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Feasibility of Olive Oil for Reducing Facial Pain of Trigeminal Neuralgia

STUDY Feasibility of Olive Oil for Reducing Facial Pain of trigeminal neuralgia.
Brief Summary:
This is a 16-week non-blinded, parallel, controlled trial to determine the feasibility and potential efficacy of an olive oil dietary intervention to alleviate facial pain caused by trigeminal neuralgia type 1 (TGN).
Detailed Description:

Trigeminal neuralgia (TGN) pain is debilitating and unpredictable. Alleviation of intensity or frequency to any degree will improve the quality of life of the individuals affected. Current medical treatments for TGN are often not effective. In some cases, the pain is a result of myelin degeneration. If diet can provide the basic building blocks for myelin regrowth, then the investigators may be able to reduce facial pain by supporting the myelin nerve sheath.

Animal studies have shown that a dietary intervention with olive oil favorably impacts myelin but no human study has been conducted to date. The investigators propose undertaking a feasibility study to determine if a comparable intervention may work in a similar way in humans. If olive oil impacts myelin repair, then pain will be decreased by this dietary intervention and quality of life will be improved. However, it is not known if individuals with TNG will be able to consume a diet relatively high in olive oil. Feasibility will include testing the logistics of distributing the olive oil intervention to the study subjects, incorporation of olive oil into the participants’ daily diets, and online/distance monitoring of compliance and reporting of pain intensity, pain frequency, and quality of life. This feasibility study will lay the groundwork for potential future studies examining the efficacy of olive oil on alleviating facial pain caused by TNG and may provide data for a power analysis for a future interventional trial.

Olive Oil Information 

Recognized for its’ abundant health benefits, olive oil is being chosen by many consumers as a preferred form of fat in diets and is being recommended by nutritionists and health professionals as one of the best alternative oils to traditional fats and oils. Olive oil has great diversity in how it can be used as an ingredient in recipes and as a food-enhancer.

Olive trees originated in Asia, but are more commonly know as an agricultural product in Mediterranean countries. Olive oil comes from the process of pitting, grinding, and pressing of the olive fruit.

In countries where olive is most highly consumed – Italy, Greece, and Spain, the incidences of cardiovascular disease is low and this is attributed the health benefits olive oil provides. One tablespoon of olive oil contains 120 calories and 14 grams of fat. However, the fat in olive oil is primarily monounsaturated which, when consumed can help reduce blood cholesterol levels leading to improved cardiovascular function.

Other Health Benefits of Olive Oil:

  • Olive oil is beneficial as an antioxidant since it contains high levels of vitamin E.
  • When consumed, olive oil promotes digestion, stimulates metabolism, and lubricates mucous membranes (olive oil contains vegetable mucilage that helps protect the gastrointestinal tract).
  • Olive oil can aid in relieving constipation. Consuming 1 teaspoon of olive oil with lemon juice (preferably on an empty stomach) can promote proper bowel movements.
  • Olive oil for skin therapy. Olive oil can be added to dry skin acting like a moisturizer and can also be applied to nails to increase nail strength and to promote healthy cuticles.

How to Choose Olive Oil:

  • Explore how you can replace butter, margarine, and low quality vegetable oils in your cooking especially in preparing salads, sautéed dishes, and sauces.
  • Purchase olive oil that is labeled as“extra virgin”, which insures that the oil has been cold pressed. Cold pressed olive oil has been produced with freshly harvested olives and has gone through less processing and has not been degraded with heating or chemicals.
  • A good quality olive oil will be golden yellow in color versus lower quality olive oils that are light green in color.
  • Note: olive oil will congeal (form as a solid) in the refrigerator, but remains a liquid at room temperature.

When used in moderation, olive oil is a nutritious fat that promotes a great deal of health benefits. Like wines, olive oils will have differences in flavor depending on the region and producer of the oils. Olive oils can also be infused with herbs, garlic, peppers and other flavorful ingredients to add extra excitement to your dishes.




