Researchers are looking for ways protect the body after acute events, such as stroke or nervous system injury, and to help with chronic nervous system diseases such as Alzheimer's, Parkinson's or multiple sclerosis (MS).
The development of neuroprotective agents is still underway, although there are some in use today.
Current neuroprotectors cannot reverse the damage already done, but they may protect against further nerve damage and slow down any degeneration, or breakdown, of the central nervous system (CNS).
Scientists are currently investigating a wide range of treatments. Some products can potentially be used in more than one disorder, as different disorders share many of the underlying mechanisms.
Contents of this article:
- The field of neuroprotection research is developing rapidly.
- Researchers aim to find a way to protect nerves against damage due to injury or disease.
- People with Alzheimer's, Parkinson's, stroke, and MS could benefit from any new drugs.
- Current drugs that show promise include riluzole, phenytoin, and amiloride.
Here are some key points about neuroprotection. More detail is in the main article.
What causes neuron damage?
Scientists hope to find neuroprotective agents that will protect against nerve damage.
To understand neuroprotection, we should first look at what kills nerves and inhibits brain function.
Different diseases that relate to the CNS have different symptoms. However, the processes by which neurons, or nerve cells, die, are similar.
Currently, these processes are thought to include the following.
An imbalance occurs between the body's production of free radicals and its ability to remove them.
Free radicals are what remain after chemical reactions occur within the body. These electrically charged particles can interact, change substances and cause cell damage.
Free radicals are the result of an oxygen-rich environment. The body needs them, but they also need to be kept in balance.
The mitochondria are specialized structures, or organelles, within cells that generate energy.
Nerve cells can die in the brain if they are overactivated.
Glutamate, a brain chemical, excites the interaction between nerve cells. It is an important step of neurotransmission, the passing of information from one nerve cell to the other.
However, too much glutamate can cause cell destruction.
Nerves that become over-stimulated by nerve impulses become damaged or non-functional.
Excitotoxicity is a key factor in nerve damage following a stroke.
When inflammation occurs in the brain or CNS, this immune response can end up killing neurons as it repairs damage or fights infection.
This can often be the cause of cell death in Alzheimer's disease, Parkinson's, and infections of the brain and the CNS.
The buildup of iron in the brain seems to play a role in degenerative diseases such as Alzheimer's, Parkinson's and amyotrophic lateral sclerosis (ALS).
Researchers are looking for substances that may help remove excess iron from the CNS. By removing iron, these substances could potentially restore balance to the brain and CNS.
Scientists are looking into the role of iron in these diseases, in the hope of finding new treatments. Excess iron may be part of a cycle of excitotoxicity and cell death.
The trouble, some believe, lies with the inflammation-causing molecules they produce.
High levels of the tumor necrosis factor (TNF) protein are found in a wide variety of CNS degenerative conditions. High levels of TNF seem to be associated with excitotoxicity and high levels of glutamate.
Types of neuroprotection
Neuroprotection aims to limit nerve death after CNS injury and to protect the CNS from premature breakdown and other causes of nerve cell death.
Neuroprotective agents counter the effects of neurodegeneration, or nerve breakdown.
Products with neuroprotective effects are grouped into the following categories.
Free radical trapping agents
These convert damaged and disease-causing, unstable free radical cells into molecules that are more stable and easier for the body to manage.
Researchers are investigating a range of possible causes of nerve damage in the hope of finding a way to stop it.
Antioxidants are agents that can interact with and reduce the impact of free radicals. They can be found in foods or supplements.
How they work is not fully understood. It seems to depend heavily on both the disease they are targeting and the many factors unique to each individual.
Vitamin E, for example, has shown antioxidant properties in Alzheimer's disease and, to a lesser extent, ALS.
However, research also suggests that vitamin E supplementation can make brain function and dementia worse in some people.
It is important to talk to a doctor before using any herbal products, over-the- counter (OTC) medications or supplements.
Many products can interact with other medicines or cause unexpected side effects.
In theory, blocking the glutamate receptors will prevent excitotoxicity and degeneration. However, some glutamate is necessary for normal nerve cell function.
Amantadine, one treatment option for Parkinson's disease, seems to work by changing the interaction between glutamate and another brain chemical.
However, side effects can include hallucinations, blurred vision, confusion, and swelling of the feet.
Amantadine may help reduce Parkinson's-triggered dyskinesia, or involuntary movements.
Apoptosis (programmed cell death) inhibitors
Apoptosis is the natural death of cells as a body ages and grows. Theoretically, anti-apoptotic agents would slow this process in neurons. Currently, these types of therapies are being used in cancer treatment research.
These have painkilling properties, but can they also affect the inflammatory processes involved in worsening Parkinson's disease and Alzheimer's.
This group of biomolecules promotes neuron growth. Scientists are looking into ways of delivering the molecules for treatment purposes.
Metal ion chelators
Since some people with Alzheimer's, Parkinson's and ALS appear to have higher-than-normal iron levels, substances that can lower iron levels may help with these diseases.
A study of rodents with Alzheimer-like disease found that iron-binding treatment improved their condition. More studies are needed.
Researchers disagree about the role of stimulants in the development of brain functioning problems like dementia.
Animal studies have suggested that caffeine is neuroprotective, but other studies conclude it may be a risk factor for developing dementia.
A recent review of research on caffeine use and dementia found that it was neither preventative nor harmful to brain function.
The blood-brain barrier protects the brain against infections and viruses, but it can also stop treatments from reaching the brain. This makes it hard to administer a treatment directly to the brain.
Gene therapy, or identifying and replacing a disease-causing gene, could solve this problem.
However, as is the case with many neuroprotectors, gene therapy has not yet proven to be consistently effective.
Drugs that show promise
Some drugs are currently being tried in people with diseases such as ALS and multiple sclerosis (MS). They are believed to provide neuroprotective effects.
The blood-brain barrier protects the brain from harmful substances, but it also hinders some treatments. Gene therapy may help overcome this obstacle.
- Riluzole is used to treat ALS. First thought to be mainly a glutamate inhibitor, it now appears to interact mostly with sodium, potassium, and calcium molecules within the CNS.The exact role it plays in helping ALS is unknown.
- Phenytoin is normally used to treat seizures. When tested on people with optic neuritis, an inflammation of the optic nerve often associated with MS, there was a reduction in nerve damage.
Amiloride is a diuretic pill used to treat congestive heart failure and high blood pressure. It has shown neuroprotective benefit in a small study of patients with MS
Research into neurodegenerative diseases and possible therapies are exciting and rapidly changing, but more work is needed before treatments can be considered safe and effective.