Recovering from stroke with proper nutrition
Nutrition and Dietary Supplements
You should seek conventional medical treatment for stroke. You should use complementary and alternative therapies only under the supervision of a health care provider. Supplements can have negative effects on certain segments of the population, and can interact negatively with prescription medications. Make sure all of your medical providers are aware of any supplements you are considering taking.
Potentially beneficial nutritional supplements include the following:
Alpha-lipoic acid. Alpha-lipoic acid works together with other antioxidants, such as vitamins C and E. It is important for growth, helps prevent cell damage, and helps the body rid itself of harmful substances. Because alpha-lipoic acid can pass easily into the brain, it has protective effects on brain and nerve tissue, and shows promise as a treatment for stroke and other brain disorders involving free radical damage. Animals treated with alpha-lipoic acid, for example, suffered less brain damage and had a four times greater survival rate after a stroke than the animals who did not receive this supplement, especially when alpha-lipoic acid is combined with vitamin E. While animal studies are encouraging, more research is needed to understand whether this benefit applies to people as well.
Calcium.. In a population-based study (one in which large groups of people are followed over time), women who took in more calcium, both through the diet and supplements, were less likely to have a stroke over a 14-year period. More research is needed to fully assess the strength of the connection between calcium and risk of stroke.
Folic Acid, Vitamin B6, Vitamin B12, and Betaine. Many clinical studies indicate that patients with elevated levels of the amino acid homocysteine are up to 2.5 times more likely to suffer from a stroke than those with normal levels. Homocysteine levels are strongly influenced by dietary factors, particularly vitamin B9 (folic acid), vitamin B6, vitamin B12, and betaine. These substances help break down homocysteine in the body. Some studies have even shown that healthy individuals who consume higher amounts of folic acid and vitamin B6 are less likely to develop atherosclerosis than those who consume lower amounts of these substances. One study found that lowering homocysteine with folic acid and vitamins B6 and B12 reduced the overall risk of stroke, but not stroke severity or disability. Despite these findings, the American Heart Association (AHA) reports that there is insufficient evidence to suggest that supplementation with betaine and B vitamins reduce the risk of atherosclerosis, or that taking these supplements prevents the development or recurrence of heart disease. The AHA does not currently recommend population-wide homocysteine screening, and suggests that folic acid, as well as vitamin B6, B12, and betaine requirements be met through diet alone. Individuals at high risk for developing atherosclerosis, however, should be screened for blood levels of homocysteine. If elevated levels are detected, a provider may recommend supplementation.
Magnesium. Population-based information suggests that people with low magnesium in their diet may be at greater risk for stroke. Some preliminary scientific evidence suggests that magnesium sulfate may be helpful in the treatment of a stroke or TIA. More research is needed to know for certain if use of this mineral following a stroke or TIA is helpful. Magnesium may lower blood pressure and potentially interact with some heart medicines.
Omega-3 Fatty Acids. Strong evidence from population-based studies suggests that omega-3 fatty acid intake (primarily from fish) helps protect against stroke caused by plaque buildup and blood clots in the arteries that lead to the brain. In fact, eating at least 2 servings of fish per week can reduce the risk of stroke by as much as 50%. However, people who eat more than 3 grams of omega-3 fatty acids per day (equivalent to 3 servings of fish per day) may be at an increased risk for hemorrhagic stroke, a potentially fatal type of stroke in which an artery in the brain leaks or ruptures. Omega-3 fatty acids may increase the chances of bleeding, especially in those taking anticoagulant medications, such as warfarin (Coumadin) or even aspirin.
The FDA recommends that pregnant women and women of childbearing age, who may become pregnant, avoid large predatory fish such as shark, tuna, and swordfish. These fish have much higher levels of methyl mercury than other commonly consumed fish. Since the fetus may be more susceptible than the mother to the adverse effects of methyl mercury, FDA experts say that it is prudent to minimize the consumption of fish that have higher levels of methyl mercury.
Potassium. Although low levels of potassium in the blood may be associated with stroke, taking potassium supplements does not seem to reduce the risk of having a stroke.
