@jenbrea Hey! So I'm getting to the point where I could write a long paper about potential overlapping connections b/t #Alzheimer's and #MECFS, but I'll summarize a few top trends in this thread! First, I brainstormed often on topic with the late Rob Moir
@jenbrea 2/ Rob’s research (done w/ Rudy Tanzi + Will Eimer at Harvard) forms the core of a potential ongoing paradigm shift in Alzheimer’s - namely that #amyloid beta may be an antimicrobial peptide that forms in response to pathogens in #brain tissue: pubmed.ncbi.nlm.nih.gov/30001512/
@jenbrea 3/ To better understand that research, read this #interview I did with Rob before he passed away last year from glioblastoma. Key to ME/CFS is his work indicates that amyloid may form in response to herpesviruses like HSV1 in the Alzheimer’s brain: microbeminded.com/2017/12/18/int…
@jenbrea 4/ We know ME/CFS cases can involve herpesviruses (especially EBV and HHV6), and that herpesviruses are neurotrophic (they preferentially infect the central #nervous system). Read this interview I did w/ Dharam Ablashi who co-discovered HHV6 for more: microbeminded.com/2020/06/28/int…
@jenbrea 5/ With that in mind, this ME/CFS brain was studied via #autopsy by a team at Temple University/UCSD (it’s an excellent analysis!): pubmed.ncbi.nlm.nih.gov/28386034/
@jenbrea 6/ In the ME/CFS brain, the team found “Abundant amyloid deposits identical to AD plaques w/ accompanying intracellular granular structures…and neurofibrillary tangles in white matter of the frontal cortex, thalamus and basal ganglia”
@jenbrea 7/ I showed that paper to Rob Moir and there are two possibilities 1) the ME/CFS subject had Alzheimer’s and had not been correctly diagnosed. Or...
@jenbrea 8/ ....amyloid cld have formed in the ME/CFS brain for other reasons. If amyloid is an antimicrobial peptide it’s possible it formed in response to neurotrophic #pathogens in a manner that contributed to ME/CFS symptoms instead?? (more research needed!)
@jenbrea 9/ There is certainly plenty of #symptom overlap 👉 ME/CFS patients often experience profound “brain fog, which, as you can see from my slide below, often actually involves loss of short #term memory/word recall 👇
@jenbrea 10/ It’s also worth noting that in Alzheimer’s, some studies show herpesvirus antiviral #drugs may prevent disease onset (this study showed a 90% decrease in #dementia risk in patients taking herpesvirus antivirals): pubmed.ncbi.nlm.nih.gov/29488144/
@jenbrea 11/ We know anecdotally that ME/CFS patients often also respond to the herpesvirus #antivirals, so that is another connection from a #clinical perspective...
@jenbrea 12/ Also this Stanford team recently showed that T cells in the cerebrospinal fluid of some patients with Alzheimer’s were responding to Epstein Barr virus: pubmed.ncbi.nlm.nih.gov/31915375/
@jenbrea 13/ That suggests that Epstein Barr #virus could be a player in both ME/CFS/Alzheimer’s. For all we know the virus could simply infect different brain regions/cell types in patients with the two different diagnoses
@jenbrea 14/ OK that’s enough info for now! Our #PolyBio team is working with the Alzheimer’s research teams mentioned in this thread to better study the trends I’ve mentioned in ME/CFS. We are currently #fundraising for the projects so fingers crossed we may learn more moving forward

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More from @microbeminded2

27 Oct
This interesting study found that skeletal #muscle cells of #ME/CFS patients showed a decrease in oxidative phosphorylation (a metabolic pathway used by #mitochondria to generate #energy). In simple terms, that caused the cells to have a dysregulated #metabolism.
2/ Not mentioned in the paper, but important to consider, is that most well-studied #viral + bacterial #pathogens “hijack” the metabolism of the cells they infect in a manner that can result in decreased oxidative phosphorylation (or similar changes in cell energy pathways).
3/ In simples terms, these #pathogens “hijack” cell metabolism to “pull” substrates out of the human mitochondrial energy pathways...and use the substrates (lipids, fatty acids, amino acids) for their own #nutritional and replication purposes!
Read 6 tweets
11 Oct
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker Walker hi - I very much disagree that #Borrelia or #EBV are typically ” long gone” in infected patients who develop chronic symptoms.
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker 2/ There is a large body of literature showing that even if such #organisms cannot be found in blood, they can persist in certain tissues or the central #nervous system where they are very hard to identify clinically
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker 3/ This is particularly obvious w/ EBV which is a #herpesvirus. Herpesviruses almost never “clear” after #infection, and symptom resolution is due to the immune system’s ability to contain the #virus in a non-replicating state
Read 10 tweets
30 Sep
Boy is it refreshing to read this thread that takes a close look at two studies being used to rationalize #vitamin D supplementation for #COVID-19. It explains how both studies have so many problems that the findings must be interpreted with great caution
2/ Why do I care? I spent part of my graduate work working on the molecular #biology of the vitamin D system (including how the various “vitamin” D metabolites impact Vitamin D Receptor activity/gene expression)
3/ Far from being simplistic “vitamins”, the various forms of “vitamin” D are actually secosteroid transcriptional activators, w/ 1-25-dihydroxyvitamin D (also called D3) also acting as a hormone
Read 11 tweets
2 Sep
Thanks for sharing my perspective in this piece @MeganEDoherty! As I mention, in these #longcovid cases, it’s very important to take the potential persistence of #COVID-19 in certain tissues and/or the central nervous system (CNS) seriously!
2/ That’s b/c #Coronaviruses have been shown capable of persisting in human #tissue or certain “anotomical sanctuaries” - for example, this team found Coronavirus RNA + antigen in the Multiple Sclerosis brain: ncbi.nlm.nih.gov/pmc/articles/P…
3/ Also in other “post-viral” syndromes like “Post-#Ebola Syndrome, viral RNA has been found in unexpected body sites like sperm, or the eyes, years after initial infection: nejm.org/doi/full/10.10…
Read 6 tweets
19 Jul
Ryan I take issue with your rash conclusion that #COVID-19 cannot survive in a persistent form in certain #LongCovid patients, and it's unfair to say that people studying the topic or discussing the possibility of COVID-19 chronic persistence are spreading rumors or causing harm!
2/ First, there is no way for you to *know* that #COVID-19 cannot persist in a latent/chronic form in certain patients. The #virus has only existed for a short time, meaning few studies on persistence have even been able to be conducted
3/ Second, have you noted all the cell types/body sites #COVID-19 can infect? (below). Have you obtained samples from all such sites in #LongCovid cases + searched for the #virus in a persistent form? (studies of cerebrospinal fluid, tissue biopsy etc?) nature.com/articles/s4159…
Read 6 tweets
14 Jul
Cool paper detailing what body sites, cell types, symptoms #COVID-19 has been connected to thus far 👉 But one thing: everyone knows that most persistent #viral (and #bacterial) pathogens are capable of #infecting/driving an equally extensive # of #symptoms, right?
2/ For example, in this interview, Dharam Ablashi (who co-discovered the #virus HHV6) explains how HHV6 has been shown capable of contributing to #cancers, type 1 #diabetes, Hashimoto’s, #MS, HPA-axis dysregulation, ME/CFS, Alzheimer’s, neuroinflammation..microbeminded.com/2020/06/28/int…
3/ ..and that the HHV6 can survive in
#microglia, astrocytes, macrophage, neurons/nerves, #pancreatic islet cells, the lung, gut epithelial cells, the #liver etc etc etc!
Read 6 tweets

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