Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult (a neurodegenerative insult) the relative . Possibilities of multimodal and neuroprotective therapies in human disease, employing currently available drugs and showing evidence of neuroprotective. Neuroprotection is a widely studied treatment option for various central nervous system (CNS) disorders including neurodegenerative diseases.
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. In the nervous system, oxidative stress has been connected to the progression of Alzheimer's, Parkinson's diseases, and other conditions.
Problems with mitochondria in neurons have been linked to autism , Alzheimer's disease , Parkinson's disease , and several mental health conditions. Problems with mitochondria elsewhere in the body are thought to be linked to chronic health issues such as diabetes and asthma.
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. Excitotoxicity is a key factor in nerve damage following a stroke.
Inflammation anywhere in the body occurs when the immune system reacts to a foreign organism or infection. Inflammation can also occur after cell damage or injury, as the body tries to repair itself.
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.
In dementia , certain proteins build up in the brain. This appears to be part of a more complex picture, as research is starting to suggest that the proteins themselves are not the problem.
High levels of TNF seem to be associated with excitotoxicity and high levels of glutamate. Neuroprotection aims to limit nerve death after CNS injury and to protect the CNS from premature breakdown and other causes of nerve cell death.
These convert damaged and disease-causing, unstable free radical cells into molecules that are more stable and easier for the body to manage. 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. 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 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.
One study has shown that half of a baby aspirin , or 40 milligrams mg per day, may decrease the risk of Alzheimer's in individuals with type 2 diabetes. This group of biomolecules promotes neuron growth. Scientists are looking into ways of delivering the molecules for treatment purposes.
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. Facebook Twitter YouTube Instagram. Examples of neuroprotective in a Sentence Recent Examples on the Web In , along with two colleagues, Nobel laureate Julius Axelrod, an American, obtained a patent on the drug for its anti-inflammatory and neuroprotective properties. Could Africa be on the verge of a weed race? First Known Use of neuroprotective , in the meaning defined above.
Learn More about neuroprotective. Resources for neuroprotective Time Traveler! Explore the year a word first appeared. Dictionary Entries near neuroprotective neuroplasticity neuropodial neuropodous neuroprotective neuropsychiatry neuropsychology neuropter.
Statistics for neuroprotective Look-up Popularity. Increased levels of oxidative stress can be caused in part by neuroinflammation, which is a highly recognized part of cerebral ischemia as well as many neurodegenerative diseases including Parkinson's disease , Alzheimer's disease , and Amyotrophic Lateral Sclerosis.
Oxidative stress can directly cause neuron cell death or it can trigger a cascade of events that leads to protein misfolding, proteasomal malfunction, mitochondrial dysfunction, or glial cell activation.
Antioxidants are the primary treatment used to control oxidative stress levels. Antioxidants work to eliminate reactive oxygen species , which are the prime cause of neurodegradation. The effectiveness of antioxidants in preventing further neurodegradation is not only disease dependent but can also depend on gender, ethnicity, and age.
Listed below are common antioxidants shown to be effective in reducing oxidative stress in at least one neurodegenerative disease:.
NMDA receptor stimulants can lead to glutamate and calcium excitotoxicity and neuroinflammation. Some other stimulants, in appropriate doses, can however be neuroprotective. More neuroprotective treatment options exist that target different mechanisms of neurodegradation.
Continued research is being done in an effort to find any method effective in preventing the onset or progression of neurodegenerative diseases or secondary injuries. From Wikipedia, the free encyclopedia. Novel therapeutic strategies for neurodegenerative disorders".
Neuroprotection researchers are looking for ways to prevent neuronal degeneration in diseases like Alzheimer's, Parkinson's, and multiple. Neuroprotection is defined as the ability for a therapy to prevent neuronal cell death by intervening in and inhibiting the pathogenetic cascade that results in cell. Neuroprotective strategies that limit secondary tissue loss and/or improve functional outcomes have been identified in multiple animal models.