The Marshall Protocol Study Site Home

Search
   
Members

Calendar

Help

Home
Search by username
   Not logged in - Login | Register 
The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Alzheimers Amyloid protein is an Antimicrobial Peptide


Alzheimers Amyloid protein is an Antimicrobial Peptide
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  ...  2  3  4  5  6  7  8  Next Page Last Page  
 

New Topic

Reply

Print
AuthorPost
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15960
Status:  Offline
 Posted: Wed Mar 7th, 2012 00:06

Quote

Reply
Who cares? And why?
 

wrotek
member


Joined: Thu Dec 30th, 2004
Location: Wroclaw, Poland
Posts: 2979
Status:  Offline
 Posted: Wed Mar 7th, 2012 01:25

Quote

Reply
Well if the study is badly done and curcumin actually shuts down VDR, we would know to avoid it.



____________________
Lyme reflux chronic pain fatigue depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15960
Status:  Offline
 Posted: Wed Mar 7th, 2012 01:27

Quote

Reply
I thought we had already decided to avoid it, except in small quantities as a spice in foods??
 

wrotek
member


Joined: Thu Dec 30th, 2004
Location: Wroclaw, Poland
Posts: 2979
Status:  Offline
 Posted: Wed Mar 7th, 2012 01:31

Quote

Reply
Oh we did ? I did not know that. It never tasted good anyway, bitter dry sand. But i like Mustard ...

Last edited on Wed Mar 7th, 2012 01:37 by wrotek



____________________
Lyme reflux chronic pain fatigue depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
Cynthia S
Foundation Staff


Joined: Wed Dec 24th, 2008
Location: N., Arizona USA
Posts: 4126
Status:  Offline
 Posted: Wed Mar 7th, 2012 10:34

Quote

Reply
If amyloid beta is an antimicrobial peptide, does it make any sense for macrophages to be gobbling it up?

Mustard comes under the heading of seasoning.  Tho I eat it in such quantities, I sometimes wonder.

Cynthia



____________________
MP start 10/08,break 1/16 - 9/16, Spondylitis'97,early Diverticulosis'98,early AMD'08,Calcium anomaly'95,TypeII Diabetes(?)'02,Degenerative hip disease'12, 25D=10.8 May'18 (preMP 125D/25D=47/43) https://marshallprotocol.com/forum30/13911-2.html
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15960
Status:  Offline
 Posted: Wed Mar 7th, 2012 11:06

Quote

Reply
Cynthia,
Macrophages clean up general cellular junk and trash, and might perhaps clean up scraps of antimicrobial. In this case, whoever, the pathogens which caused the monocytes and macrophages to produce the amyloid-beta in the first place have almost certainly vanished in the process of the researchers trying to get access to the tissue, so all bets are off with respect to what actually might be happening a live human being :)
 

Chloe Ringer
Member
 

Joined: Fri Dec 18th, 2009
Location: Baltimore, Maryland USA
Posts: 265
Status:  Offline
 Posted: Thu Mar 8th, 2012 06:54

Quote

Reply
I'm reminded of a paragraph on biotechnology by Wendell Berry in his book, Citizen Papers:

"Richard Strohman, of the University of California-Berkeley, has proposed that the problems of biotechnology arise, not because the science is new, but because it is old.  He sees it as a development of a now outdated paradigm according to which scientists have undertaken to supply simple solutions to complex problems, without due regard to the complexity of the problems.  The proper scientific response to this, he says, is to enlarge the context of the work."



____________________
MP Dec'09(no breaks)/LymeDisease'78(#1)'05(#2)/high liver enzymes, liver/stomach inflammation, high mitochondrial antibodies, autoimmune hepatitis, joint/muscle pain, dizziness, IBS, brain fog, neuropathy, neck/sinus pain, fatigue, osteoporosis/last 25D=9
lorenzo von matterhorn
Member*


Joined: Wed Jan 6th, 2010
Location: Bergen, Norway
Posts: 685
Status:  Offline
 Posted: Tue Mar 13th, 2012 04:15

Quote

Reply
http://www.newsroom.ucla.edu/portal/ucla/scientists-pinpoint-how-vitamin-229702.aspx

macrophages gobbling up Amyloid Beta..



