In two independent studies, several prominent scientists funded by Cure Alzheimer’s Fund including Rudy Tanzi, Rob Moir, and Sam Gandy, along with their colleagues, have demonstrated that viruses, and herpes in particular, are involved in Alzheimer’s disease. The herpes virus can influence the activity of many human genes—including several that affect the risk of Alzheimer’s.
The Research Papers are available in Neuron:
Alzheimer’s Disease-Associated beta-amyloid is rapidly seeded by Herpesviridae to Protect against Brain Infection: https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9
Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Dirsuption of molecular, Genetic, and Clinical Networks by Human Herpes Virus: https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5
“Even more Evidence for the Link Between Alzheimer’s and Herpes”
In two independent studies, several prominent scientists funded by Cure Alzheimer’s Fund including Rudy Tanzi, Rob Moir, and Sam Gandy along with their colleagues have demonstrated that viruses, and herpes in particular, are involved in Alzheimer’s disease. The herpes virus can influence the activity of many human genes – including several that affect the risk of Alzheimer’s.
A Common Virus May Play a Role in Alzheimer’s Disease:
Human Aβ protects against herpesviridae in AD mouse and 3D human neuronal cell cultures
Fibrilization mediates Aβ antiherpetic activities, entrapping viruses in β-amyloid
Herpesviridae infections dramatically accelerate Aβ-amyloidosis in AD models
Amyloid-β peptide (Aβ) fibrilization and deposition as β-amyloid are hallmarks of Alzheimer’s disease (AD) pathology. We recently reported Aβ is an innate immune protein that protects against fungal and bacterial infections. Fibrilization pathways mediate Aβ antimicrobial activities. Thus, infection can seed and dramatically accelerate β-amyloid deposition. Here, we show Aβ oligomers bind herpesvirus surface glycoproteins, accelerating β-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 β-amyloidosis in brain. These data support the notion that Aβ might play a protective role in CNS innate immunity, and suggest an AD etiological mechanism in which herpesviridae infection may directly promote Aβ amyloidosis.
Common viral species frequently detected in normal, aging brain
Increased HHV-6A and HHV-7 in brains of subjects with Alzheimer’s disease (AD)
Findings were replicated in two additional, independent cohorts
Multiscale networks reveal viral regulation of AD risk, and APP processing genes
Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD.
From the Archive: Read early insights from Dr. Rudy Tanzi, Dr. Robert Moir, and colleagues on how amyloid-beta protects against microbial infection published in Science Translational Medicine: http://stm.sciencemag.org/content/8/340/340ra72