suggests that a enceinte swath of the population could be vulnerable to Alzheimer ’s disease . Two other strains of the virus , HHV-6A and HHV-7 , have also been base to be more common in the brain of departed Alzheimer ’s patients than in the oecumenical universe .
More research will be needed to further understand the possible human relationship between the two . If more finding support the theory , then it ’s potential that antiviral drug or vaccine targeting herpes might also reduce the chances of amyloid genus Beta buildup .
[ h / tAtlantic ]
