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Lowering some antibodies to increase longevity?

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#1 Ark

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Posted 01 July 2015 - 09:53 PM


I'm wondering if lowering certain antibodies would increase longevity and what role modulation of the immune system play directly with telomerase and related biological functions.

We know the immune system antibodies play a role with some chronic fatigue patients, and when certain antibodies are suppressed the fatigue is lifted using immune suppressing drugs. Although not directly related, it does go to show the intricate relationship with cross functions of the immune system is relatively new in science. My thoughts what if antibodies set the clock of telomeres to some extent? In a fashion untethered to standard anti-aging approaches?


If so what supplements could help selectively counter negative antibodie effects without compromising the needed immunity?

Cheers,!

Edited by Ark, 01 July 2015 - 09:58 PM.

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#2 OneScrewLoose

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Posted 01 July 2015 - 10:59 PM

I would wager to say that we know next to nothing about the potential for this. I wouldn't be messing with antibodies for longevity, when there are known things like Selegiline and Vitamin D that work.


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#3 Ark

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Posted 02 July 2015 - 04:06 AM

I'm looking for studies online but Google is coming up short for my questions. Can anyone link some current medical research in this area, I'm assuming that animal studies are useless therefore computer models probably hold the most potential for any further insights.
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#4 playground

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Posted 02 July 2015 - 10:05 AM

Hi Ark,

 

you said above:

We know the immune system antibodies play a role with some chronic fatigue patients, and when

certain antibodies are suppressed the fatigue is lifted using immune suppressing drugs.

 

That's new for me, i'd not encountered this idea before. 

Do you have a link for that ?


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#5 Ark

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Posted 02 July 2015 - 12:33 PM

It won't let me post any links, something is wrong with my account, mods help?

#6 playground

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Posted 02 July 2015 - 03:43 PM

Thank Ark,

....for supplying the anti-body link.

 

For other readers of this thread, here is the link:

http://www.newscient...ml#.VZVb17ykVC2

 

playground


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#7 nowayout

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Posted 02 July 2015 - 04:25 PM

Well, anti-inflammatory treatments (NSAIDs, anti-TNF biologicals, and aspirin) are known to reduce risk of certain aging-related conditions (e.g., Alzheimer).  These don't mainly affect antibody-related immunity, though. 


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#8 Ark

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Posted 03 July 2015 - 12:29 AM

Does anyone else think there might be some marit to low dose treatment using Rituximab say once a year,- would be beneficial impact for longevity/life extension?


Cheers,!

Edited by Ark, 03 July 2015 - 12:33 AM.

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#9 synthetic

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Posted 03 July 2015 - 05:44 AM

The Rituximab Norway trial presents positive findings; follow-up studies would be nice. The studies were indicated in chronic fatigue syndrome. Literature on life extension limiting. Extrapolating the Norway results in chronic fatigue syndrome would promote longevity/resilience due to improvements in mental and physical state from the chronic fatigue syndrome manifestation(s).

 

Would I expect Rituximab to markedly increase life extension, I would not presume. The note of Rituximab used in cancer treatment was mentioned; I'm not inclined to think Rituximab decreases rates of cancer formation, thus increasing life expectancy.

I recommend Selegiline and positive vitamins and minerals; the 2-3 other studies on rates with Selegiline concluded that Selegiline was positively correlated for the increase in the rats longevity. I have a few articles that mentioned telemere mechanism(s) in cell health. I've thought on how people are approaching life extension; I'm always finding research publications with findings of new biological markers, mechanism discoveries, and biological interactions. The most recent studies I have seen were on small celled organisms; actual cells, yeast, files, bacterium; in vivo studies on these mentioned studies very limiting.

 

When I run into a few sources, I'll link you!


Edited by synthetic, 03 July 2015 - 05:47 AM.

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#10 nowayout

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Posted 03 July 2015 - 01:37 PM

Does anyone else think there might be some marit to low dose treatment using Rituximab say once a year,- would be beneficial impact for longevity/life extension?

 

The theory is that rituximab helps chronic fatigue because it supposedly suppresses an autoimmune reaction where healthy tissues are attacked by the immune system. 

 

This has nothing to do with aging - as far as I know, nobody has linked aging to the kind of autoimmune reaction hypothesized in CFS.  In healthy people, rituximab seems more likely to be harmful than beneficial. 

 

Remember, the immune system is essential for clearing out tissues that have been damaged or mutated.  It is essential in protecting us from cancer.  It may help getting rid of senile cells.  Deficiencies in immune function are hypothesized to be an important contributor to aging. 

 


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#11 synthetic

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Posted 03 July 2015 - 04:09 PM

 

Does anyone else think there might be some marit to low dose treatment using Rituximab say once a year,- would be beneficial impact for longevity/life extension?

