Just recently, features of psychiatric disorders such as schizophrenia were suggested to be due to a decrease of brain memory center’s inhibitory neurons. HSV-infection is primarily limited to mucosal epithelial cells and neurons, and autophagy is critical in antiviral defense in neurons. Given that type I IFN treatment failed to completely block HSV-1 replication and induce cell death in neurons, some xenobiotical factors might be considered triggering replication of neurotropic HSV-1, and lead to a loss of inhibitory neurons.
HSV1 is capable of infecting all cell lines, glia included. On the other hand, any physical stress that induces a physiological stress reaction with activation of hormonal responses, interleukins and what have you, may trigger a HSV1 flare up. Why inhibitory neurons in particular?
Jyrki,
It’s about a finding announced on January 6, 2015, namely: "Scientists at Columbia University's Mortimer B. Zuckerman Mind Brain Behavior Institute, Columbia University Medical Center (CUMC), and the Université Paris Descartes have found that deficits in social memory--a crucial yet poorly understood feature of psychiatric disorders such as schizophrenia--may be due to a decrease in the number of a particular class of brain cells, called inhibitory neurons, in a little-explored region within the brain's memory center”. This crucial discovery links pretty well with our recent revelation of multiple potentially active dioxin-responsive elements in the promoter area of HSV-1 gene, which reflects ability of the HSV-1 gene to be trans-activated by a body burden amount of dioxin in human cells, including brain’s neurons.
Ilya
So selective neural damage, mediated by activation of HSV1, would be triggered by an environmental toxin? Interesting idea, but in terms of translational research, you may have a long road ahead... HSV1 has been suggested to be the culprit in many neurological and psychiatric diseases, but so far the evidence is anything but convincing. On the other hand, there is no denying that HSV1 works in mysterious ways http://www.neurology.org/content/83/21/1888.short
J
Let me re-reply to your reply with just two not “mysterious ideas” but proven facts, one epidemiological, and another – mechanistic one, both supporting the above mentioned point that Arctic regions accumulated extremely potent dioxin-like compounds thru the marine food chains ("food web"). (1) According to recent studies, your lovely Finland has the highest incidence of Alzheimer’s disease in the world. Namely, a ratio of Alzheimer Dementia/Death per 100K: Finland – 34.9, Iceland – 25.1, USA – 24.8. (2) In addition to our in cilico and experimental data with HSV-1 infected cells other that neurons, the following recent paper directly fits the very target of the problem: “Critical Role of TAK1-Dependent Nuclear Factor-κB Signaling in 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced Astrocyte Activation and Subsequent Neuronal Death”, May 2015 · Neurochemical Research 05/2015; 40(6). DOI:10.1007/s11064-015-1585-2
I.T.
P.S. What if we would try collaborate with your lab, The Alzheimer Society of Finland, or other Scandinavian experts on studying the above vital to all Arctic region countries' problem?
Well, I seriously doubt that the incidence of Alzheimer's in reality is significantly higher in Finland than in the caucasian population overall. Totally different aspect is, how often and by which criteria the diagnosis is made in healthcare. For example, I know for certain, that there is very clear a bias in favor of AD diagnosis, especially in mild cognitive decline and mild dementia, as well as mild VD, since certain social benefits go with the diagnosis.
Thanks for the offer, but I'm 100% occupied in our follow-up birth-risk cohort study.
http://alzheimerdisease.tv/alzheimers-disease-finland-sweden/
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Hämeenlinna 2006, s. 23–39.
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