An epilepsy drug: A new way to treat osteoarthritis pain?


An existing epilepsy drug may have the potential to be used as a treatment for osteoarthritis.

  • Osteoarthritis is a painful and chronic condition that makes performing specific movements harder and more painful.
  • Managing osteoarthritis can be a struggle, so researchers have been trying to find medications that can help.
  • A recent study found that a particular sodium channel in neurons and cartilage cells may be a pivotal area to target, leading to reduced pain and joint damage from osteoarthritis.
  • This sodium channel may be successfully inhibited by the drug Carbamazepine, a medication that helps treat epilepsy.

Even with the renovations of modern medicine, certain chronic conditions, like osteoarthritis, remain difficult to manage. Research areas include finding ways to halt joint damage and improve pain symptoms.

A study published in NatureTrusted Sourceexamined how targeting the sodium channel Nav1.7 could help treat osteoarthritis. Using mouse models and cell analysis, researchers determined that this sodium channel is present in neurons and cartilage cells and that inhibiting it may be the key to osteoarthritis treatment.

The researchers further found that blocking the action of these sodium channels with the medication Carbamazepine can help minimize damage to joints and improve pain in osteoarthritis. This medication typically treats epilepsy, but this research demonstrates its potential to be used to treat other chronic conditions.

While this research is preliminary, it points to potential treatment options for osteoarthritis.

The target of a new osteoarthritis treatment

The current study focused on a way to slow the joint damage caused by osteoarthritis rather than focusing on pain relief alone. Researchers noted that osteoarthritis involves cartilage breakdown and pain. At the cellular level, this involves chondrocytesTrusted Source, or cartilage cells and neurons, which are involved in the pain response from osteoarthritis.

Researchers were particularly interested in understanding the presence and work of voltage-gated sodium channelsTrusted Source in the cartilage cells. These sodium channels are a specific type of protein found in cell types.

To start, researchers examined chondrocytes in people with osteoarthritis. They found that the Nav1.7 sodium channels are present in chondrocytes and that the amount is increased in osteoarthritis.

Using mouse models, researchers genetically deleted Nav1.7 and studied the results. They found that in dorsal root gangliaTrusted Source neurons, the junction boxes for nerves as they exit the spinal column, this deletion contributed to pain reduction. In the chondrocyte cells in mice, the deletion contributed to much less structural damage and progression of osteoarthritis and less pain-related behavior from the osteoarthritis.

The results concluded that inhibiting these channels could be the key to slowing osteoarthritis progression and minimizing pain. Researchers looked at several components to test this hypothesis and some of the underlying mechanisms involved.

Dr. Yoon noted the following:

“The study investigating Nav1.7 is important to create disease modifying medicines for osteoarthritis. Understanding the cellular mechanisms underlying osteoarthritis and creating targeted therapies to address both pain and the actual disease itself will be necessary to modify the impact of this disease.”

Carbamazepine for osteoarthritis

One key area of interest is that the researchers were then able to test if the drug Carbamazepine affected osteoarthritis progression in mice. Carbamazepine inhibits Nav1.7 channels, and doctors use it in the treatment of conditions like epilepsy and bipolar disorder.

They found that the Carbamazepine helped with pain and lowered amounts of cartilage loss.

Study author Chuan-Ju Liu, PhD, Charles W. Ohse Professor and Translational Orthopaedic Lab Director in the Department of Orthopaedics at Yale University School of Medicine, explained the key findings of the research to Medical News Today:

“Our discovery of the sodium channel Nav1.7 as a target for both pain relief and disease modification represents a significant stride towards a novel therapeutic strategy to slow down or prevent osteoarthritis progression while concurrently alleviating associated pain. Inhibiting Nav1.7 channels with specific inhibitors has shown promising results in slowing joint damage across various animal models of osteoarthritis. Expanding on this, our investigations with the non-specific Nav-blocking drug, Carbamazepine, also demonstrated a robust protective effect against joint degeneration in mouse osteoarthritis models.”

