You are here: Welcome to the MPKB » Welcome to the MPKB » Marshall Protocol » Minocycline
Home

Differences

This shows you the differences between two versions of the page.

Link to this comparison view

Both sides previous revisionPrevious revision
home:mp:minocycline [09.02.2019] – [Minocycline] sallieqhome:mp:minocycline [09.14.2022] (current) – external edit 127.0.0.1
Line 5: Line 5:
 Minocycline hydrochloride, also known as minocycline, is a broad spectrum tetracycline antibiotic, and was the base antibiotic of the Marshall Protocol. Minocycline hydrochloride, also known as minocycline, is a broad spectrum tetracycline antibiotic, and was the base antibiotic of the Marshall Protocol.
  
-Minocycline is recognized as a DMARD (Disease-Modifying Anti-Rheumatic Drug) by the American College of Rheumatology, which recommends its use as a treatment for mild rheumatoid arthritis.(({{pubmed>long:18512708}})) To minimize its [[home:othertreatments:antibacterials:highdose|dose-dependent immunosuppressive effects]], the Marshall Protocol uses minocycline at pulsed doses [[home:protocol:mp_antibiotics:dosing|much lower]] than otherwise prescribed by rheumatologists.+Minocycline is recognized as a DMARD (Disease-Modifying Anti-Rheumatic Drug) by the American College of Rheumatology, which recommends its use as a treatment for mild rheumatoid arthritis.(({{pmid>long:18512708}})) To minimize its [[home:othertreatments:antibacterials:highdose|dose-dependent immunosuppressive effects]], the Marshall Protocol uses minocycline at pulsed doses [[home:protocol:mp_antibiotics:dosing|much lower]] than otherwise prescribed by rheumatologists.
  
 Either generic or brand name is appropriate to use. Either generic or brand name is appropriate to use.
Line 62: Line 62:
  
  
-Minocycline has been in use for over 40 years yet continues to be effective against MRSA(({{pubmed>long:18221183}})) and to reduce disease severity even after follow-up several years later.(({{pubmed>long:10446869}}))+Minocycline has been in use for over 40 years yet continues to be effective against MRSA(({{pmid>long:18221183}})) and to reduce disease severity even after follow-up several years later.(({{pmid>long:10446869}}))
  
    
Line 69: Line 69:
 {{tag>Other_medication MP}} {{tag>Other_medication MP}}
  
 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
Line 76: Line 77:
 Chef Bama</blockquote> Chef Bama</blockquote>
  
-[[http://www.medscape.com/viewarticle/728141|Minocycline Promising in Fragile X Syndrome]]+[[https://www.medscape.com/viewarticle/728141|Minocycline Promising in Fragile X Syndrome]]
  
  
Line 85: Line 86:
 Minocycline, a clinically used tetracycline for over 40 years, crosses the blood-brain barrier and prevents caspase up-regulation. It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (ALS) and is in clinical trial for sporadic ALS. Because apoptosis also occurs after brain and spinal cord (SCI) injury, its prevention may be useful in improving recovery. We analyzed minocycline's neuroprotective effects over 28 days following contusion SCI and found significant functional recovery compared to tetracycline. Histology, immunocytochemistry, and image analysis indicated statistically significant tissue sparing, reduced apoptosis and microgliosis, and less activated caspase-3 and substrate cleavage.  Minocycline, a clinically used tetracycline for over 40 years, crosses the blood-brain barrier and prevents caspase up-regulation. It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (ALS) and is in clinical trial for sporadic ALS. Because apoptosis also occurs after brain and spinal cord (SCI) injury, its prevention may be useful in improving recovery. We analyzed minocycline's neuroprotective effects over 28 days following contusion SCI and found significant functional recovery compared to tetracycline. Histology, immunocytochemistry, and image analysis indicated statistically significant tissue sparing, reduced apoptosis and microgliosis, and less activated caspase-3 and substrate cleavage. 
  
-//**BW Festoff**// (({{pubmed>long:16638021}})) </blockquote>+//**BW Festoff**// (({{pmid>long:16638021}})) </blockquote>
  
-Also, minocycline partially inhibits caspase-3 activation and photoreceptor degeneration after photic injury.(({{pubmed>long:15990464}}))+Also, minocycline partially inhibits caspase-3 activation and photoreceptor degeneration after photic injury.(({{pmid>long:15990464}}))
  
 <blockquote> <blockquote>
-Minocycline inhibits the growth of glioma by inducing autophagy.(({{pubmed>long:21079420}}))+Minocycline inhibits the growth of glioma by inducing autophagy.(({{pmid>long:21079420}}))
  
 Minocycline effectively inhibited tumor growth and induced autophagy in the xenograft tumor model of C6 glioma cells. These results suggest that minocycline may kill glioma cells by inducing autophagic cell death. When autophagy was inhibited, minocycline still induced cell death through the activation of caspase-3. Thus, minocycline is a promising agent in the treatment of malignant gliomas. Minocycline effectively inhibited tumor growth and induced autophagy in the xenograft tumor model of C6 glioma cells. These results suggest that minocycline may kill glioma cells by inducing autophagic cell death. When autophagy was inhibited, minocycline still induced cell death through the activation of caspase-3. Thus, minocycline is a promising agent in the treatment of malignant gliomas.
Line 98: Line 99:
    * https://marshallprotocol.com/view_topic.php?id=55&forum_id=37    * https://marshallprotocol.com/view_topic.php?id=55&forum_id=37
  
-===== References =====+===== References =====</nodisp> 
home/mp/minocycline.txt · Last modified: 09.14.2022 by 127.0.0.1
© 2015, Autoimmunity Research Foundation. All Rights Reserved.