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Trigeminal Neuralgia Electronic Diary Trial

Noema Pharma announces completion of enrollment in the Trigeminal Neuralgia Electronic Diary (TNED) validation study

Study to validate the novel Patient-Reported Electronic Diary designed to more efficiently and accurately measure disease burden associated with trigeminal neuralgia

LIBRATN (NOE-101 Phase 2/3 study in Trigeminal Neuralgia) is on track to report top-line data in H1 2024

BASEL, Switzerland/ Boston, MA, September 6, 2022 – Noema Pharma, a clinical-stage biotech company targeting debilitating central nervous system (CNS) indications,today announces it has completed participant enrollment and data collection in the validation study of a novel Trigeminal Neuralgia Electronic Diary (TNED). The results will be presented at a scientific meeting and published in a specialized peer-reviewed journal.

The TNED validation study was conducted in two leading centers in the US and Europe, the result of a collaboration between University College London Hospitals UCLH/UCL in the UK, the Kaizen Brain Center in the US, the Trigeminal Neuralgia Association UK, and Noema Pharma. Thirty participants with a confirmed diagnosis of trigeminal neuralgia (TN) volunteered to complete the electronic diary. The diary,which was completed daily, includes a self-assessment of the different aspects of their condition; frequency and severity of intermittent attacks, also known as “flare-ups”, the duration of associated continuous pain when present, and the impact of these attacks on personal, social, and professional functioning. While the analysis of the validation data is ongoing, the electronic diary was generally found to be easy to use and enabled participants to accurately describe the burden of trigeminal neuralgia (TN).

“The TNED is a better alternative to the conventional paper-and-pencil method that is used to report the different aspects of facial pain,” said Professor Joanna Zakrzewska Principal Investigator of the LIBRA trigeminal neuralgia study at UCLH/UCL. “In addition to being patient friendly and easy to use, TNED is the first electronic diary designed specifically for people who suffer from TN. It measures different aspects of the condition and will allow regular measurement of the different aspects of the condition. In addition to being an excellent research tool for TN clinical studies, TNED can be used by patients with TN in clinical practice as a reliable tool to communicate symptom severity and frequency to their health care provider leading to improved quality of care as it enables assessment of the timing of flare ups and the efficacy of medication.”

“It’s very exciting to have completed the recruitment of the TNED validation study. This research tool is very well received by patients with TN, easy to use, and has the potential of becoming a routine activity with minimal burden on patients. We see great potential for the TNED to become a state-of-the-art research tool to be used in all TN clinical trials, including Noema’s LIBRATN,” said George Garibaldi, President and Head of Research and Development at Noema Pharma“Treatment options are scarce in TN with only one treatment that was approved over 50 years ago. We believe that patients suffering from TN deserve the benefit of the latest innovations and discoveries. Through the TNED, Noema is making a significant contribution to research in this field.”T

TN, also called “tic douloureux”, is a chronic severe pain condition that affects the trigeminal nerve, which carries sensation from the face to the brain. TN is a form of neuropathic pain, associated with nerve injury or a nerve lesion. New cases of TN affect 4 to 5 of every 100,000 people in the United States each year.

Noema is investigating the effect of NOE-101 (basimglurant), a highly selective, potent, and cell-penetrant negative allosteric modulator of mGlu5 receptors for the management of pain associated with TN. It was effective in controlling pain in multiple animal models predictive of a therapeutic effect in neuropathic pain. The currently ongoing placebo-controlled clinical study named LIBRATN (NCT05217628) aims to recruit up to 200 participants in centers across Europe and the U.S. Top-line data from the study is expected in H1 2024. 

About Noema Pharma
Noema Pharma ( is a clinical-stage Biotech company targeting debilitating central nervous system (CNS) indications characterized by imbalanced neuronal networks. The company is actively developing three mid-clinical-stage therapeutic product candidates in-licensed from Roche. Basimglurant, an mGluR5 inhibitor, is Phase 2b-ready for two indications: persistent seizures in Tuberous Sclerosis Complex and severe pain in Trigeminal Neuralgia. Gemlapodect, a PDE10A inhibitor, is currently enrolling a Phase 2a clinical trial in patients with Tourette Syndrome.

