Molecule PSR 1 Can Repair Damaged Nerve Cells

Today's post from sciencedaily.com (see link below) looks at the discovery of a unique 'wonder' molecule that can eliminate diseased cells but also apparently regenerate damaged nerve cells. The fact that it can re-join and fuse together broken axons in the central nervous system (frequent causes of neuropathic symptoms) is astonishing and has many implications for the future of neuropathy treatment. That said, as with so many of these findings, we're a long way from translating the theory into effective treatment models but take comfort from the fact that new discoveries are being made and will lead to improvements for future generations

Research findings have implications for regenerating damaged nerve cells 
Date:January 7, 2015 Source:University of Colorado at Boulder
 
Summary:

Two new studies have identified a unique molecule that not only gobbles up bad cells, but also has the ability to repair damaged nerve cells. Known as the phosphatidylserine receptor, or PSR-1, the molecule can locate and clear out apoptotic cells that are pre-programmed to die as well as necrotic cells that have been injured and are causing inflammation. Programmed cell death, or apoptosis, is a natural process that kills billions of cells in a typical human body each day.
 
Two new studies involving the University of Colorado Boulder and the University of Queensland (UQ) in Brisbane, Australia have identified a unique molecule that not only gobbles up bad cells, but also has the ability to repair damaged nerve cells.

Known as the phosphatidylserine receptor, or PSR-1, the molecule can locate and clear out apoptotic cells that are pre-programmed to die as well as necrotic cells that have been injured and are causing inflammation, said CU-Boulder Professor Ding Xue, who led one study and co-authored the other. Programmed cell death, or apoptosis, is a natural process that kills billions of cells in a typical human body each day.

But it is the finding that the PSR-1 molecule also can help reconnect and knit together broken nerve fibers, called axons, that has caught the attention of both science teams.

"I would call this an unexpected and somewhat stunning finding," said Xue of CU-Boulder's Department of Molecular, Cellular and Developmental Biology. "This is the first time a molecule involved in apoptosis has been found to have the ability to repair severed axons, and we believe it has great therapeutic potential."

Xue is the lead author on a paper being published Jan. 7 in Nature Communications that details how PSR-1 recognizes and removes cells that are pre-programmed to die or damaged. He also is co-author of the companion paper being published in Jan. 7 in Nature led by Associate Professor Massimo Hilliard of the UQ's Queensland Brain Institute that shows the major role played by PSR-1 in the regeneration of nerve axons, a holy grail of sorts for neurologists involved with patients who have suffered central nervous system damage from accidents or diseases.

Both studies relied on a popular lab organism known as C. elegans, a nearly microscopic nematode that is fast growing, translucent and has a sequenced genome showing that nearly half its genes are closely related to corresponding human genes.

"This will open new avenues to try and exploit this knowledge in other systems closer to human physiology and hopefully move toward solving injuries," said Hilliard. In the future, neurosurgery may be combined with molecular biology to deliver positive clinical outcomes and perhaps treat conditions like spinal cord or nerve injuries, he said.

During programmed cell death, apoptotic cells flag themselves for elimination by moving a specific cell membrane component known as phosphatidylserine (PS) from the inner membrane to the cell surface, setting them up to be engulfed. "These are what we call 'eat me' signals," said Xue.

In contrast, broken axons in nerve cells send PSR-1 molecules an SOS alert. "The moment there is a cut to the nerve cell we see a change in the cell membrane PS composition, which acts as a signal to PSR-1 molecules in the other part of the nerve that essentially says "I am in danger, come and save me," said Xue.

One of the most encouraging finding is that PSR-1 plays an early role in the axonal fusion process required for neuroregeneration, said Xue. "Whether human PSR has the capacity to repair injured axons is still unknown," he said. "But I think our new research findings will spur a number of research groups to chase this question."

While biomedical researchers have had some successes in repairing peripheral nerves and nerve clusters outside the brain and spinal cord in humans, there currently is no effective way to regenerate broken nerve cells in the central nervous system, said Xue. Such nerve damage can cause partial or total paralysis.

Xue, who first identified the PSR-1 receptor in 2003, said the collaboration between CU-Boulder and UQ has pushed scientific discovery forward. "We are trying to understand how PSR-1 removes cells through apoptosis and necrosis, and they are trying to understand if molecules involved in apoptosis also play a role in the neuroregeneration process," said Xue.

