Brain inflammation

It could all just be down to energy supply, all of our bodily processes consume energy the brain especially, if we can't we can't supply enough energy to our legs to work properly maybe the same is true of our brains.

 

Coffee pressure Gave me a good laugh at least

 

I think that the Good thing is there’s atleast some neuro-imaging research happening now so we don’t have to hypothesise forever. Whether microglia are activated, active or not and how much is possible to explore

 

They are by the empty academic vessels who make most noise, just as coronary artery disease has been. To someone trained in inflammatory pathology these proclamations make little sense.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3887148/

https://parkinsonsnewstoday.com/201...-new-repurposed-therapies-brain-inflammation/

I can keep posting additional links if you wish.

 

Search for prions (prpsc) and inflammation.

In the beginning there was consenses there was no inmunneresponse. Now it is a different story.

 

Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. bchesebro@niaid.nih.gov.
https://www.ncbi.nlm.nih.gov/pubmed/30650564

Neuroinflammation, Microglia, and Cell-Association during Prion Disease.

Our current understanding is that microglia are beneficial during prion infection and critical to host defense against prion disease.

 

https://www.ncbi.nlm.nih.gov/pubmed/28714865

Microglia in prion diseases.

On the positive side, recent findings suggest that therapeutic strategies modulating microglial activation and function may have merit in prion disease.

 

Interesting location. (@chrisb)

I think often times when it comes to brain inflammation people conflate the appearances of acute brain inflammation, like in encephalitis, with brain inflammation in chronic conditions which I suspect is less overt. I think this holds true with many commonly accepted markers that ME/CFS patients may inadvertantly fall in-range. This holds true for cognitive testing as well.

As a medical community, broadly speaking, we don't calibrate well for the chronically ill.

 

I'm not an expert on prions, but the above 2 posts seem contradictory to me.

1. Microglial are beneficial during prion infection and
2. Modifying/reducing their activation may be a good thing in prion disease.

which, in my mind, reduces down to

1. Microglial activation is an important part of the response to infection, so
2. Lets disable them as it reduces pesky symptoms.

 

In conclusion, microglial activation during prion disease progression is a complex and multistep process, with activated microglia comprising a heterogeneous population with diverse functions. At early stages of prion infection, microglia respond to PrPSc deposits and consequently increase their phagocytic capacity to remove PrPSc. However, this phagocytosis is insufficient, and sustained PrPSc accumulation leads to neuronal damage, which could in turn trigger the microglia to switch to a proinflammatory phenotype and exert detrimental effects in the brain (Figure 1).

 

No need. That was the sort thing I was referring to - empty vessels.

 

Lot of empty vessels out there. A lot. As far as I can tell, they float just fine.

But hey, I know all too well what passes as opinion - or even dogma - in some areas can be crap, so I hear your concerns.

 

Rats! I was afraid you'd say that.

Yet, as always, I appreciate your honesty.

Bill