Vitamin C. Having low levels of vitamin C contributes to the development of atherosclerosis and other damage to blood vessels and the consequences, such as stroke. Vitamin C supplements may also improve cognitive function if you have suffered from multiple strokes.
Vitamin E. Eating plenty of foods rich in vitamin E, along with other antioxidants like vitamin C, selenium, and carotenoids, reduces your risk for stroke. In addition, low levels of vitamin E in the blood may be associated with risk of dementia (memory impairment) following stroke. Animal studies also suggest that vitamin E supplements, possibly in combination with alpha-lipoic acid, may reduce the amount of brain damaged if taken prior to the actual stroke. Researchers suggest testing this theory in people who are at high risk for stroke. Thus far, however, some large, well-designed studies of people suggest that it is safest and best to obtain this antioxidant via food sources, and that supplements do not provide any added benefit.
Others. Additional supplements that require further research but may be useful as part of the treatment or prevention of stroke include:
- Coenzyme Q10 (CoQ10). CoQ10 works as an antioxidant and may reduce damage following a stroke. CoQ10 may increase the ability of the blood to clot and therefore interfere with some blood-thinning medicines, such as warfarin (Coumadin) and others.
- Selenium. Low levels can worsen atherosclerosis and its consequences. However, scientists do not know whether taking selenium supplements will help.
Herbs
The use of herbs is a time-honored approach to strengthening the body and treating disease. Herbs, however, contain active substances that can trigger side effects and interact with other herbs, supplements, or medications. For these reasons, you should take herbs only under the supervision of a health care provider knowledgeable in the field.
Bilberry (Vaccinium myrtillus). A close relative of the cranberry, bilberry fruits contain flavonoid compounds called anthocyanidins. Flavonoids are plant pigments that have excellent antioxidant properties. This means that they scavenge damaging particles in the body known as free radicals and may help prevent a number of long-term illnesses, such as heart disease. Bilberry may slow blood clotting and therefore may increase the risk of bleeding in people who take blood-thinning medications, such as warfarin (Coumadin), aspirin, and others.
Garlic (Allium sativum). Clinical studies suggest that fresh garlic and garlic supplements may prevent blood clots and destroy plaque. Blood clots and plaque block blood flow and contribute to the development of heart attack and stroke. Garlic may also be beneficial for reducing risk factors for heart disease and stroke like high blood pressure, high cholesterol, and diabetes. Homocysteine, similar to cholesterol, may contribute to increasing amounts of blood clots and plaque in blood vessels. If you take aspirin or other blood thinners like warfarin (Coumadin), ACE inhibitors (a class of blood pressure medications), sulfonylureas for diabetes, birth control medications, medications for HIV, or statins for high cholesterol, talk to your doctor before using garlic supplements.
Ginkgo (Ginkgo biloba). Gingko may reduce the likelihood of dementia following multiple strokes (often called multi-infarct dementia) by preventing blood clot formation. Most providers choose to use medications for this effect rather than herbs. Ginkgo may also decrease the amount of brain damage following a stroke. While animal studies support these possible benefits of ginkgo, more research is needed. Also, ginkgo should not be used with blood-thinning medications, such as warfarin (Coumadin), aspirin, and others, unless specifically instructed by your provider.
Ginseng (Panax ginseng). Asian ginseng may decrease endothelial cell dysfunction. Endothelial cells line the inside of blood vessels. When these cells are disturbed, it may lead to a heart attack or stroke. The potential for ginseng to quiet down the blood vessels may prove to be protective against these conditions. More research is needed. Ginseng can have stimulating effects that may be harmful to certain people. Ginseng may also thin your blood and, therefore, should be used only under the supervision of a doctor, particularly if you are taking blood-thinning medication, such as warfarin (Coumadin), aspirin, and others.
Turmeric (Curcuma longa). Early studies suggest that turmeric may prevent heart attack or stroke. Animal studies have shown that an extract of turmeric lowered cholesterol levels and inhibited the oxidation of LDL (bad) cholesterol. This is helpful because oxidized LDL deposits in the walls of blood vessels and contributes to the formation of atherosclerotic plaque and other damage to the vessels. Turmeric may also prevent platelet build up along the walls of an injured blood vessel. Platelets collecting at the site of a damaged blood vessel cause blood clots to form and contribute to blocking the artery as well. Turmeric may also thin your blood and, therefore, should only be used under the supervision of a provider, particularly if you are taking blood-thinning medications, such as warfarin (Coumadin), aspirin, and others. More research is needed to determine whether these effects apply to people.