CU-Boulder postdoctoral researcher Yu-Zen Chen, a Nature Communications paper co-author, said the team currently is trying to find ways to raise the level of the PSR-1 in nematode cells, which likely would promote faster healing in nerve axons. "We think the higher the PSR-1 level, the higher the repair capacity of the molecule," said Chen.

Xue said C. elegans is an ideal organism to use in the hunt for new therapeutics to treat nerve damage because of its relatively small, well-known genome and short life span -- just a few days. "This makes drug screening much easier, faster and less expensive than using a mouse model, for instance," said Xue.

"The big finding is that we have a single receptor that does two different jobs," Xue said. "We don't have a solution yet for treating people with nerve damage, but we feel these findings offer promise in seeking new and effective therapeutics."

Story Source:

The above story is based on materials provided by University of Colorado at Boulder. Note: Materials may be edited for content and length.

Journal References:
Hengwen Yang, Yu-Zen Chen, Yi Zhang, Xiaohui Wang, Xiang Zhao, James I. Godfroy, Qian Liang, Man Zhang, Tianying Zhang, Quan Yuan, Mary Ann Royal, Monica Driscoll, Ning-Shao Xia, Hang Yin, Ding Xue. A lysine-rich motif in the phosphatidylserine receptor PSR-1 mediates recognition and removal of apoptotic cells. Nature Communications, 2015; 6: 5717 DOI: 10.1038/ncomms6717
Brent Neumann, Sean Coakley, Rosina Giordano-Santini, Casey Linton, Eui Seung Lee, Akihisa Nakagawa, Ding Xue, Massimo A. Hilliard. EFF-1-mediated regenerative axonal fusion requires components of the apoptotic pathway. Nature, 2015; 517 (7533): 219 DOI: 10.1038/nature14102

http://www.sciencedaily.com/releases/2015/01/150107122912.htm

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HIV Related Neuropathy

Today's video is an Australian view of how HIV can cause neuropathy, whether from the virus itself or the drugs. It comes from PainClinician.com (see link below) and is basically a teaching video for other medical professionals. The difference with most of the other neuropathy videos posted here on the blog, is that if this is what medical students are learning, then we can look at the disease from the point of view of the doctors who treat us. It seems to be full of up to date information and reflects modern medical thinking but apart from the odd scientific term here and there, which may not be so easily understood, the vast majority of the 11 minutes, is pretty interesting to the average neuropathy and HIV patient and explains a few areas which may have previously seemed vague.




http://painclinician.com/video/hiv_related_neuropathy

Hepatitis C And Neuropathy

Today's post from hepcsupport.org (see link below) talks about the link between hepatitis C and neuropathy. It is suspected that the blood condition EMC which is associated with hepatitis C, is responsible for causing nervous system abnormalities, thus explaining why so many people with hepatitis C also display symptoms familiar to many neuropathy patients. In this case, new treatments for hepatitis C are emerging and becoming more widely available. There's even a good chance that a combination therapy similar to the HIV anti-viral combos will be available for Hepatitis C patients. The research so far however, on the links between Hep C, EMC and Neuropathy, is thin on the ground to say the least.

A PAINFUL CONNECTION: HCV, CRYO, NEUROPATHY

By Mary Lou Reazor|March 24th, 2013|

There is a very strong association between HCV and a blood condition called Essential Mixed Cryoglobulinemia (EMC). People with hepatitis c, who suffer numbness or tingling of their extremities, know from experience there is also an association between HCV and Neuropathy. Increasingly, their claims are finding support according to researchers and clinical physicians.

Among other symptoms, EMC can cause nervous system abnormalities. Researchers have not explained the connection between HCV, Neuropathy and EMC, nor have they found significantly effective treatments, but knowledge is sure to increase as more people are diagnosed with HCV and its symptoms.

Neuropathy refers to any disease of the nervous system, resulting from localized inflammation of nerves. Patients complain of numbness, tingling and muscle weakness. Symptoms appear in the body’s extremities, the condition is called “Peripheral Neuropathy”. A physical exam may also reveal decreased deep tendon reflexes.

In both Encephalopathy and Neuropathy, the key change is inflammation of blood vessels (Vasculitis). The vessels are responding to immune system products floating in the blood vessels directly. The immune-globulins that are involved are called Cryoglobulins because they turn into a cool gel at cool temperatures. Since cold temps readily affect the small and middle-sized vessels in the extremities, the Cryoglobulins are more likely to form in them. Cryoglobulemia is the condition of having cyroglobulins in the blood.