Needs to be tested in humans

While this research is promising, it also has certain limitations. The main limitation is that the findings are derived from mouse models. Researchers also only included cell samples from a limited number of patients, which could have influenced the study’s findings. Experts must be cautious and do more research before seeing how this data applies to people with osteoarthritis.

Dr. Liu noted the following areas of continued research:

“There is still a long way to go in translating current findings from animal models to human applications. We need to understand why a low number of sodium channels has such significant effects on chondrocyte biology. Additionally, further testing is essential to explore the comparative effects of various sodium channel inhibitors on chondrocytes, cartilage, and different osteoarthritis models.”

“Our next steps involve assessing new therapeutic strategies focused on blocking Nav1.7 channels and exploring gene therapy approaches to reduce the production of these channels. This research aims to bridge the gap between animal models and human treatments, bringing us closer to a future where osteoarthritis is more manageable, enabling patients to lead healthier and happier lives.”
— Dr. Chuan-Ju Liu, study author

How to manage osteoarthritis symptoms

OsteoarthritisTrusted Source is a common subtype of arthritis. When people have osteoarthritis, there is breakdown and damage in the joints, leading to pain, swelling, and movement struggles. Osteoarthritis affects various joints and can range in severity.

Study author Dr. Liu said there were challenges with treating osteoarthritis.

“Osteoarthritis, the most common form of arthritis, affects over [7.6%Trusted Source] of the global population and is a leading cause of disability. Unfortunately, there’s currently no cure, and existing treatments mainly focus on relieving pain without addressing the underlying cartilage breakdown. Patients often resort to invasive surgeries like total knee or hip replacements,” he told Medical News Today.

There are certain things people can do that may help to minimize their risk of developing osteoarthritis, such as maintaining a healthy body weight and exercising regularly.

Management of osteoarthritis involves a number of strategies, often to help with symptom relief. There is growing evidence of the effectiveness of a range of exercises for knee osteoarthritis, including aerobic exercise, strength training, and balance training. A range of medications can relieve pain, and people may also try injections of corticosteroids or hot and cold therapy. However, it can be difficult to find effective strategies that prevent disease progression.

Dr. Steve Yoon, a board certified physiatrist and director of The Regenerative Sports and Joint Clinic at Cedars-Sinai Kerlan-Jobe Institute in Los Angeles, who was not involved in the study, explained that common treatments for osteoarthritis “require a multidisciplinary approach.”

Managing osteoarthritis

“Modalities such as ice and heat can be used topically. Topical creams and ointments used may include anesthetic and anti-inflammatory medications as well as cannabidiol (CBD). Oral medications including acetaminophen and ibuprofen may be used for more serious pain control. Physical therapy will include a strength and low impact exercise program.”
— Dr. Steve Yoon

An epilepsy drug: A new way to treat osteoarthritis pain?


osteoarthritis pain?

  • Osteoarthritis is a painful and chronic condition that makes performing specific movements harder and more painful.
  • Managing osteoarthritis can be a struggle, so researchers have been trying to find medications that can help.
  • A recent study found that a particular sodium channel in neurons and cartilage cells may be a pivotal area to target, leading to reduced pain and joint damage from osteoarthritis.
  • This sodium channel may be successfully inhibited by the drug Carbamazepine, a medication that helps treat epilepsy.

Even with the renovations of modern medicine, certain chronic conditions, like osteoarthritis, remain difficult to manage. Research areas include finding ways to halt joint damage and improve pain symptoms.

A study published in NatureTrusted Sourceexamined how targeting the sodium channel Nav1.7 could help treat osteoarthritis. Using mouse models and cell analysis, researchers determined that this sodium channel is present in neurons and cartilage cells and that inhibiting it may be the key to osteoarthritis treatment.

The researchers further found that blocking the action of these sodium channels with the medication Carbamazepine can help minimize damage to joints and improve pain in osteoarthritis. This medication typically treats epilepsy, but this research demonstrates its potential to be used to treat other chronic conditions.

While this research is preliminary, it points to potential treatment options for osteoarthritis.

