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.
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.
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.
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.
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.
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
Alzheimer’s Disease Research Grants–Private sources of funds
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.
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.
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.
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%.
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.
Japanese investigators from Kobe University identified CXC11 as a chemokine uniquely expressed in primary HHV-6B infections. They also confirmed a previous finding that cytokine CCL2 (MCP-1) plays a role in HHV-6B primary infections. Both CXCL11 and CCL2 are expressed in several neuroinflammatory conditions including epilepsy, Alzheimer’s disease and traumatic brain injury.
A group from Italy’s University of Bologna report that genetic defects in antimicrobial defense mechanisms can leave some individuals vulnerable to sub-clinical infections that lead to cognitive decline as they age. They found variations in specific antiviral genes that correlate with HHV-6 DNA levels in brain tissue and blood from patients with Alzheimer’s disease.
New data suggests HHV-6 and EBV are associated with the development of Alzheimer’s in elderly persons.