Sometimes a scientific airfield appear to make little forward motion for years , before promulgation come in a rush . At least to non - neuroscientists , that attend to be the case with the connection between the herpes virus and Alzheimer ’s disease . Just last month a paper reported that nous tissues from mass with Alzheimer ’s aretwice as likelyto have been infected with two common strains of herpes virus as tissues from hoi polloi without , and now we may know why .
Last calendar month ’s research was n’t the first to propose a link between herpes virus and dementia , although it was the most convincing . NowDr Rudolph Tanziof Massachusetts General Hospital has shown that genus Beta - amyloid proteins , which forge plaque in the brains of people with Alzheimer ’s disease , maw herpes virus computer virus particle , preventing immediate damage to the brain . Unfortunately , once the memorial tablet have been “ seed ” in reaction to the virus they keep growing , with black consequences later on .
The body of work has focalize on the HSV-1 virus , which preponderantly make cold sore , not the rarer but more noted HSV-2 , which is associated with more frequent re - occurrences of genital infections .
Beta - amyloid plaque have been see waste product with no utilitarian purpose of their own . However , Tanzi and colleague found that mice infect with HSV-1 survive significantly longer if they can verbalise beta - amyloid than if they can not .
describe inNeuron , the squad showed that the protein truss to the computer virus and prevents it from aggress the brain , but at the cost of inducing plaques much originally in the mouse ’s lives than normal .
“ Our finding reveal a dim-witted and direct chemical mechanism by which herpes virus infections trigger the deposition of brain amyloid as a defense response in the brain , " Tanzi said in astatement . " In this style , we have merged the infection hypothesis and amyloid hypothesis into one ‘ Antimicrobial Response Hypothesis ’ of Alzheimer ’s disease . ”
The work suggests that controlling Alzheimer ’s may not be as simple as direct beta - amyloid , since its absence seizure could lead to even swifter damage . On the other hand , ifforthcoming trialsof a herpes vaccine prove effectual we may find it going some path to solve even big problems than the ones against which it was designed .
However , while herpes may be the most common infectious agent stimulating genus Beta - amyloid growth , it ’s not unique . Tanzi and colleagues havepreviously shownthe protein has a protective role against fungal and bacterial infections . therefore , while a vaccine against , or discourse for , herpes virus might help trim the number of Alzheimer ’s cases , we ’ll call for something much more comprehensive to stop the disease totally .
Tanzi is lead the “ Brain Microbiome Project ” , exploring the hypothesis that , like the intestine , the brain ordinarily has a population of good microbes whose gap makes agency for pathogen to take over .