The target of a new osteoarthritis treatment

The current study focused on a way to slow the joint damage caused by osteoarthritis rather than focusing on pain relief alone. Researchers noted that osteoarthritis involves cartilage breakdown and pain. At the cellular level, this involves chondrocytesTrusted Source, or cartilage cells and neurons, which are involved in the pain response from osteoarthritis.

Researchers were particularly interested in understanding the presence and work of voltage-gated sodium channelsTrusted Source in the cartilage cells. These sodium channels are a specific type of protein found in cell types.

To start, researchers examined chondrocytes in people with osteoarthritis. They found that the Nav1.7 sodium channels are present in chondrocytes and that the amount is increased in osteoarthritis.

Using mouse models, researchers genetically deleted Nav1.7 and studied the results. They found that in dorsal root gangliaTrusted Source neurons, the junction boxes for nerves as they exit the spinal column, this deletion contributed to pain reduction. In the chondrocyte cells in mice, the deletion contributed to much less structural damage and progression of osteoarthritis and less pain-related behavior from the osteoarthritis.

The results concluded that inhibiting these channels could be the key to slowing osteoarthritis progression and minimizing pain. Researchers looked at several components to test this hypothesis and some of the underlying mechanisms involved.

Dr. Yoon noted the following:

“The study investigating Nav1.7 is important to create disease modifying medicines for osteoarthritis. Understanding the cellular mechanisms underlying osteoarthritis and creating targeted therapies to address both pain and the actual disease itself will be necessary to modify the impact of this disease.”

Carbamazepine for osteoarthritis

One key area of interest is that the researchers were then able to test if the drug Carbamazepine affected osteoarthritis progression in mice. Carbamazepine inhibits Nav1.7 channels, and doctors use it in the treatment of conditions like epilepsy and bipolar disorder.

They found that the Carbamazepine helped with pain and lowered amounts of cartilage loss.

Study author Chuan-Ju Liu, PhD, Charles W. Ohse Professor and Translational Orthopaedic Lab Director in the Department of Orthopaedics at Yale University School of Medicine, explained the key findings of the research to Medical News Today:

“Our discovery of the sodium channel Nav1.7 as a target for both pain relief and disease modification represents a significant stride towards a novel therapeutic strategy to slow down or prevent osteoarthritis progression while concurrently alleviating associated pain. Inhibiting Nav1.7 channels with specific inhibitors has shown promising results in slowing joint damage across various animal models of osteoarthritis. Expanding on this, our investigations with the non-specific Nav-blocking drug, Carbamazepine, also demonstrated a robust protective effect against joint degeneration in mouse osteoarthritis models.”

Needs to be tested in humans

While this research is promising, it also has certain limitations. The main limitation is that the findings are derived from mouse models. Researchers also only included cell samples from a limited number of patients, which could have influenced the study’s findings. Experts must be cautious and do more research before seeing how this data applies to people with osteoarthritis.

Dr. Liu noted the following areas of continued research:

“There is still a long way to go in translating current findings from animal models to human applications. We need to understand why a low number of sodium channels has such significant effects on chondrocyte biology. Additionally, further testing is essential to explore the comparative effects of various sodium channel inhibitors on chondrocytes, cartilage, and different osteoarthritis models.”

“Our next steps involve assessing new therapeutic strategies focused on blocking Nav1.7 channels and exploring gene therapy approaches to reduce the production of these channels. This research aims to bridge the gap between animal models and human treatments, bringing us closer to a future where osteoarthritis is more manageable, enabling patients to lead healthier and happier lives.”
— Dr. Chuan-Ju Liu, study author

How to manage osteoarthritis symptoms

OsteoarthritisTrusted Source is a common subtype of arthritis. When people have osteoarthritis, there is breakdown and damage in the joints, leading to pain, swelling, and movement struggles. Osteoarthritis affects various joints and can range in severity.

Study author Dr. Liu said there were challenges with treating osteoarthritis.

