CBD oil

I’m testing CBD oil for some of our seniors with pain.

CBD oil is made by extracting CBD from the cannabis plant, then diluting it with a carrier oil like coconut or hemp seed oil. It’s gaining momentum in the health and wellness world, with some scientific studies confirming it may ease symptoms of ailments like chronic pain and anxiety.

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CBD oil is made by extracting CBD from the cannabis plant, then diluting it with a carrier oil like coconut or hemp seed oil. It’s gaining momentum in the health and wellness world, with some scientific studies confirming it may ease symptoms of ailments like chronic pain and anxiety.

 

 

Sensory neurons regulate how we recognize pain, touch, and the movement

‘Busybody’ Protein May Get On Your Nerves, But That’s A Good Thing

Summary: Researchers have identified a protein that is critical for pain signaling.

Source: Salk Institute.

Sensory neurons regulate how we recognize pain, touch, and the movement and position of our own bodies, but the field of neuroscience is just beginning to unravel this circuitry. Now, new research from the Salk Institute shows how a protein called p75 is critical for pain signaling, which could one day have implications for treating neurological disorders as well as trauma such as spinal cord injury.

“The p75 protein is a busybody. It plays a role in many different signaling pathways,” says Salk Professor Kuo-Fen Lee, holder of the Helen McLoraine Chair in Molecular Neurobiology and co-senior author of the new work. “This complexity makes the protein interesting to study. In this latest research, we discovered that, in addition to its other functions, it’s also required for the survival of certain pain-sensing neurons.” The results are published October 17, 2017, in Cell Reports.

Previous research by Lee’s lab had shown that p75 is involved in a signaling pathway that regulates the development of sensory neurons–cells which transmit our sensation of pain, touch and muscle tension–in the dorsal root ganglia.

In this latest study, the investigators collaborated with a team at the University of Michigan led by co-senior author Brian Pierchala to further learn about the role of p75 in the development of sensory neurons. They studied mice lacking p75 only in the sensory neurons. When these mice were born, their sensory neurons were normal. But by the time they were six months old, some of those sensory neurons had degenerated, particularly the populations of cells that usually transmit pain signals.

It turned out that p75 partners with another class of receptors, called the GDNF (glial cell-derived neurotrophic factor) receptor family. The p75 protein binds to one such receptor called Ret, which is associated with some neurological conditions as well as certain types of cancer. Members of the GDNF family support the survival of sensory neurons that transmit the pain signal and p75 enhances this survival-promoting effect by interacting with Ret. When p75 was removed, the survival-promoting signal from GDNF family members was reduced and the sensory neurons that need this signal to survive gradually degenerated.

Image shows the p75 protein in the ns.

“In this particular study, one of the remarkable findings is that this relationship between Ret and p75 exists at all. It’s something that wasn’t previously known,” says Zhijiang Chen, a postdoctoral fellow in Lee’s lab and one of the paper’s co-first authors. “This research adds further significance to the role of p75 as a master regulator for many different signaling pathways that are vital for the nervous system to function normally.”

Lee says that although he doesn’t know of any human disorders that are associated with the loss of p75 in particular, pain sensation is obviously vital for quality of life. “We do know of people who have these kinds of sensory deficits, and it can be serious problem,” he says. “Thanks to this research, we now know more about the broad influence of the p75 protein.”

Future studies will look at the role p75 plays in two other types of cells — glial cells and skin cells. The investigators also plan to look in more detail at the role of p75 in different parts of the body.

“We know that in the sacral region, there is a high percentage of sensory neurons with strong p75 expression,” Lee says.

ABOUT THIS NEUROSCIENCE RESEARCH ASALK INSTITUTECLE

Other authors on the study are Bertha Dominguez, Yoshinobu Harada, Tasha Bengoechea of Salk; Weichun Lin of UT Southwestern Medical School; and Christopher R. Donnelly and Alan S. Halim of the University of Michigan.

Funding: This research was supported by grants from the NIH, the Clayton Foundation, the Schlink Foundation, the Gemcon Family Foundation, and the Joe W. and Dorothy Dorsett Brown Foundation.

Source: Salk Institute
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Salk Institute.
Original Research: The study will appear in Cell Reports.


Neurotrophins

The low-affinity nerve growth factor receptor (nerve growth factor receptor (TNFR superfamily, member 16), also called the LNGFR or p75 neurotrophin receptor) is one of the two receptor types for the neurotrophins, a family of protein growth factors that stimulate neuronal cells to survive and differentiate. LNGFR is a member of the tumor necrosis factor receptor (TNF receptor)superfamily – indeed, LNGFR was the first member of this large family of receptors to be characterized.[5][6]

The neurotrophins are composed of four proteins, all of which bind to the LNGFR: nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4).

