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Fenamate NSAIDs inhibit the NLRP3 inflammasome and protect against Alzheimer’s disease in rodents

Never Give Up

Collecting improvements, until there's a cure.
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This seems to have a powerful effect of memory in Alzheimer's patients.

http://www.nature.com/ncomms/2016/160811/ncomms12504/full/ncomms12504.html

In summary, we have shown that fenamate NSAIDs are potent and selective inhibitors of the NLRP3 inflammasome, which act through inhibition of VRAC, a novel player in NLRP3 inflammasome regulation. Fenamate NSAID inhibition of NLRP3 is rapidly reversible which offers significant clinical benefit. We have characterized their activity both in vitro and in vivo and propose that fenamate NSAIDs can be rapidly repurposed as drugs to target the NLRP3 inflammasome in inflammatory diseases such as Alzheimer’s disease.

Is anyone aware of any research related to this in ME patients?
 

Hutan

Senior Member
Messages
1,099
Location
New Zealand
Some background information that might help interpret this:

There are various classes of NSAIDs (Non-steroidal Anti-inflammatory Drugs):
http://emedicine.medscape.com/article/2172136-overview
  • Acetic acids
  • COX-2 inhibitors - Celexicob
  • Fenemates - Meclofenamate and Mefenamic acid
  • Oxicam derivatives - eg Meloxicam (Mobic)
  • Propionic acids - eg Fenoprofen and Ibuprofen
  • Salicylates eg Aspirin
ETA: the article in the OP also mentions Flufenamic acid as one of the fenemates
 

Hutan

Senior Member
Messages
1,099
Location
New Zealand
Meclofenemate doesn't sound great if our mitochondria are already limping along.

https://edsinfo.wordpress.com/2016/05/07/nsaids-cause-heart-damage/

The UC Davis researchers compared naproxen, considered the safest over-the-counter NSAID, with a more potent anti-inflammatory, the prescription drug meclofenamate sodium (MS).

They found that meclofenamate sodium (MS)

  • increased reactive oxygen species,
  • impaired mitochondrial function,
  • decreased proteasome function, and
  • increased cardiac cell death.
Naproxen did not affect proteasome function or cause heart cells to die, but it did impair mitochondrial function and increase reactive oxygen species produced in cardiac cells.

“We were surprised to see that many of the NSAIDs we tested were causing the cardiac cell to die when used for prolonged periods,” said Gomes. “Some people are taking these drugs too often, and this is a problem. These drugs are abused.”

(Although, I couldn't see the details of the study. Sounds as though it was on mouse cardiac cells in vitro so perhaps more systemic benefits couldn't be observed.)