 

The theory is that rituximab helps chronic fatigue because it supposedly suppresses an autoimmune reaction where healthy tissues are attacked by the immune system. 

 

This has nothing to do with aging - as far as I know, nobody has linked aging to the kind of autoimmune reaction hypothesized in CFS.  In healthy people, rituximab seems more likely to be harmful than beneficial. 

 

Remember, the immune system is essential for clearing out tissues that have been damaged or mutated.  It is essential in protecting us from cancer.  It may help getting rid of senile cells.  Deficiencies in immune function are hypothesized to be an important contributor to aging. 

 

 

I agree.


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#12 shadowhawk

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Posted 03 July 2015 - 07:24 PM

Very interesting.  If the immune system was working  correctly (as we want) then it would only be doing what we want but when it doesn't?


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#13 Fenix_

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Posted 04 July 2015 - 12:11 AM

Assuming a healthy immune system, what would the advantage be of refreshing the body's supply of B cells? It seems like doing so would lower the threshold for infection in some cases. Although maybe having newer B cells would be more adaptable, and less prone to inappropriate autoimmune response (just speculating here)?


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#14 Fenix_

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Posted 06 July 2015 - 07:52 PM

http://neurosciencenews.com/b2m-neurogenesis-cognitive-decline-2197/

"A blood-borne molecule that increases in abundance as we age blocks regeneration of brain cells and promotes cognitive decline, suggests a new study by researchers at UC San Francisco and Stanford School of Medicine.

The molecule in question, known as beta-2 microglobulin, or B2M, is a component of a larger molecule called MHC I (major histocompatibility complex class I), which plays a major role in the adaptive immune system. A growing body of research indicates that the B2M-MHC I complex, which is present in all cells in the body except red blood cells and plasma cells, can act in the brain in ways not obviously related to immunity–guiding brain development, shaping nerve cell communication, and even affecting behavior."


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#15 Ark

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Posted 17 July 2015 - 09:01 PM

I found this interesting.

http://www.scienceda...50715133504.htm

#16 Ark

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Posted 17 July 2015 - 09:04 PM


MRI scan. (stock image)
Credit: © George.M. / Fotolia
New research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides the first direct evidence linking traumatic brain injury to Alzheimer's disease and chronic traumatic encephalopathy (CTE) -- and offers the potential for early intervention to prevent the development of these debilitating neurodegenerative diseases. TBI can result from repetitive contact sport injuries or from exposure to military blasts, and is one of the most significant risk factors for both Alzheimer's disease and CTE.