Nerve growth factor, the prototypical growth factor, is a protein secreted by a neuron’s target. NGF is critical for the survival and maintenance of sympathetic and sensory neurons. NGF is released from the target cells, binds to and activates its high-affinity receptor tropomyosin receptor kinase A (TrkA), and is internalized into the responsive neuron. The NGF/TrkA complex is subsequently trafficked back to the cell body. This movement of NGF from axon tip to soma is thought to be involved in the long-distance signaling of neurons.
The activation of TrkA by NGF is critical in inducing the survival and differentiation caused by this growth factor.
However, NGF binds at least two receptors on the surface of cells that are capable of responding to this growth factor, TrkA (pronounced “Track A”) and the LNGFR.

Trk family of receptor tyrosine kinases

TrkA is a receptor tyrosine kinase (meaning it mediates its actions by causing the addition of phosphate molecules on certain tyrosines in the cell, activating cellular signaling). There are other related Trk receptors, TrkB and TrkC. Also, there are other neurotrophic factors structurally related to NGF: BDNF (for Brain-Derived Neurotrophic Factor), NT-3 (for Neurotrophin-3) and NT-4 (for Neurotrophin-4). While TrkA mediates the effects of NGF, TrkB binds and is activated by BDNF, NT-4, and NT-3, and TrkC binds and is activated only by NT-3.

Neurotrophins activating LNGFR may signal a cell to die via apoptosis, but this effect is counteracted by anti-apoptotic signaling by TrkA, TrkB, or TrkC signaling in cells that also express those receptors. LNGFR functions in a complex with Nogo receptor (NgR, Reticulon 4 receptor) to mediate RhoA-dependent inhibition of growth of regenerating axons exposed to inhibitory proteins of CNS myelin, such as Nogo, MAG or OMgP. LNGFR also activates a caspase- dependent signaling pathway that promotes developmental axon pruning, and axon degeneration in neurodegenerative disease.


I massage with coconut oil the buttocks, upper legs, lower back and stomach of my elderly seniors to relieve pain as most of them have lower body pain.

Connie

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My scientist friend asked how to detox or clean his body from toxins

Over the years, I have experienced family and friends dying of cancer. I observed their lifestyle and toxins they are exposed to. So to answer my friend’s question on how to detox and the mechanism of cleaning our body or getting rid of toxins, I listed some items for Dos and Donts.

Our lymphatic system which travels opposite our blood is responsible for cleaning our blood.  Search for lymphatic, massage and detox in this site http://www.clubalthea.com

When we clean the many bad foods or toxins that entered our body, we must clean our liver first, our laboratory.  It is closely linked to our heart that during our last breath, our liver is the first and last signal that our heart gets to shut down.

Detox or cleaning our cells from toxins is the key to living longer, the anti-aging process we all are seeking for. In my 50s, I could have died long time ago if I was born centuries ago with no clean water, fresh produce and raising a dozen children. Each child is minus 5 years of a woman’s age.

Detox is like cleaning the toilet. The following are detox tips and anti-aging tips to clean your cells:

Dos in cleansing your body from toxin, also detoxes your liver

  • Massage
  • Adequate sleep
  • Filtered water
  • Lemon
  • Baking soda (pinch in your drinking water)
  • Activated charcoal
  • Digestive enzymes from pineapple and papaya
  • Apple cider vinegar
  • Wash produce with salt or diluted vinegar
  • No over ripe fruits and left over foods or 3-day old rice ( aflatoxin , mycotoxin )
  • No charred BBQ
  • Whole foods ; sulfur rich as they are anti-inflammatory (ginger, garlic, turmeric, coconut, walnuts)
  • Deep breathing thru nose and blow out thru mouth
  • Prayer: May God’s light energy be with you and say Amen to accept it.
  • Resveratrol from Berries, kiwi, citrus fruit
  • Fasting
  • Activated charcoal
  • Clean air

Donts are ways that when practiced or consumed can kills our nerve cells and produce toxins in our cells.

  • Avoidance of too much caffeine, iron and sugar, these are food for cancer
  • Other metal toxins
  • TRANS fat
  • Processed
  • Plastics in food
  • Stress
  • Shift work: not sleeping from 10pm to 4 am
  • Radiation
  • Over medications, chemo, other carcinogens
  • Avoid exposure to fumes, chemicals (formaldehydes,carcinogens,toxins)

 

——-

Hi Connnie,

And what is your recipe for liver detox and the mechanism by which it works to accomplish that?

