HHV-6A infection of microglia cells increases inflammatory markers and Aβ and tau expression dramatically, supporting the hypothesis that plaque development in Alzheimer’s disease may be an innate immune response to pathogens
HHV-6B induces ER stress in primary monocytes, impairing their survival and differentiation into dendritic cells
Investigators propose that the induction of endoplasmic reticulum stress, likely exacerbated by autophagy inhibition, could contribute to the immune suppression induced by HHV-6B in exanthem subitem patients.
Differential gene expression pattern shared in herpesviruses, Alzheimer’s & Parkinson’s patients
Researchers from GlaxoSmithKline found a significant overlap in differentially expressed genes shared by those with herpesvirus infections, Alzheimer’s and Parkinson’s. On the other hand, there was no significant overlap between herpesviruses and Type 2 diabetes or Huntington’s disease.
Herpesvirus acquires protein corona that facilitates the formation of Alzheimer’s plaques
Swedish researchers report that viruses interact with proteins to form a coating or protein corona that facilitates the formation of amyloid plaque, supporting previous findings by Harvard’s Rudy Tanzi and Robert Moir.
Single-cell transcriptomic analysis of Alzheimer’s brains showed early changes that are highly cell-type specific with APOE strongly upregulated in the microglia
MIT examined transcription across tens of thousands of individual cells in both Alzheimer’s and healthy brains and found APOE strongly upregulated in the microglia and perturbation in myelination-related processes in multiple cell types including oligodendrocytes.
Could autophagy dysregulation link neurotropic viruses to Alzheimer’s disease?
The cellular housekeeping function of autophagy may play a role in Alzheimer’s as dysfunction could result in the accumulation of amyloid. HHV-6A, HHV-6B and HSV1 can infect central nervous system cells and dysregulate autophagy.
Herpesviruses may reduce NK cell cytotoxicity in Alzheimer’s
MS patients with a particular haplotype on natural killer cells are more susceptible to HHV-6A infection. Similarly, HHV-6A/B may contribute to Alzheimer’s by utilizing a specific NK cell inhibitory receptor to disrupt the ability of NK cells to clear infected cells.
HHV-6 small non-coding RNA proposed as an indicator of an early stage of HHV-6 reactivation
German investigators have identified a marker for what they believe is the earliest stage of viral reactivation, or “transactivation” marked by transcription of several viral small non-coding RNAs in the absence of detectable viral replication. The group believes that these viral small RNAs could be developed as biomarkers.
Biospecimen Repositories for Alzheimer’s Disease
NIH NeuroBioBank (brain tissues from various neurological diseases) BrainNet Europe – 19 brain banks in 11 European countries UK Brain Banks Network Australian Brain Bank Network – accepts requests from outside Australia
Private funding available for Alzheimer’s research
Alzheimer’s Disease Research Grants–Private sources of funds
National Institute on Aging encourages grant proposals on HHV-6A & HHV-7 in Alzheimer’s
NIH leaders of the National Institute on Aging (NIA) encouraged investigators with experience in virology and infectious disease to apply for funding to study Alzheimer’s disease. The encouragement came at a workshop held at the Alzheimer’s Association International Conference in Chicago on July 22nd.
Gene-expression network analysis points to HHV-6A as a key driver in upregulating genes leading to Alzheimer’s disease progression
Investigators at Mt Sinai used “big data” models to determine that the genes involved with fighting Alzheimer’s are the same ones that fight virus. They found HHV-6A and HHV-7 to be more abundant in Alzheimer’s brains, and singled out HHV6-A as a key modulator of the genes involved in amyloidosis and neuronal death.
HHV-6 and HSV1 dramatically accelerate amyloid plaque production in Alzheimer’s model
Researchers at Harvard studied how neurons responded to the presence of herpesviruses HSV1 and HHV-6, and found that they rapidly induce amyloid plaque production within 24 to 48 hours.
Antiviral therapy reduces risk of dementia in Taiwan seniors with a history of acute herpesvirus infections
Large insurance data studies in Taiwan have found that seniors with shingles or serious HSV1 infections have a 2-3 fold increased risk of certain forms of dementia, and that antiviral treatment can reduce that risk by 90%.
Decreased HHV-6 IgG in Alzheimer’s
Investigators from Uppsala University in Sweden found that HHV-6 IgG reactivity was significantly lower in Alzheimer’s Disease patients compared to controls. The authors suggest reduced immunity may be one reason why past studies have found increased levels of HHV-6 DNA in the brains of Alzheimer’s patients compared to controls.
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