There are several possible new treatments in “the pipeline”. There are several anti-viral agents that have shown promise in clinical trials, and researchers are developing several HCV specific protease inhibitors similar to those used for HIV retro-virus.

http://hepcsupport.org/a-painful-connection-hcv-cryo-neuropathy/

B Vitamins Alpha Lipoic Acid and other Nutrients for Neuropathy

There have been other posts on the blog (see alphabetical list on the right) about both Alpha Lipoic Acid and nutrients in general which may or may not help with neuropathy. Today's post comes from MDJunction (see link below) and is an excellent account, though without any indication of the writer's qualifications. That said, she says nothing that isn't found on most related sites on the Web (and provides more detail than most) and that may, in your opinion, be verification enough.
The general concensus from neurologists is that they support B-Vitamins and both Alpha Lipoic Acid and Acetyl-L Carnitine as supplements which may improve neuropathic problems but you should be aware that neither is cheap and in most countries, neither is covered by any sort of insurance policy. If the case is proved, it seems unfair to discriminate on the basis of who can and who can't afford a treatment but that's a whole other story!
Also, always take extra B-vitamins with advice from your doctor - it's easy to create an imbalance in your body and cause more harm than good.
If you decide to try supplements, (after consultation with your doctor) shopping around on the Net may help reduce costs.

Peripheral Neuropathy- Nutrients
Jackie
Mar 23 2011

Neuropathy: Nutrient Therapies

Although there has been virtually no research on the use of nutrient therapies for HIV-related neuropathies, there has been a fair amount of research (mostly in other countries) on their use for diabetic neuropathies. Since it appears likely that at least some of the mechanisms for the nerve damage may be similar in the two diseases (inflammation and oxidative damage to the nerves combined with B vitamin deficiencies), there is reason to believe that therapies which have proven useful for diabetics may also work for at least some people living with HIV who develop neuropathy. Many people living with HIV have reported to me that they have successfully eliminated neuropathy with some combination of the nutrient therapies discussed here. Thus, in addition to the other treatments mentioned, I would stress the importance of therapy with the B vitamins and other nutrients, especially acetyl-L-carnitine, gamma-linolenic acid, alpha-lipoic acid, magnesium, and chromium. I would definitely consider including the nutrients that have been shown to help rebuild the myelin sheath around nerves and/or improve nerve functioning such as choline, inositol, gamma linolenic acid, B6, B12, niacin, thiamine, biotin, folic acid, and magnesium.

Biotin, choline, inositol, and thiamine are B vitamins that have all been found useful in treating the peripheral and autonomic neuropathies found in diabetes and may also help with HIV-related neuropathies. In a study at the University of Athens, it was shown that regular, long-term use of biotin in diabetics was very effective both for improvement in nerve conduction and relief of pain. Improvement in nerve conduction occurred after only 4-8 weeks of therapy. In this study, biotin was given via daily intramuscular injection (10 mg/day) for 6 weeks; then 3 times per week (10 mg), intramuscularly, for 6 weeks; then 5 mg/day taken orally for up to two years. The researchers hypothesize that deficiency, inactivity, or unavailability of biotin in diabetics may result in disordered activity of the biotin-dependent enzyme, pyruvate carboxylase, leading to an accumulation of pyruvate and/or a depletion of aspartate, either of which could adversely affect nervous system metabolism. There are a number of reasons why HIV-positive persons may be deficient in biotin and, thus, potentially at risk for a similar problem. It has been suggested that those with neuropathy symptoms might try 10-15 mg/day orally, taken in conjunction with the other B vitamins found useful for improving nerve function.

B12 deficiency is a known cause of neuropathy so this vitamin, along with its coworker folic acid, should certainly be included in any program aimed at eliminating this symptom. Typical symptoms of peripheral neuropathy related to B12 deficiency include the type of leg and foot pains experienced by many. B6 deficiencies are also known to cause both carpal tunnel syndrome (with symptoms of numbness, tingling, and pain in the hands and wrists) and degeneration of peripheral nerves and may be responsible for some peripheral neuropathy problems.