“Osteoarthritis, the most common form of arthritis, affects over [7.6%Trusted Source] of the global population and is a leading cause of disability. Unfortunately, there’s currently no cure, and existing treatments mainly focus on relieving pain without addressing the underlying cartilage breakdown. Patients often resort to invasive surgeries like total knee or hip replacements,” he told Medical News Today.

There are certain things people can do that may help to minimize their risk of developing osteoarthritis, such as maintaining a healthy body weight and exercising regularly.

Management of osteoarthritis involves a number of strategies, often to help with symptom relief. There is growing evidence of the effectiveness of a range of exercises for knee osteoarthritis, including aerobic exercise, strength training, and balance training. A range of medications can relieve pain, and people may also try injections of corticosteroids or hot and cold therapy. However, it can be difficult to find effective strategies that prevent disease progression.

Dr. Steve Yoon, a board certified physiatrist and director of The Regenerative Sports and Joint Clinic at Cedars-Sinai Kerlan-Jobe Institute in Los Angeles, who was not involved in the study, explained that common treatments for osteoarthritis “require a multidisciplinary approach.”

Managing osteoarthritis

“Modalities such as ice and heat can be used topically. Topical creams and ointments used may include anesthetic and anti-inflammatory medications as well as cannabidiol (CBD). Oral medications including acetaminophen and ibuprofen may be used for more serious pain control. Physical therapy will include a strength and low impact exercise program.”
— Dr. Steve Yoon

Epilepsy drug could help treat Alzheimer’s disease


University of British Columbia researchers say a new epilepsy drug holds promise as a treatment for Alzheimer’s disease.

The findings, published today in Alzheimer’s Research & Therapy, reinforce the theory that brain hyperexcitability plays an important role in Alzheimer’s disease, and that anticonvulsant drugs—drugs that prevent or reduce the severity of seizures—represent a promising treatment that deserve further human studies.

In previous studies, several groups have tested the effects of the widely used anticonvulsant drug levetiracetam in both rodent models as well as two clinical trials in patients with early signs of Alzheimer’s disease. The findings suggest it may slow some of the symptoms of the disease, including memory loss.

In this newest research, Dr. Haakon Nygaard, the Fipke Professor in Alzheimer’s Research in UBC’s Faculty of Medicine, tested the effects of brivaracetam, an anticonvulsant drug still in clinical development for epilepsy, and closely related to levetiracetam. Since it is 10 times more potent than levetiracetam, it can be used at lower dosages. Nygaard and his colleagues found that it completely reversed memory loss in a rodent model of Alzheimer’s disease.

While the drug appears effective, the researchers are unclear how it works to reverse memory loss. Nygaard also points out that the current study represents very preliminary data with respect to treating patients with Alzheimer’s disease.

“Now we have many different research groups using antiepileptic drugs that engage the same target, and all point to a therapeutic effect in both Alzheimer’s disease models, and patients with the disease,” said Nygaard, a researcher with the Djavad Mowafaghian Centre for Brain Health. “Both of these drugs are likely to be tested in larger clinical trials in Alzheimer’s disease over the next five to 10 years.”

“Larger clinical studies in human subjects will be needed before we can determine whether anticonvulsant therapy will be part of our future therapeutic arsenal against Alzheimer’s.”

Background

Alzheimer’s is the most common cause of dementia among older people. It slowly destroys memory and cognitive skills, and eventually the ability to carry out simple, daily tasks. In 2011, 747,000 Canadians were living with dementia, a number expected to rise to 1.4 million by 2031.

It’s been known for a few decades that patients with Alzheimer’s have an increased risk of seizures, especially in people with a family history of the disease. There is now a growing body of evidence that certain mechanisms related to how the brain is wired are shared between Alzheimer’s and epilepsy This led researchers to test anticonvulsant drugs as potential treatments for Alzheimer’s. While some drugs like levetiracetam and brivaracetam appear to work, others do not. In this study, Nygaard and his colleagues also tested the anticonvulsant ethosuximide but found that it was not effective in reversing symptoms in an Alzheimer’s model.