While MRV administered peripherally led to brain infection and neuroinflammation, it did not increase Aß deposition
HHV-6A promotes inflammation in astrocytoma cells by dysregulating autophagy
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
A potential mechanism by which HHV-6A infection could promote Alzheimer’s Disease
HHV-6A was found to both enhance expression and inhibit degradation of amyloid precursor protein in vitro.
The role of HHV-6 in dysregulating autophagy
HHV-6, like some other herpesviruses, dysregulates autophagy in multiple cell types, with important biological consequences.
HHV-6A/B in brain disease: proposed criteria for establishing causation
Three top experts on HHV-6A/B teamed up to write a comprehensive review and propose criteria for establishing HHV-6A/B to MS, epilepsy and Alzheimer’s disease.
HHV-6A and the suppression of miR155 in Alzheimer’s pathology
Dysregulation of the microRNA miR155 is associated with pathophysiological progression of Alzheimer’s disease. HHV-6A has been shown to suppress miR155.
Clonally expanded CD8 T cells in spinal fluid of Alzheimer’s patients suggest an adaptive immune response to pathogens
Researchers at the NIH used RNA-Seq cells from skin and blood to study the underlying mechanisms in DIHS/DRESS and identified both HHV-6 and JAK-STAT pathways as potential targets. Central memory CD4+T cells were enriched with HHV-6B.
NINDS/NIH investigators find very little HHV-6 RNA or DNA in either Alzheimer’s or control brains
A team led by Steven Jacobson, PhD at NINDS analyzed RNA-seq datasets from 901 brains, and found only 1.2% of Alzheimer’s patients and 0.4% of controls positive for HHV-6 RNA. They also found HHV-6 DNA in less than 4% of samples tested by ddPCR.
The debate continues over RNA-seq analysis of HHV-6A in Alzheimer’s
Two groups have challenged the widely-publicized 2018 study in 2018, that found increased HHV-6A & 7 abundance and an association with clinical and pathology scores in Alzheimer’s. The topic has become the focus vigorous debate.
HHV-6A induces dysregulation of autophagy in neurons and astrocytoma cells, increasing beta-amyloid and tau
Building on their prior work, an Italian team has shown that HHV-6A is able to induce dysregulation of autophagy in neurons and astrocytoma cells, increasing amyloid beta and tau production.
HHV-6A activates microglia and increases Aβ and tau expression
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.
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