____________________
Emotional&cognitive issues, food intolerance 125D50 25D19 PH1Sep09 PH2Oct09 (28/01)25D3.6 low lux nada sun
wrotek
member


Joined: Thu Dec 30th, 2004
Location: Wroclaw, Poland
Posts: 2979
Status:  Offline
 Posted: Sat Mar 31st, 2012 02:54

Quote

Reply
Interesting differences between curcumin and 1,25-D in this paper.



____________________
Lyme reflux chronic pain fatigue depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
mvanwink5
Support Team


Joined: Fri Nov 5th, 2010
Location: Newland, North Carolina USA
Posts: 3696
Status:  Offline
 Posted: Sat Mar 31st, 2012 07:55

Quote

Reply
From the paperThe mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.I am not sure what they are saying here, are they really saying the VDR was on the cell surface membrane? These researchers need serious help in writing technical papers for clarity. I am not saying I am better, but I have never heard of the VDR being on the cell surface before.

The paper might have an interesting find if the difference in curcumin and 1,25D was only due to VDR stabilization differences as they assert, but I can't see that they showed that (though they seem to infer that). They utilized a technique based on mass spectrometry, which showed that 1a,25–dihydroxyvitamin D3 stabilized many more critical sites on the vitamin D receptor than did the curcuminoids.
Best regards,
Mike

PS Sometimes I wonder if these researchers would conclude police are the cause of crime because they are frequently found at the scene of crimes, and therefore we need to reduce how many policemen there are (amyloid beta is an amp)?



____________________
Lyme joints, EMF sensitive, MP start 8/10; 25D <4ng/ml 6/19; vegetarian; olmesartan only-240mg/d, RF shielding required, My Progress: http://tinyurl.com/z2stwo8
Russ
inactive member
 

Joined: Fri Mar 24th, 2006
Location: Hartford, Connecticut USA
Posts: 812
Status:  Offline
 Posted: Sat Mar 31st, 2012 08:31

Quote

Reply
mvanwink5 wrote: From the paperThe mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.
Is this implying that VDR activation is dependent on calcium? 

mvanwink5
Support Team


Joined: Fri Nov 5th, 2010
Location: Newland, North Carolina USA
Posts: 3696
Status:  Offline
 Posted: Sat Mar 31st, 2012 09:56

Quote

Reply
Russ,
As I understanding the paper it is after the VDR agonist has docked that the Ca becomes involved.
Best regards,
Mike



____________________
Lyme joints, EMF sensitive, MP start 8/10; 25D <4ng/ml 6/19; vegetarian; olmesartan only-240mg/d, RF shielding required, My Progress: http://tinyurl.com/z2stwo8
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15960
Status:  Offline
 Posted: Sat Mar 31st, 2012 10:01

Quote

Reply
Don't dwell on these biology papers too much - this is a far more complex issue than any of these research groups have ever dreamed. Each only gives you a small glimpse into the actual mechanisms in play...
 

Russ
inactive member
 

Joined: Fri Mar 24th, 2006
Location: Hartford, Connecticut USA
Posts: 812
Status:  Offline
 Posted: Sat Mar 31st, 2012 14:25

Quote

Reply
Interesting.  Thanks.

Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Wed Aug 14th, 2013 03:17

Quote

Reply
Study identifies new culprit that may make aging brains susceptible to neurodegenerative diseases

http://tiny.cc/ot2s1w

"The study, to be published Aug. 14 in the Journal of Neuroscience, reveals that with advancing age, a protein called C1q, well-known as a key initiator of immune response, increasingly lodges at contact points connecting nerve cells in the brain to one another. Elevated C1q concentrations at these contact points, or synapses, may render them prone to catastrophic destruction by brain-dwelling immune cells, triggered when a catalytic event such as brain injury, systemic infection or a series of small strokes unleashes a second set of substances on the synapses"

"No other protein has ever been shown to increase nearly so profoundly with normal brain aging," said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.


"The brain has its own set of immune cells, called microglia, which can secrete C1q. Still other brain cells, called astrocytes, secrete all of C1q's complement-system "teammates." The two cell types work analogously to the two tubes of an Epoxy kit, in which one tube contains the resin, the other a catalyst"

"
Most cells in the body have their own complement-inhibiting agents. This prevents the wholesale loss of healthy tissue during an immune attack on invading pathogens or debris from dead tissue during wound healing. But nerve cells lack their own supply of complement inhibitors. So, when astrocytes get activated, their ensuing release of C1q's teammates may set off a synapse-destroying rampage that spreads "like a fire burning through the brain," Barres said"

Last edited on Wed Aug 14th, 2013 03:19 by Bane

GillyB
Support Team


Joined: Tue Jul 10th, 2012
Location: Olympia, Washington USA
Posts: 3614
Status:  Offline
 Posted: Wed Aug 14th, 2013 04:29

Quote

Reply
Maybe I'm stating the obvious, but the researcher is assuming that the buildup up is age-related.

