Amyloid beta is turning out to be an effective antimicrobial not a rouge dangerous byproduct. The slowness to recognize its function illustrates the danger of pursing only proximate explanations without thinking deeply about why selection shaped mechanisms to make such a molecule. Two new papers this month clinch the case. ALZforum offers a lovely succinct summary of these advances.
A paper by Readhead et al. published June 21 in Neuron shows herpesviruses 6 and 7 are more common in brains with Alzheimer’s than those of controls. A paper due out July 11 from the Tanzi and Moir group at Mass General clinches the case. “herpesvirus glycoprotein B binding induces Aβ fibrillization, mediating protective activities against neurotropic herpes simplex virus 1 (HSV1) and human herpesvirus 6 (HHV6).” Details below.
Readhead B, Haure-Mirande JV, Funk CC, Richards MA, Shannon P, Haroutunian V, Sano M, Liang WS, Beckmann ND, Price ND, Reiman EM, Schadt EE, Ehrlich ME, Gandy S, Dudley JT. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus. Neuron 99, 1–19
Eimer WA, Kumar DK, Shanmugam NK, Washicosky KJ, Rodriguez AS, György B, Breakefield XO, Tanzi RO, Moir RD.Alzheimer’s disease-associated β-amyloid is rapidly seeded by herpesviridae to protect against brain infection. Neuron. 2018 Jul 11.