Discover and read the best of Twitter Threads about #neuroinflammation

Most recents (9)

A significant number of COVID19 patients develop '#longCOVID', a condition defined by long-lasting debilitating, often neurological, symptoms. The pathophysiology of long COVID is unknown. 1/
Here comes a new Preprint that presents in-vivo evidence of widespread #neuroinflammation in long COVID, using a quantitative assessment, [18F]DPA-714 PET, in two long COVID patients. 2/
The researchers reanalyzed historical data from three matched healthy control subjects, for comparison purposes. Both patients with long COVID had widespread increases in [18F]DPA-714 binding throughout the brain. 3/
Read 4 tweets
Excited to share our new paper out at @NatImmunol today! We discovered the limiting factor for #brain #Tregs is #IL2, and developed a new #genetherapy to treat #traumaticbraininjury and other #neuroinflammatory pathologies. 1/12…
The work started more than 10 years ago, after my brother Russell died following a #traumaticbraininjury. The more I read into it, the more treatable #neuroinflammation seems. Obviously there is a #brain delivery problem, but stopping #inflammation is basic #immunology! 2/12 Image
We had a great post-doc, @EmanuelaPasciu1, drive a project showing #Tcells in mouse and human brain, with key functions. Among these T cells were a small population of anti-inflammatory #Tregs, again in mouse and human. 3/12…
Read 12 tweets
This is the most straightforward explanation for chronic symptoms in at least a subset of #LongCovid patients. Partly b/c if the #virus is still present its activity can directly contribute to other phenomena also being documented in LongCovid
2/ Persistence of #SARS-CoV-2 in tissue could lead to shedding of spike protein into blood, which can catalyze the ongoing formation of microclots and hyperactivated platelets
3/ Persistence of SARS-CoV-2 can lead to ongoing downregulation of interferon and/or T cell signaling by the virus, creating an optimal atmosphere for activation of EBV or other #pathogens normally controlled by such immunity
Read 10 tweets
Was passiert eigentlich im Körper von #PostCovid-Patienten und warum sind manche betroffen und andere nicht? Was ist die Pathophysiologie hinter den häufig neurologischen Symptomen und (wie) hängt das mit #MECFS zusammen?
Ein 🧵 und Erklärungsansatz
@LongCovidKids @long_covid
Dass SARS-CoV2 nicht nur die Lunge sondern den gesamten Körper, insbesondere die Gefäße, angreift und potentiell schädigt, ist inzwischen bekannt. In Erklärungsansätzen bzgl. der Beschwerden die noch lange anhalten #longcovid oder auch erst mit einer gewissen Latenz
(Wochen-Monate nach Infektion) beginnen #postcovid werden immer wieder Autoantikörper, Endothelitis (Entzündung der Gefäßinnenwände), Durchblutungsstörungen und eine Unterversorgung des Körpers mit Sauerstoff erwähnt.
Read 11 tweets
Dr. @eyolab is presenting now! #BIIAtTheBench
@eyolab Some cool transcriptional data from this paper today: #BIIAtTheBench #BIIW21
@eyolab A great PI goes where the data go! Integrated #SexDifferences because a trainee brought compelling data for #P2RY12 gene! #BIIW21 #BIIAtTheBench
Read 9 tweets
In a meeting I watched today, microglia priming was mentioned in #LongCovid and #ME/CFS. It’s important to clarify what “microglia priming” means. Microglial priming does not mean that after a trigger has “cleared” microglia remain perpetually activated
2/ Instead, microglia priming goes like this 👉 When microglia or other glial cells detect #infection, injury, or inflammatory mediators, they enter a state of activation in which they change morphology and release their own neuroexcitatory inflammatory mediators
3/ Then, after activating, they retain a “primed” functional state which causes an even more robust response to *subsequent* infectious/immune/#inflammatory challenges. And as cells, microglia live long lives (they are not replaced as often as many other cell types)
Read 13 tweets
#BHB inhibits #inflammasome activation to attenuate #Alzheimer’s disease #pathology | Journal of #Neuroinflammation |

“Here, we find BHB levels are lower in red blood cells and brain parenchyma of AD patients when compared with non-AD controls...…
...Furthermore, exogenous BHB administration reduced plaque formation, microgliosis, apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) speck formation, and caspase-1 activation in the 5XFAD mouse model of AD.”
“Taken together, our findings demonstrate that BHB reduces AD pathology by inhibiting NLRP3 inflammasome activation. Additionally, our data suggest dietary or pharmacological approaches to increase BHB levels as promising therapeutic strategies”
Read 3 tweets
Yet another team ties #neuroinflammation to persistent brain infection 👉 Here, RNA seq + western blot + antibody testing identified pegvirus inside the #brain cells of two patients who died from encephalitis (and not controls):… ImageImage
Important that pegvirus acted as an intracelluar #pathogen (viral antigens were found inside glial cells + lymphocytes + astrocytes)☝️..w/ their presence in lymphocytes suggesting the “cells might serve as a Trojan horse for #viral infection of the brain parenchymal cells.” ImageImage
Also important is that detection of #pegvirus-antigen in the pre-transplantation bone marrow biopsy of one subject 👉 “indicated that this patient was infected at least 15 years before #neurological presentation, suggesting a period of viral latency.” Image
Read 3 tweets

The 10 publications below provide scientific evidence that patients with #MECFS have #brain abnormalities in #neuroinflammation, #metabolism, #neurological connections and blood perfusion

#pwME suffer from #chronicillness

#pwME are #SickNotWeak
1. These studies “provide evidence of #neuroinflammation in #MECFS.. as well as evidence of the possible contribution of neuroinflammation to the pathophysiology of #MECFS

2. This Australian study found abnormalities in the #brain MRIs and peripheral Blood Pressure and Heart Rate in #MECFS patients including the Vasomotor centre, midbrain and hypothalamus

Read 14 tweets

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