From: Male friend in his late 50s whose brother died of pancreatic cancer

Shared genetic influence on frailty and chronic widespread pain: a study from Twins UK 

Shared genetic influence on frailty and chronic widespread pain: a study from Twins UK 

Abstract

Introduction

frailty is an increased vulnerability to adverse health outcomes, across multiple physiological systems, with both environmental and genetic drivers. The two most commonly used measures are Rockwood’s frailty index (FI) and Fried’s frailty phenotype (FP).

 

Material and methods

The present study included 3626 individuals from the TwinsUK Adult Twin Registry. We used the classical twin model to determine whether FI and FP share the same latent aetiological factors. We also investigated the relationship between frailty and chronic widespread musculoskeletal pain (CWP), another holistic age-related condition with significant clinical impact.

 

Results

 

FP and FI shared underlying genetic and environmental aetiology. CWP was associated with both frailty measures, and health deficits appeared to mediate the relationship between phenotypic frailty and pain. Latent genetic factors underpinning CWP were shared with frailty. While frailty was increased in the twins reporting pain, co-twin regression analysis indicated that the relationship between CWP and frailty is reduced after accounting for shared genetic and environmental factors.

 

Conclusions

 

Both measures of frailty tap the same root causes, thus this work helps unify frailty research. We confirmed a strong association between CWP and frailty, and showed a large and significant shared genetic aetiology of both phenomena. Our findings argue against pain being a significant causative factor in the development of frailty, favouring common causation. This study highlights the need to manage CWP in frail individuals and undertake a Comprehensive Geriatric Assessment in individuals presenting with CWP. Finally, the search for genetic factors underpinning CWP and frailty could be aided by integrating measures of pain and frailty.


Chronic widespread muscoloskeletal pain

Chronic widespread muscoloskeletal pain (CWP) is prevalent in the general population and associated with high health care costs, so understanding the risk factors for chronic pain is important for both those affected and for society. In the present study we investigated the underlying etiological structure of CWP to understand better the association between the major clinical features of fatigue, depression and dihydroepiandrosterone sulphate (DHEAS) using a multivariate twin design.

Methodology/Principle Findings

Data were available in 463 UK female twin pairs including CWP status and information on depression, chronic fatigue and serum DHEAS levels. High to moderate heritabilities for all phenotypes were obtained (42.58% to 74.24%). The highest phenotypic correlation was observed between fatigue and CWP (r = 0.45), and the highest genetic correlation between CWP and fatigue (rg = 0.78). Structural equation modeling revealed the AE Cholesky model to provide the best model of the observed data. In this model, two additive genetic factors could be detected loading heavily on CWP—A2 explaining 40% of the variance and A3 20%. The factor loading heaviest on DHEAS showed only a small loading on the other phenotypes and none on fatigue at all. Furthermore, one distinct non-shared environmental factor loading specifically on CWP—but not on any of the other phenotypes—could be detected suggesting that the association between CWP and the other phenotypes is due only to genetic factors.

Conclusions/Significance

Our results suggest that CWP and its associated features share a genetic predisposition but that they are relatively distinct in their environmental determinants.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140289

 

How the Naked Mole Rat Escapes Inflammatory Pain

Summary: Findings from a study of naked mole rats could be important for helping develop pain therapies for humans.

Source: MDC.

In injuries and inflammation, naked mole-rats do not develop normal hypersensitivity to temperature stimuli. This is due to a tiny change in a receptor molecule on cells called TrkA, as a research team from the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) has now discovered. The work, which appears in the journal Cell Reports, may be important for pain therapy in humans.

When an animal suffers an injury or inflammation, nearby tissue usually becomes highly sensitive to pain. Skin becomes red and puffy, for example, and is hypersensitive to heat. This condition, called “thermal hyperalgesia,” acts as a warning that helps animals avoid further injuries.

The only known animals unable to feel thermal hyperalgesia are naked mole-rats, rodents which live in extremely harsh conditions in underground tunnels. MDC researchers Dr. Damir Omerbasic and Dr. Ewan St. J. Smith from Prof. Gary Lewin’s lab now found out the reasons and presented their work in the latest issue of the journal Cell Reports.

Hyperalgesia is mediated by the signaling molecule Nerve Growth Factor (NGF), which is also responsible for the growth of new nerves, especially during embryonic development. Hyperalgesia occurs when inflamed or injured tissue releases NGF molecules which subsequently bind to protein molecules on the surfaces of specialized, pain-sensing nerve cells. These surface proteins are called TrkA receptors, and when they are stimulated by NGF they relay a signal into the nerve cell. This causes other proteins to interact with the receptor, starting a cascade of biochemical signals which ultimately makes the cell oversensitive to thermal stimuli.

A naked mole mole-rat in a laboratory. NeuroscienceNews.com image is credited to Laura-Nadine Schuhmacher, Cambridge University.