In a study published today in the online edition of the journal Nature, the researchers found that a misshapen isoform of the tau protein can develop as soon as 12 hours after TBI, setting in motion a destructive course of events that can lead to widespread neurodegeneration. Importantly, the researchers have developed a potent antibody that can selectively detect and destroy this highly toxic protein.
"TBI is a leading cause of death and disability in children and young adults and also affects approximately 20 percent of the more than two million troops who have deployed to Iraq and Afghanistan," said co-senior author Kun Ping Lu, MD, PhD, Chief of the Division of Translational Therapeutics in the Department of Medicine at BIDMC and Professor of Medicine at Harvard Medical School (HMS). "Our study shows that an early neurodegenerative process induced by the toxic tau protein can begin just hours after a traumatic brain injury. In both cell models of stress and in mouse models simulating sport- and military-related TBI, the production of this pathogenic protein, called cis P-tau, disrupts normal neurological functioning, spreads to other neurons and leads to widespread neuronal death. We have developed a potent monoclonal antibody that can prevent the onset of widespread neurodegeneration by identifying and neutralizing this toxic protein and restoring neurons' structural and functional abilities."
Alzheimer's disease is the most common form of dementia in older individuals and currently affects more than 5 million Americans and 30 million people worldwide. Chronic traumatic encephalopathy is a degenerative brain disease associated with a number of neurological symptoms including risk-taking, aggression and depression. CTE can also lead to progressive dementia.
Previous research has shown that abnormal phosphorylation of the tau protein underlies Alzheimer's and other neurodegenerative diseases. In recent years, the Lu laboratory discovered that tau exists in two isoforms, or shapes -- one functioning and one disease-causing.
"Healthy tau protein is found in the brain and serves to assemble and support microtubules, the 'scaffolding systems' that give neurons their unique shape and are integral to memory and normal brain functioning," explained Lu. But in Alzheimer's, CTE and other neurodegenerative diseases, collectively called tauopathies, tau becomes tangled and unable to function properly.
"Recent studies of CTE in the brains of boxers, American football players and blast-exposed veterans have identified extensive neurofibrillary tau tangles," he said. "But, because these tangles were not detected until months or, more likely, years after TBI, it has not been known whether tauopathy is a cause or a consequence of TBI-related neurodegenerative disease. We have now shown that it is a cause of these diseases."
Co-senior author of the new study Xiao Zhen Zhou, MD, also an investigator in BIDMC's Division of Translational Therapeutics and Assistant Professor of Medicine at HMS, had previously developed polyclonal antibodies capable of distinguishing between two distinct isoforms of the phosphorylated tau protein. The isoform known as trans is in a relaxed shape and is important for normal brain functioning. The other isoform, known as cis, is in a twisted shape and is prone to becoming tangled. Cis P-tau is an early pathogenic protein leading to tauopathy and memory loss in Alzheimer's disease.
"In this new study, we wanted to find out whether cis P-tau is present following TBI and, if so, how to eliminate it from the brain without disrupting the healthy functioning of trans P-tau," said Zhou. "We generated a monoclonal antibody able to detect and eliminate cis P-tau very early in the disease process."
Monoclonal antibody technology is a popular drug development approach. Working like a lock and key, it enabled the investigators to both detect and neutralize only the toxic cis P-tau.
After confirming the existence of this toxic cis tau isoform in the brain tissue of humans who had died of CTE, the authors simulated contact-sport and blast-related injuries in mouse models, and found that the brain's induction of cis P-tau is dependent on injury severity and frequency.
"Mild TBI, also known as a concussion, results in moderate and transient cis P-tau induction," explained Lu. "However, repetitive concussions, as might occur in contact sports, can result in robust and persistent cis P-tau induction. This is similar to what is produced following a single severe TBI caused by a blast or impact."
Subsequent experiments revealed that the cis P-tau protein disrupts the brain's microtubule scaffolding systems and the transport of mitochondria, the powerhouse that provides energy for neuronal function, and eventually leads to neuron death by apoptosis. The research also showed that, over time, cis P-tau progressively spreads throughout the brain. Treating TBI with cis antibody eliminated the toxic cis P-tau, prevented widespread tauopathy and neuron death and restored brain structure and function.
"These experiments told us that cis P-tau has the ability to kill one neuron after another, eventually leading to widespread neurofibrillary tangles and brain atrophy, which are the hallmark lesions of both Alzheimer's disease and CTE," said Lu. "We have determined that cis P-tau is an early driver of neurodegenerative disease after brain injury and that tauopathy it is a cause of TBI-related Alzheimer's disease and CTE. We have also determined that the cis antibody can treat TBI and prevent its long-term consequences in mouse models. The next important steps will be to establish cis P-tau as a new biomarker to help enable early detection, and to humanize the cis antibody for treating patients with TBI."
"Alzheimer's disease and chronic traumatic encephalopathy are terrible diseases that progressively rob individuals of their memory, judgment and ability to function," said study coauthor Alvaro Pascual-Leone, MD, PhD, Chief of the Division of Cognitive Neurology at BIDMC and Professor of Neurology at HMS. Pascual-Leone also serves as Associate Director of the Football Players Health Study (FPHS) at Harvard University, a multi-year initiative to discover new approaches to diagnose, treat and prevent injuries in professional football players.
"High-profile cases of CTE, such as that of the late football player Junior Seau, have vividly demonstrated the tragic consequences of this affliction," he added. "We need to learn more about CTE's causes in order to develop better ways of diagnosing and treating it, and this study offers us a promising early intervention to prevent the pathologic consequences of this disease. These findings additionally offer us a new way to approach Alzheimer's disease, which poses a staggering unsustainable burden throughout the world. Alzheimer's afflicts both individuals and their families and, it deprives society of the contributions of experienced and wise elders."
The study was funded, in part, by National Institutes of Health grants (T32HD040128, UO1NS86659-01; P30AG13846; R01AG029385, R01CA167677; RHL111430; R01AG046319) as well as grants from the Alzheimer's Association and from the Football Players Health Study at Harvard University, a research partnership with the National Football League Players Association.
Lu and Zhou have interests in Pinteon Therapeutics, Inc., which has licensed Pin 1 technology from BIDMC.

#17 Ark

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Posted 27 February 2016 - 02:33 PM

http://www.psypost.o...zophrenia-41251

#18 xEva

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Posted 27 February 2016 - 05:44 PM

Does anyone else think there might be some marit to low dose treatment using Rituximab say once a year,- would be beneficial impact for longevity/life extension?


Cheers,!

 

 

I think so! but where would you get it? I looked just now and it is very expensive (except maybe in India).

 

According to wiki "Rituximab destroys B cells and is therefore used to treat diseases which are characterized by excessive numbers of B cells, overactive B cells, or dysfunctional B cells."