The Company has completed validation studies and is pursuing the development of NOE-115 in Behavioral Metabolic Cluster disorders. It is also planning to develop NOE-109 an mGluR2/3 inhibitor, in undisclosed indications. Noema Pharma was founded in 2020 by the leading venture capital firm Sofinnova Partners. Investors include Polaris Partners, Gilde Healthcare, Invus and Biomed Partners.


Noema Pharma
Luigi Costa
Chief Executive Officer

LifeSci Advisors – Guillaume van Renterghem
+41 (0) 76 735 01 31 

LifeSci Advisors – Bernhard Schmid
+41 (0) 44 447 12 21


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FPA – New Life for Cancer Drug

New life for cancer drug that reprograms pain pathway to fight chronic pain

Chronic pain associated with nerve injury and chronic bone pain from metastatic cancer are unmet medical needs. This sober sentence vastly understates the crushing and devastating impact of these forms of pain on victims’ lives, their families, and their social and professional lives.

“I just can not sleep any more because turning in bed hurts, my spine hurts lying down, and sitting up to sleep hurts even more. During daytime, I have constant brain fog, interrupted by pain that within minutes gets worse (10-out-of-10) against a background of constant burning pain which gets worse toward the afternoon and evening. I hurt more when I go to the bathroom. The pain medication makes my brain fog worse, I feel like a zombie, I am badly constipated and itch all over.” That is how a patient with bone cancer pain feels. Testimony from victims of chronic nerve injury pain, through peripheral nerve damage from diabetes or medications, or in the aftermath of shingles, indicates that their lives are equally turned upside down from the pain.

New treatments against pain are needed. What is the desired profile ? “New drugs and other therapies against chronic pain need to be safe, i.e the fewer side effects the better, especially non-addictive and non-sedative, and effective. For example they should work against nerve injury pain and cancer pain, finally and practically, with minimal time to official drug approval. “Since chronic pain, like many chronic diseases, has an important root in genetic switches being reprogrammed in a ‘bad’ way, a disease-modifying treatment for chronic pain should reset the genetic switches, not just cover up the pain as with opioid and aspirin/tylenol-like painkillers,” says Dr. Wolfgang Liedtke, who practiced pain medicine for the last 17 years at Duke University Medical Center in Durham, NC, USA, and directed the former Liedtke-Lab to elucidate basic pain mechanisms. Dr. Liedkte moved to an executive position at Regeneron Pharmaceuticals in Tarrytown NY, in April 2021.

Liedtke’s Duke team, jointly with colleagues from University of California Irvine, tackled the problem by starting with a collection of “junkyard of cancer drugs”, 1,057 compounds originating from two Compound Libraries of the National Cancer Institute. Liedtke picked cancer drugs because a sizeable number of them influence epigenetic regulation of genes, which stops rapidly dividing cancer cells from dividing, but can reset maladaptive genetic switches in non-dividing nerve cells. In order to identify useful candidate anti-pain drugs from this starting pool, Liedtke’s team devised a screening method that relied on brain nerve cells from genetically-engineered mice that were “knockin” for a convenient reporter gene system so that compounds that enhance expression of an anti-pain target gene would generate a bio-luminescent signal which can be readily measured, allowing 1,057 compounds to be tested.

The selected anti-pain target gene was Kcc2 which encodes a chloride extruding transporter molecule, KCC2. KCC2 churns out chloride from nerve cells, low chloride means strong function of inhibitory neurotransmission, also in pain pathways, thus silencing the pain signal, or not allowing it to break through. In essentially all forms of chronic pain studied in experimental animals and also human spinal cord models, KCC2 disappears from the primary pain gate in the dorsal spinal cord. Liedtke’s team identified 137 first-round winners, i.e Kcc2 gene expression-enhancers, which then were retested iteratively, with a yield of four final co-winners. Kenpaullone was selected for work-up because the compound had a strong record of protecting nerve cells in human ALS models, also hearing and brain neurons from damage. In mice, Kenpaullone functioned effectively against pain caused by nerve constriction injury and by cancer cells seeding in the femur. Pain relief was profound, long lasting and with protracted onset, indicative of Kenpaullone impacting gene regulation.