Homeopathy
Although an experienced homeopath might prescribe a regimen for treating stroke that includes one of the remedies listed below, the scientific evidence to date does not confirm the value of homeopathy for this purpose.
- Acontitum napellus. For numbness or paralysis after a cerebral accident.
- Belladonna. For stroke that leaves the person very sensitive to any motion, with vertigo and trembling.
- Kali bromatum. For stroke resulting in restlessness, wringing of the hands or other repeated gestures, insomnia, and night terrors.
- Nux vomica. For cerebral accident with paresis (muscular weakness caused by disease of the nervous system), expressive aphasia (language disorder), convulsions, and great irritability.
Acupuncture
Many studies have been conducted on the effects of acupuncture during stroke rehabilitation. These studies show that acupuncture reduces hospital stays and improves recovery speed. Acupuncture has been shown to help stroke patients regain motor and cognitive skills and to improve their ability to manage daily functioning. Based on the available data, the National Institutes of Health recommend acupuncture as an alternative or supplemental therapy for stroke rehabilitation. In general, the evidence indicates that acupuncture is most effective when initiated as soon as possible after a stroke occurs, however positive outcomes have been found for acupuncture started as late as 6 months following a stroke.
People who have suffered a stroke often have a deficiency of qi in the liver meridian and a relative excess in the gallbladder meridian. In addition to a primary needling treatment on the liver meridian and the supporting kidney meridians, moxibustion (a technique in which the herb mugwort is burned over specific acupuncture points) may be used to enhance therapy. Treatment may also include performing acupuncture on affected limbs. Certain scalp acupuncture techniques that have been developed by Chinese, Korean, and Japanese practitioners also show promise.
Chiropractic
Chiropractors do not treat stroke, and high velocity manipulation of the upper spine is considered inappropriate in individuals who are taking blood-thinning medications, or other medications used to reduce the risk of stroke. It should also be noted that chiropractic spinal manipulation of the neck is associated with an exceedingly small risk of causing stroke (reports range from 1 per 400,000 to 1 per 2,000,000).
Traditional Chinese Medicine
In Traditional Chinese Medicine, there are reports of more than 100 substances that have been used to treat stroke. In fact, pharmacologic research of these substances focuses on understanding the ingredients and their mechanisms of action in order to develop new drugs.
Prognosis and Complications
There are many possible complications associated with stroke, including:
- Seizures
- Paralysis
- Cognitive (thinking) deficits
- Speech problems
- Emotional difficulties
- Daily living problems
- Pain
- Memory deficits
Many people begin to recover from a stroke almost immediately after it has occurred.
The recovery process is most rapid in the first 3 months after a stroke, but improvement will continue for 6 months to a year. Many stroke survivors even report that they slowly continue to regain function for years after their stroke. It is very important not to lose hope.
Connie’s comments: I would start with bananas, figs, oranges, avocado, walnut, fish, olive oil, colored foods and soups with bone marrow from beef, chicken or turkey. I prefer supplements of Lifepak and AGELOC at:
http://www.clubalthea.pxproducts.com
We are inviting all to the nutrition test business to measure your anti-oxidant levels. See Dr Oz Pharmanex scanner in YouTube. Email motherhealth@gmail.com if you are a pharma rep or doctor or health care pros.
Anxiety with Dementia decreased with calcium and magnesium nutrients
Anxiety with Dementia decreased with calcium and magnesium nutrients
Anxiety with Dementia decreased by calcium and magnesium nutrients
My client who is 92 yrs old with early Dementia is shouting less at night and more calm. After 4 weeks of taking care of her and with introduction of nutritional supplementation rich in calcium and magnesium, she did not shout last night. I also spent some time massaging her head and face after I massage her legs between the hours of 6 to 7 pm. We still need to get a protective top mattress cover for her hospital bed to prevent bed sores and provide more comfort. I also served cooked – boiled sweet potatoes last night. When I shop for her food, I include eggs, nutrition drink, blueberries, lemon, avocados, bananas, oranges, salmon, veggies for soups (cilantro, carrots, celery, onions, garlic).