 

Interesting that some viruses are known to hide in B-cells. For exaplme EBV hides there and periodically reactivates, in order to infect more B cells. I just saw a study where a year of acyclovir lowered the number of infected B-cells. To get rid of all  EBV with just acyclovir would take many years. I see in rituximab a potentially more effective therapy. One could take acyclovir and rituximab together, rituximab probably in short, rare pulses on top of continuous acyclovir. 

 

It could be worth a try. But where would you get it for less than $500 per 500 mg vial?


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#19 Ark

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Posted 28 February 2016 - 12:16 PM

Group buy

#20 xEva

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Posted 28 February 2016 - 03:49 PM

Do we have anybody living in India? I thought I saw a ridiculously low price in some medIndia (-?) price list, but could not find it again.

#21 Ark

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Posted 29 February 2016 - 05:51 AM


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YOU ARE AT:Home»Research»Mental Health»Small study finds immunotherapy improves cognition in patients with schizophrenia
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Small study finds immunotherapy improves cognition in patients with schizophrenia 0
BY MEDICAL COLLEGE OF GEORGIA ON FEBRUARY 25, 2016 MENTAL HEALTH
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A recent study of a handful of patients supports mounting evidence that targeted suppression of inflammation packaged with standard therapy can improve the cognitive ability of patients with schizophrenia, physician-scientists report.

After just two intravenous doses in eight weeks of tocilizumab, an immune-suppressing drug regularly prescribed for rheumatoid and juvenile arthritis, study participants had significantly improved cognitive ability, said Dr. Brian J. Miller, a psychiatrist at the Medical College of Georgia at Augusta University.



“This adds to the growing evidence that inflammation plays a role in patients with schizophrenia and again suggests that targeting inflammation may be a viable therapeutic target, at least for cognitive impairment, which is a huge area of unmet need,” Miller said.

Cognitive problems typically are a major source of dysfunction and disability in these patients and can be among the earliest symptoms of schizophrenia, said Miller, corresponding author of the report in the Journal of Clinical Psychiatry.

Anywhere from 25 to 50 percent of patients may have inflammation in the brain contributing to that dysfunction. Problems range from having trouble remembering important numbers to impairment of executive function that enables them to analyze, organize, and generally manage their lives.

Tocilizumab targets the receptor for IL-6, a protein which helps regulate inflammation that is often elevated in patients with schizophrenia. Higher IL-6 levels also have been correlated with a smaller hippocampus, a center for learning and memory in the brain, as well as experiencing more psychiatric symptoms.

The five study patients did not experience improvement in overall levels of psychiatric symptoms, such as hallucinations and delusions, more classic symptoms of schizophrenia, which were already well-controlled with antipsychotics, Miller said.

Nonsteroidal anti-inflammatory drugs, including aspirin, have been tried in these patients, but tend to be less potent and have multiple mechanisms of action, Miller said. “If we see improvements with this drug, then we know it’s not due to other effects.”

Increasing evidence of inflammation’s role in schizophrenia, means that Miller already routinely tests his patients’ blood level of C-reactive protein, an indicator of inflammation and IL-6 levels, and he may try a variety of anti-inflammatory drugs in addition to an antipsychotic.

While he did not pretest in these study patients, Miller later learned that while all appeared to benefit from the targeted anti-inflammatory therapy, only half had elevated C-reactive protein level. That finding is another reason a larger, double-blind study is needed, he said.

While given intravenously for the study, a newer injectable version of tocilizumab also is now available, Miller said. Drugs that directly target IL-6, rather than its receptor, are now available as well and Miller recently received a grant from the nonprofit Stanley Medical Research Institute to examine the effectiveness of one of these drugs, siltuximab, in patients with blood evidence of inflammation. Since he already sees most of his patients monthly, giving these types of drugs should not be much of an additional burden for them.

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#22 Logic

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Posted 29 February 2016 - 10:42 AM

Ark: "I'm wondering if lowering certain antibodies would increase longevity and what role modulation of the immune system play directly with telomerase and related biological functions..."

 

Yes!
The question is why does the immune system get out of whack in the 1st place.

The answers seem to be:

  • AGE's
  • Low level chronic infections.
  • A more and more leaky gut and gut dysbiosis with age.

I dont have the time to write out a dissertation on the subject, but if we can fix those..!

Googlesitesearch in the search dropdown menu! (top. 2nd from right)


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#23 Ark

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Posted 09 December 2016 - 07:28 PM

https://news.virgini...write-textbooks

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#24 Ark

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Posted 10 December 2016 - 01:32 AM

I would be interested in knowing more about the immune systems antibody levels of supercenterians and compare them to healthy normal people. I wonder if there are any tests being conducted like the one I'm imagining.




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