Says Liedtke “At this stage, we knew we had met the basic requirement of our screen of shelved cancer drugs, namely identified Kcc2 gene expression-enhancers, and demonstrated that they are analgesics in valid preclinical pain models.” Thus encouraged, Liedtke’s team addressed whether Kenpaullone affected spinal cord processing of pain, with affirmative findings, then whether the pain-relaying nerve cells in the dorsal spinal cord can lower their elevated chloride, caused by nerve injury, by Kenpaullone treatment – again with resoundingly affirmative results. This was great news and prompted the investigators to query how exactly Kenpaullone works in nerve cells so that the Kcc2 gene is expressed stronger.

They discovered the underlying signaling mechanism, a key element of it completely new. Kenpaullone inhibits the kinase GSK3-beta which adds phosphate tags to other proteins which in turn switches their function powerfully. They found that the kinase target of GSK3beta is delta-catenin, delta-cat, which when phosphorylated is tagged for the cellular garbage bin. That means that chronic pain, via activation of GSK3-beta leads to loss of delta-cat in pain relaying neurons. What is the original function of delta-cat in relation to pain relay, and in relation to gene expression of Kcc2 ?  Liedtke’s team found that non-phosphorylated delta-cat transfers into the cell’s nucleus and binds to the Kcc2 gene’s DNA in its promoter region, where it switches back on the switched-off Kcc2 gene. To prove the relevance of this pathway for pain, they devised a gene-therapeutic approach so that phosphorylation-resistant delta-cat becomes the payload of an AAV9 gene-therapy viral vector, which infects spinal cord dorsal horn neurons. Injection of this gene therapy vector into the cerebrospinal fluid of mice was similarly analgesic as Kenpaullone.

These findings suggest that Kenpaullone and similarly-acting kinase-inhibitory compounds, also delta-cat gene therapy can become new tools in our toolbox against chronic “refractory” pain, also caused by nerve injury, also caused by cancer bone pain, likely against other forms of chronic pain where Kcc2 is not expressed well (trigeminal pain), and possibly other neurologic and psychiatric disorders where this mechanism appears to contribute to disease.

Amidst Duke co-authors, 1st author Dr. Michele Yeo successfully elucidated basic regulation of the Kcc2 gene together with Liedtke for more than a decade and ran the 1,057 compound screen, co-first author Dr. Yong Chen provided skillful animal experimentation, and co-senior author Dr. Ru-Rong Ji (Director of Translational Pain Research) and his team covered dedicated assessment of spinal cord relay mechanisms. Collaboration with Dr Jorge Busciglio’s laboratory at UC Irvine was key to validate human relevance of Kenpaullone.

Summary Figure
Upper right “Junkyard of cancer” drugs were screened, akin to sieving through sand, looking for gold nuggets. Kenpaullone was identified as a “winner”, capable of switching on the Kcc2 gene, which previous research predicted to be beneficial for chronic pain.
Upper left Nerve injury pain and bone cancer pain are serious and pressing unmet medical needs. Preclinical models were used totest Kenpaullone which proved to be highly effective in both.
Middle panels, left-hand Nerve injury by constriction or cancer cells populating a bone activates GSK3ß, an enzyme that tags other proteins with phosphate. In nerve cells dedicated to pain relay in the spinal cord, GSK3ß tags d-catenin
(d-CAT), which routs d-CAT to the cellular garbage bin. Without d- CAT in the cells’ nucleus, the Kcc2 gene remains switched off. This in turn makes the pain relay neurons run full of chloride which makes them electrically more jittery, with chronic “refractory” pain a result.
Right-hand panel Treatment with Kenpaullone inhibits GSK3b’s phosphate-tagging capability, so that d-CAT becomes untagged, which clears the way to the nerve cells’ nucleus. There it binds to the DNA region of the Kcc2 gene critical for switch-on or switch-off, the promoter. By binding there, d- CAT reverts the switch-off to switch-on and the Kcc2 gene is running again, making KCC2 protein. KCC2 in turn pumps chloride ions out of the pain-relay nerve cells, making them electrically more stable. This leads to circuit repair and pain relief, based on resetting of the genetic switches. Instead of Kenpaullone, d-CAT can serve as payload of a gene therapy approach that directs expression of d-CAT and hence KCC2 to pain relay nerve cells in the spinal cord.