TrkA receptors evolved in an ancient animal and have been passed down to all its descendants. TrkA is so important that it has been protected from most evolutionary change.

When the researchers compared the receptor of naked mole-rats to TrkA receptors in other mammals, they found minute differences in a region of the molecule that projects into the cell interior. This region triggers the biochemical signaling cascade and is virtually identical in all mammals.

In naked mole-rats, the differences in this portion of the receptor alter a few of the protein’s building blocks and severely diminishes the signal-relaying action of the TrkA receptor. The researchers found that it took ten times the amount of NGF compared to TrkA receptors from other animals to trigger the signaling cascade, explaining why naked mole-rats are almost completely insensitive to thermal hyperalgesia.

NGF has another important function: it stimulates the growth and maintenance of nerves as the nervous system develops in the embryo. That’s why defects of the TrkA receptor in other mammals often lead to a degeneration of the nervous system during embryonic development. “The nervous system of the naked mole-rat can develop normally because while the function of its TrkA receptors is lowered, it is not completely abolished,” principal investigator Gary Lewin explains. “Evolution has selected a version of the molecule that can send just enough signal to build a proper nervous system, but not enough to make cells hypersensitive to pain.”

The difference surely makes life more bearable for the rodents, which live underground in densely packed colonies. Injuries and inflammations are common, and under the same conditions other mammals would suffer intense, continual pain.

That’s a daily experience for many people who suffer from chronic pain. In many cases the problem also involves NGF and TrkA; treatments that block the binding of these two molecules have had very positive effects in clinical trials. It’s another example, Gary says, of how basic research – even when it starts in a very unusual animal – could pave the way toward new human therapies.

ABOUT THIS PAIN RESEARCH ARTICLE

Damir Omerbasic and Ewan St. J. Smith contributed equally to this work. This study was funded by the European Research Council (ERC) and the Alexander von Humboldt foundation.

Source: Vera Glaßer – MDC
Image Source: NeuroscienceNews.com image is credited to Laura-Nadine Schuhmacher, Cambridge University..
Original Research: Full open access research for “Hypofunctional TrkA Accounts for the Absence of Pain Sensitization in the African Naked Mole-Rat” by Damir Omerbašić, Ewan St. J. Smith, Mirko Moroni, Johanna Homfeld, Ole Eigenbrod, Nigel C. Bennett, Jane Reznick, Chris G. Faulkes, Matthias Selbach, and Gary R. Lewin in Cell Reports. Published online October 11 2016 doi:10.1080/23297018.2016.1207202

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
MDC “How the Naked Mole Rat Escapes Inflammatory Pain.” NeuroscienceNews. NeuroscienceNews, 11 October 2016.
<http://neurosciencenews.com/inflammatory-pain-mole-rat-5271/&gt;.

Abstract

Hypofunctional TrkA Accounts for the Absence of Pain Sensitization in the African Naked Mole-Rat

Highlights
•TRPV1 ion channels in naked mole-rat nociceptors are not sensitized by NGF
•Naked mole-rat TRPV1 channels are sensitized by NGF in mouse nociceptors
•NGF activation of naked mole-rat TrkA receptors does not sensitize TRPV1
•One to three amino acids in the naked mole-rat TrkA receptors may render it hypofunctional

Summary
The naked mole-rat is a subterranean rodent lacking several pain behaviors found in humans, rats, and mice. For example, nerve growth factor (NGF), an important mediator of pain sensitization, fails to produce thermal hyperalgesia in naked mole-rats. The sensitization of capsaicin-sensitive TRPV1 ion channels is necessary for NGF-induced hyperalgesia, but naked mole-rats have fully functional TRPV1 channels. We show that exposing isolated naked mole-rat nociceptors to NGF does not sensitize TRPV1. However, the naked mole-rat NGF receptor TrkA displays a reduced ability to engage signal transduction pathways that sensitize TRPV1. Between one- and three-amino-acid substitutions in the kinase domain of the naked mole-rat TrkA are sufficient to render the receptor hypofunctional, and this is associated with the absence of heat hyperalgesia. Our data suggest that evolution has selected for a TrkA variant that abolishes a robust nociceptive behavior in this species but is still compatible with species fitness.

“Hypofunctional TrkA Accounts for the Absence of Pain Sensitization in the African Naked Mole-Rat” by Damir Omerbašić, Ewan St. J. Smith, Mirko Moroni, Johanna Homfeld, Ole Eigenbrod, Nigel C. Bennett, Jane Reznick, Chris G. Faulkes, Matthias Selbach, and Gary R. Lewin in Cell Reports. Published online October 11 2016 doi:10.1080/23297018.2016.1207202

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