Alzheimer's

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Alzheimer's Disease (AD) is the most common form of dementia, accounting for 60 to 80 percent of dementia cases. It is "a type of dementia that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks."[1]

Notable studies[edit | edit source]

Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.[2]
  • 2018, Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus[3] (SUMMARY)
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.[3]

Learn more[edit | edit source]

References[edit | edit source]

  1. "What Is Alzheimer's?". alz.org. 
  2. 2.0 2.1 Itzhaki, Ruth F. (2018). "Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer's Disease". Frontiers in Aging Neuroscience. 10. doi:10.3389/fnagi.2018.00324. ISSN 1663-4365. 
  3. 3.0 3.1 Readhead, Ben; Haure-Mirande, Jean-Vianney; Funk, Cory C.; Richards, Matthew A.; Shannon, Paul; Haroutunian, Vahram; Sano, Mary; Liang, Winnie S.; Beckmann, Noam D. (2018). "Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus". Neuron. 99 (1): 64–82.e7. doi:10.1016/j.neuron.2018.05.023. ISSN 0896-6273. 
  4. Johnson, Cort (Aug 2, 2016). "Reversing Alzheimer's: What It Could Mean for ME/CFS and Fibromyalgia - Health Rising". Health Rising. Retrieved Oct 23, 2018. 
  5. Belluck, Pam (Jun 21, 2018). "A Common Virus May Play Role in Alzheimer's Disease, Study Finds". Retrieved Oct 23, 2018. 
  6. Itzhaki, Ruth (Oct 23, 2018). "There is mounting evidence that herpes leads to Alzheimer's". bbc.com. BBC - Future. Retrieved Oct 23, 2018. 

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.