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Australian Organisations Raising Awareness about Trigeminal Neuralgia

Our organisation has been a registered Charity since 2003 and next year will be our 20th Anniversary.  We work tirelessly to ensure all sufferers receive support and our new website has certainly raised our profile in the digital space

In 2018 another organisation was established in Victoria founded by Skye and Peta called FightingTN

These two ladies have created an amazing community where local business support their fund raising by offering a % of profits.

All funds raised by FightingTN are directed to the brain org who utilise the funds for research.

You can buy product on their website, see upcoming events, create and register your own fundraising event too.

Every year FightingTN hosts an awareness day event for Light up in Teal

We are all working for the same outcome  – a cure for Trigeminal Neuralgia.







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Trigeminal Neuralgia Research – The Facial pain Research Foundation

YouTube Trigeminal Neuralgia: The Facial Pain Research Foundation – Kim Birchiel MD

Research is happening around the world to better understand Trigeminal Neuralgia and this foundation has nine research programs ongoing

The Facial Pain Research Foundation – it’s time to find a cure! (

In Search of a Cure: Finding the Genes that Predispose to Trigeminal Neuralgia

A compressed trigeminal nerve is sometimes the reason why a patient suffers. However, it’s a fact that many people, if imaged, would present a similar compression, but experience no pain. Why? That question inspired our scientists to hypothesize there is a genetic predisposition to TN. Their plan is to find these defective genes in TN sufferers, which could then provide targets for designing customized drugs or gene therapy. For their analysis, they collected DNA samples from nearly 1,000 patients at seven US locations, one in Canada, and one in the UK. Their findings from this analysis may unlock the mystery of why some people suffer, and so many others do not.

Scott Diehl, Ph.D.
Kim Burchiel, M.D.
Ze’ev Seltzer, BMS, DMD

Towards Gene Therapy for Trigeminal Neuralgia

The primary goal of this project, led by Dr. Todd Golde at the University of Florida, is to identify a novel gene therapy approach to treat and cure TN and related neuropathic pain. Gene therapies rely on a modified viral vector to enable delivery of the genetic “payload” to cells. In this case, the viral vector is, in essence, the “shuttle” that enables the payload to be delivered to the nerve. There are many potential genetic “payloads” that might be used to dampen or block pain signaling in the nerve. Our team’s research involves systematically evaluating various viral vector shuttles, and various delivery methods. In addition, they will generate payloads that suppress pain signaling by either knocking out (CRISPR mediated gene silencing), or reducing the level (miRNA based antisense approaches) of factors important in pain signaling.

Todd Golde, M.D., Ph.D.
Robert Caudle, Ph.D.
Yona Levites, Ph.D.
John Neubert, DDS, Ph.D.

Identifying Sensory Genes That Are Critical to Neuropathic Pain, Including Trigeminal Neuralgia

We believe we still don’t know all of the elements responsible for the initiation of Trigeminal Neuralgia pain. The question is which genes are critical and can these be selectively regulated to manage TN, but, to date, the focus of the field has been on a relatively small number of genes.  Dr. Allan Basbaum is examining a relatively large number, and wider variety of, genes using the “one gene at a time” approach. This study was prompted to a great extent by his team’s comprehensive analysis of a dorsal root ganglion (DRG) from intact and nerve-injured mice. This analysis identified almost 1200 genes that affected pain after the injury. To prioritize genes for future study as causing TN, they chose some that have been reported repeatedly in the scientific literature, genes that showed the greatest change in expression after injury, and the so-called dark genes which until recently have largely been ignored. The plan is to identify the genes that impact TN, and then create or find the therapies needed to “manage or fix” them to end the pain.

Dr. Allan Basbaum, Ph.D.

Mapping Towards a Cure: Finding the Brain Signature Centers that Cause Trigeminal Neuralgia

Led by Dr. John Neubert at the University of Florida, our team of researchers hypothesized that specific neural centers in the brain and spinal cord are active prior to, and during, a TN attack, essentially “lighting up” with activity. These neural centers hold the key to providing pain relief, as they give us a specific area to target for curative treatments- if we can block these centers, we can prevent the pain. Using highly advanced magnetic resonance imaging, our team has scanned over 60 TN patients, and located what we believe are the “pain centers” of TN patients.