Choline and inositol also seem to be very important parts of the combination of vitamins needed for neuropathy resolution. Diabetic neuropathy is known to be associated with a reduction in myo-inositol levels in nerves and tissues. The decreased level of myo-inositol is believed to cause a decrease in the activity of the sodium-potassium pump and, thus, to change the sodium permeability of nerves. Both diets high in inositol and inositol supplementation have been shown to improve diabetic neuropathy. Researchers at the University of Alabama found a statistically significant improvement in nerve function in diabetics placed on a diet high in inositol. Included in the diet were high-inositol foods such as cantaloupe, peanuts, grapefruit, and whole grains. Other researchers have reported that supplementation with inositol in doses of 2-6 grams per day has resulted in improvements in neuropathy. Robert Atkins, M.D., has reported his successful use of 2-6 grams per day for reversing diabetic neuropathy, and notes that physicians at St. James Hospital in Leeds, England, have reported good results with even smaller dosages.

In addition to the use of inositol itself, treatment with acetyl-L-carnitine can help raise nerve myo-inositol content. Florida researchers have found that peripheral nerve function in diabetes is linked to nerve myo-inositol content and that acetyl-l-carnitine can raise the levels of myo-inositol in the nerves of animals with experimentally induced diabetes. It also apparently protects the nerve membranes from free-radical damage, as evidenced by reduced malondialdehyde levels in the animals treated with acetyl-l- carnitine.

Thiamine has also been seen to be useful in treating diabetic neuropathy. Stanley Mirski, M.D., has reported that a large percentage of his diabetic patients who suffer from neuropathy have achieved improvements with daily thiamine supplementation in doses of 50-100 mg. Using a fat-soluble form of thiamine such as thiamine tetrahydro-furfuryl disulfide may be preferable because of the relatively poor absorption of water-soluble forms of this vitamin. This type is contained in Cardiovascular Research's Allithiamine. A large number of HIV-positive people have reported to me their successful elimination of neuropathy with the combined use of the B vitamins discussed here. The information on acetyl-l- carnitine is too recent for much in the way of anecdotal reports to have surfaced, but it might be an important addition to improve the chances for successful elimination of neuropathy.

Alpha-lipoic acid has long been used in Europe for the treatment of peripheral neuropathy in diabetics. A number of controlled clinical trials have shown its usefulness for reducing both the pain and numbness suffered by those with diabetic neuropathy, and its use for this condition is approved in Germany. Its antioxidant properties may help protect the nerves from the inflammation and oxidative damage that HIV induces, as has been shown to be true with diabetic neuropathy. Because of its liver protective and antioxidant benefits, it has been included as a component of the programs of many of my clients for several years now. It may have contributed to the success of the neuropathy elimination programs some of them have used.

Gamma linolenic acid is an essential fatty acid found in borage oil, grape seed oil, black currant oil, and evening primrose oil that has been shown to be successful in reversing nerve damage in diabetics suffering from peripheral neuropathy. In a double-blind, placebo-controlled study using 480 mg of GLA daily, all the diabetics given the fatty acid experienced gradual reversal of nerve damage and improvement in the symptoms related to the peripheral neuropathy, while those on placebo gradually worsened. It is thought that GLA may help to rebuild the myelin sheath around the nerves, thus restoring proper nerve conduction.

Magnesium is also known to be necessary for nerve conduction; deficiency is known to cause peripheral neuropathy symptoms. Thus, including optimal amounts of magnesium might contribute to elimination of neuropathy. There have also been reports of chromium deficiency causing peripheral neuropathy. I learned this too recently for chromium to have been included in most of the neuropathy therapy programs used by my clients in the past and, thus, I'm not sure what it might contribute. However, chronic infection is known to deplete body stores of chromium, so adding a dose of perhaps 200-400 mcg/day to a complete nutrient protocol might be reasonable.

In addition to all the nutrient supplements, an analysis of data coming out of the Immune Enhancement Program in Portland, Oregon, appears to show that their program, which includes Chinese herbs along with acupuncture and various other therapeutic approaches, results in improvement in neuropathy for some.

If you are considering supplementation with any of the B vitamins discussed above, never forget that although B vitamins are by and large non-toxic, any individual B vitamin should always be taken along with the full B complex to prevent imbalance in the body. Long-term use of very high doses of individual B vitamins taken alone, without the rest of the B complex, can induce imbalances or deficiencies in other B vitamins.

