| First Author | Eimer WA | Year | 2018 |
| Journal | Neuron | Volume | 99 |
| Issue | 1 | Pages | 56-63.e3 |
| PubMed ID | 30001512 | Mgi Jnum | J:270047 |
| Mgi Id | MGI:6269094 | Doi | 10.1016/j.neuron.2018.06.030 |
| Citation | Eimer WA, et al. (2018) Alzheimer's Disease-Associated beta-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection. Neuron 99(1):56-63.e3 |
| abstractText | Amyloid-beta peptide (Abeta) fibrilization and deposition as beta-amyloid are hallmarks of Alzheimer's disease (AD) pathology. We recently reported Abeta is an innate immune protein that protects against fungal and bacterial infections. Fibrilization pathways mediate Abeta antimicrobial activities. Thus, infection can seed and dramatically accelerate beta-amyloid deposition. Here, we show Abeta oligomers bind herpesvirus surface glycoproteins, accelerating beta-amyloid deposition and leading to protective viral entrapment activity in 5XFAD mouse and 3D human neural cell culture infection models against neurotropic herpes simplex virus 1 (HSV1) and human herpesvirus 6A and B. Herpesviridae are linked to AD, but it has been unclear how viruses may induce beta-amyloidosis in brain. These data support the notion that Abeta might play a protective role in CNS innate immunity, and suggest an AD etiological mechanism in which herpesviridae infection may directly promote Abeta amyloidosis. |