John Neubert, DDS, Ph.D.
Marcello Febo, Ph.D.
Mingzhou Ding, Ph.D.
Robert Caudle, Ph.D.

Evaluation of a Cellular Therapeutic for the Treatment of Trigeminal Pain

Neurona Therapeutics is a pre-clinical stage biotechnology company that was founded by four leading-edge neuroscientists and stem cell pioneers at The University of California, San Francisco. Led by Dr. Cory Nicholas, Ph.D., Neurona has formed a strategic research collaboration with the Facial Pain Research Foundation, to develop a human inhibitory interneuron therapeutic (neuro-stem cells) for the treatment of neuropathic pain conditions like TN.  As an example of the unique collaboration we foster between our scientists, our researchers at The University of Florida are providing the animal subjects to test whether Neurona’s neural stem-cells can stop neuropathic facial pain in animals. If successful, we will then move to human trials.

Dr. Cory Nicholas, Ph.D.
Dr. John Neubert, Ph.D.
Dr. Allan Basbaum, Ph.D. 

Determining Efficacy of CODA ‘Switch’ Receptors in a Model of Neuropathic Pain

CODA Biotherapeutics, Inc., is a preclinical-stage biopharmaceutical company developing a gene therapy to stop TN. Led by Dr. Orion Keifer, CODA has formed a strategic research collaboration with the Facial Pain Research Foundation, with the goal of utilizing CODA’s chemogenetic gene therapy platform to identify and develop potential new therapies and cures for Trigeminal Neuralgia, and related neuropathic pain. Under the collaboration, CODA is working with the FPRF to establish a research continuum that is dedicated to identifying the mechanisms underlying neuropathic facial pain and to developing groundbreaking therapeutic strategies that aim to permanently stop the pain.

Orion P. Keifer, Jr., M.D., Ph.D.

Cholesterol Homeostasis in Peripheral Nerve Myelin with a Focus on Statins

The aim of this research, led by Dr. Lucia Notterpek, Ph.D., was to prove that unhealthy and/or damaged myelin- the protective coating of nerves- is the reason why some patients have TN pain. We have confirmed this in animal subjects, and treatments to stop their pain by repairing this damaged myelin have been successful. We hope to achieve this in humans organically, through dietary supplements, rather than with medications, and believe this will be an effective therapy for those who’ve developed TN as a result of myelin-related causes.

Dr. Lucia Notterpek, Ph.D.
Dr. Susan Percival, Ph.D.
Dr. Wendy Dahl, Ph.D.

Exploring Neuropeptide Guided Botulinum Light Chain for Use in Blocking Pain Transmission

The overall long-term goal of this project is to begin a search for new, novel, pain control therapies to supplant highly addictive opioids.  Dr. Rob Caudle at the University of Florida has chosen botulinum toxins as his therapeutic agent, which have already proven very successful in treating migraine headaches.  However, he has modified these toxins with a unique research approach. The newly created substances are directed to the appropriate sensory neurons, which Dr. Caudle and his team have identified, where they are internalized, and disrupt neurotransmission- the result of which, is the inhibition of pain.

Robert Caudle, Ph.D.

The Role of TMD in the Diagnosis of Trigeminal Neuralgia

There is considerable confusion regarding the diagnosis of TMD (Temporomandibular Disorder), and because of the lack of good diagnostic tools, many TMD patients end up being referred to neurologists and neurosurgeons as TN patients. Since there is significant symptom overlap between the two conditions, some of these TMD patients end up being mistakenly treated for TN.

The study will quantify how often TMD patients are mistakenly referred as TN patients. It will determine how many patients fit the diagnostic tools for both TN and TDM, and will define new diagnostic tools that will correctly predict a TMD patient. The result being a new protocol to screen oral facial pain patients for TMD suspects. The benefit of this work will be that TMD patients will be less likely to be treated for TN, and TN patients less likely to be treated for TMD because of an overlap in symptoms and the lack of good diagnostic tools.

Kim Burchiel, M.D