"No other protein has ever been shown to increase nearly so profoundly with normal brain aging," said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.

Perhaps it's a consequence of immune system dysfunction instead.




____________________
MP start Jun'12, once again on an MP break | Degenerative Disc Disease, Osteoarthritis, Post-Lyme, depression/anxiety, GI. Most recent serum 25D: 6/15 -18
Carry on, and keep MP'ing
Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Wed Aug 14th, 2013 09:37

Quote

Reply
GillyB wrote:Perhaps it's a consequence of immune system dysfunction instead.
This:)

Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Thu Aug 7th, 2014 01:09

Quote

Reply
Link between vitamin D, dementia risk confirmed

http://www.sciencedaily.com/releases/2014/08/140806161659.htm

"Similar results were recorded for Alzheimer's disease, with the moderately deficient group 69 per cent more likely to develop this type of dementia, jumping to a 122 per cent increased risk for those severely deficient"

"The study also found evidence that there is a threshold level of Vitamin D circulating in the bloodstream below which the risk of developing dementia and Alzheimer's disease increases. The team had previously hypothesized that this might lie in the region of 25-50 nmol/L, and their new findings confirm that vitamin D levels above 50 nmol/L are most strongly associated with good brain health"

Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Thu Aug 7th, 2014 01:29

Quote

Reply
Alzheimer's Associated β-Amyloid Protein Inhibits Influenza A Virus and Modulates Viral Interactions with Phagocytes.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0101364

Accumulation of β-Amyloid (βA) is a key pathogenetic factor in Alzheimer's disease; however, the normal function of βA is unknown. Recent studies have shown that βA can inhibit growth of bacteria and fungi. In this paper we show that βA also inhibits replication of seasonal and pandemic strains of H3N2 and H1N1 influenza A virus (IAV) in vitro. The 42 amino acid fragment of βA (βA42) had greater activity than the 40 amino acid fragment. Direct incubation of the virus with βA42 was needed to achieve optimal inhibition. Using quantitative PCR assays βA42 was shown to reduce viral uptake by epithelial cells after 45 minutes and to reduce supernatant virus at 24 hours post infection. βA42 caused aggregation of IAV particles as detected by light transmission assays and electron and confocal microscopy. βA42 did not stimulate neutrophil H2O2 production or extracellular trap formation on its own, but it increased both responses stimulated by IAV. In addition, βA42 increased uptake of IAV by neutrophils. βA42 reduced viral protein synthesis in monocytes and reduced IAV-induced interleukin-6 production by these cells. Hence, we demonstrate for the first time that βA has antiviral activity and modulates viral interactions with phagocytes.


Helicobacter pylori filtrate impairs spatial learning and memory in rats and increases β-amyloid by enhancing expression of presenilin-2

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3990046/

"Injection of H. pylori filtrate significantly increased Aβ42 both in the hippocampus and cortex, together with an increased level of presenilin-2 (PS-2), one key component of γ-secretase involved in Aβ production. Incubation of H. pylori filtrate with N2a cells which over-express amyloid precursor protein (APP) also resulted in increased PS-2 expression and Aβ42 overproduction"

Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Sat Sep 20th, 2014 02:28

Quote

Reply
Down Syndrome helps researchers understand Alzheimer's disease

http://www.sciencedaily.com/releases/2014/09/140918150832.htm

http://brain.oxfordjournals.org/content/137/9/2556


"Our findings indicate that many adults with Down syndrome can tolerate amyloid-β deposition without deleterious effects on cognitive functioning."


 Current time is 07:45
Page:  First Page Previous Page  ...  2  3  4  5  6  7  8  Next Page Last Page  



* We can help you understand chronic disease, but only your physician is licensed to give you medical care *

Powered by WowBB 1.7 - Entire site Copyright © 2004-2020 Autoimmunity Research Foundation, All Rights Reserved
Click here to view our PRIVACY POLICY
Page processed in 0.3110 seconds (95% database + 5% PHP). 19 queries executed.