About Alpha Lipoic Acid

Alpha-lipoic acid (ALA), also known as lipoic acid (or thioctic acid), is a sulfur-containing fatty acid found inside every cell of the human body. The main function of alpha-lipoic acid is to generate the energy required to keep living organisms alive and functioning. Lipoic acid plays a key role in a variety vital energy-producing reactions in the body that turn glucose (blood sugar) into energy.

Alpha-lipoic acid is a potent biological antioxidant that has been shown to slow the oxidative damage in cells, and in many cases stabilize or even reverse cell damage. Alpha-lipoic acid is so effective as an anti-oxidant because it works on both water and fat-soluble free radicals that cause oxidation and cell damage in the body. Notwithstanding its popularity, the exact mechanism responsible for the medicinal affects of alpha-lipoic acid is still not fully understood.

Some research suggests that certain nerve diseases may occur as a result of free radical damage. Since alpha-lipoic acid can reach all parts of a nerve cell it can potentially protect nerve cells against such damage. This is the rationale behind studies on the potential benefits of alpha-lipoic acid for diabetic neuropathy.

Experimental studies show that alpha-lipoic acid may exhibit a renal protective effect in individuals with diabetes. Alpha-lipoic acid increases glucose uptake in the cells and appears to reduce symptoms of diabetic complications including cataract formation, vascular damage, and polyneuropathy (nerve damage). A study published in Diabetic Medicine in 1999 showed that patients treated with 600 mg of ALA 3 times daily for 3 weeks had improvement of diabetic symptoms from polyneuropathy. In another study using 600 to 1,800 mg of ALA daily, individuals treated showed improved insulin sensitivity. Most studies supporting the use of alpha-lipoic acid to reduce symptoms of diabetic peripheral neuropathy employed intravenous alpha-lipoic. Evidence for the use of oral lipoic acid, in connection with diabetes remains weak and contradictory.

Another group of nerve cells in diabetics, the autonomic nerves, which control the function of internal organs, may also become damaged. When this same phenomenon occurs in the heart, a condition known as cardiac autonomic neuropathy, it leads to irregularities of heart rhythm. There is some evidence that alpha-lipoic acid may be helpful for this condition.

Some in the scientific community believe that alpha-lipoic acid can actually reverse the damage in aging cells of the brain. Alpha lipoic acid has also been used both in oral and topical forms as a way for keeping skin healthy and young in appearance. There have been studies documented in medical literature indicating that supplemental ALA may even be beneficial in patients with glaucoma.

NutritionalTree.com is a great consumer resource that collects user reviews for alpha lipoic acid products.

Dosage

The common dosage of alpha-lipoic acid for complications of diabetes is 100 to 200 mg three times daily. In studies that found benefit of supplementing with alpha-lipoic acid, several weeks of treatment were often necessary for effects to develop. However, some studies have indicated as much as 600-1,800 mg per day of alpha-lipoic acid for optimal benefit in people with specific health concerns such as diabetes, liver cirrhosis and atherosclerosis.

If you are healthy and want to promote optimal health, a dose of 30 - 300 mg per day may be sufficient.

Lipoic acid appears to have no significant side effects at dosages up to 1,800 mg daily.

http://www.mdjunction.com/diary/jackies-journey-back-to-health/peripheral-neuropathy-nutrients

HOMOEOPATHIC REMEDIES FOR DYSENTERY

Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica(amoebic dysentery).

HOMOEOPATHIC REMEDIES

MERCURIUS COR 30- MERCURIUS SOL 30- Begin the treatment with Merc cor. if there is much blood  or with Merc sol. If there is much mucus. Cutting pains are present and stools are scanty. Tenesmus before and after stools.

NUX VOMICA 30- Stools contain much mucus. There are abdominal pains before stools and these are relieved after stool

ALOE SOC. 30—Stools contain a lot of mucus or are jelly like. There is burning and pain in the rectum . Patient is afraid of passing flatus as he is not sure whether the urge is for stool or flatus. Bleeding from the rectum

CHAPARRO- It is an excellent remedy for chronic dysentery and diarrhea

COLCHICUM AUTUM. 30- Autumnal dysentery when days are hot and nights are cold

TROMBIDIUM 30—Dysentery worse by eating and drinking. Stools only after eating. Much pain, before and after stool. Burning in the anus

THUJA OCC. 200- An excellent remedy for amoebic dysentery

SEPTICAEMINUM 30- It cures magically the dysentery which is produced in camp life

BAPTISIA TIC. 30- Dysentery  of old people. Dysentery during typhoid fever

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