I prefer the quality supplements, LIFEPAK and AGELOC products at :
http://www.clubalthea.pxproducts.com
Connie
Nervous system nutrients
Our nervous system requires several dozen minerals, vitamins, fatty acids and amino acids to function at all properly. Deficiencies of nutrients such as calcium, magnesium, zinc, omega-3 fatty acids, and vitamins A, B-complex, C, D3 and E are common, especially if you eat refined foods.
Anxiety and demographic characteristics
Sex
Although anxiety symptoms and disorders tend to be more common in women within the non-demented elderly (Stanley & Beck, 2000), most studies using dementia samples did not find sex differences: only two of thirteen studies found greater levels of anxiety among women with AD (Bungener et al., 1996; Ferretti et al., 2001). These two studies, however, used anxiety scales that have not been previously validated in individuals with dementia. Thus, the bulk of the evidence suggests a lack of relationship between sex and anxiety in individuals with dementia (Ballard, Boyle, & Bowler, 1996; Ballard et al., 2000; Hwang et al., 2004; Mendez, McMurtray, Chen, Shapira, Mishkin, & Miller, 2006; Orrell & Bebbington, 1996; Ownby, Harwood, Barker, & Duara, 2000; Paulsen, Ready, Hamilton, Mega, & Cummings, 2001; Porter et al., 2003; Shankar et al., 1999; Teri et al., 1999; Tsang et al., 2003).
Age
Of the nine studies we identified, one found greater anxiety in older patients (Bungener et al., 1996). This study, already cited above, used anxiety scales that have not been validated in dementia. Another study (Ferretti et al., 2001) found greater anxiety in older patients in one sample but not the other; moreover, the association between anxiety and age disappeared after controlling for other variables of interest. The other studies found no relationship between age and anxiety (Ballard et al., 1996; Ballard et al., 2000; Mendez et al., 2006; Orrell & Bebbington, 1996; Paulsen et al., 2001; Shankar et al., 1999; Tsang et al., 2003).
Education
The two studies we identified found no relationship between anxiety and years of education in FTD (Mendez et al., 2006) and AD (Ownby et al., 2000).
Race/ethnicity
Two studies (Chen, Borson, & Scanlan, 2000; Ortiz, Fitten, Cummings, Hwang, & Fonseca, 2006) examined the prevalence of anxiety symptoms in individuals with dementia of different ethnic groups. In one study (Chen et al., 2000), African-Americans with dementia had lower anxiety than Asians and Hispanics with dementia, even after controlling for dementia severity, age, sex, and education. In another study (Ortiz et al., 2006), Hispanics with dementia had higher anxiety than Caucasians with dementia, even after controlling for age, sex and education. In contrast, Hispanics and Caucasians without dementia did not differ in anxiety symptoms. Thus, current data suggest that anxiety may be more prevalent in Hispanics and Asians with dementia than African-Americans and Caucasians with dementia.
Anxiety and dementia subtype
Six studies (Aarsland, Cummings, & Larsen, 2001; Ballard et al., 2000; Lyketsos et al., 2000; Porter et al., 2003; Skoog, 1993; Sultzer, Levin, Mahler, High, & Cummings, 1993) compared anxiety prevalence in distinct, well-defined types of dementia (see Table 2). In one study (Skoog, 1993), rates of OCD, phobia, and GAD did not differ between AD and vascular dementia (VaD). Among four studies that examined rates of anxiety symptoms in AD and VaD, two found greater anxiety in VaD (Ballard et al., 2000; Porter et al., 2003), and the other two did not find any significant difference (Lyketsos et al., 2000; Sultzer et al., 1993). In both studies with null findings, anxiety was qualitatively greater in the AD group. Moreover, in one study (Sultzer et al., 1993), sample size was relatively small (N=28 in each group), and in the other study (Lyketsos et al., 2000), rates of anxiety symptoms were unusually low (8% in the AD group and 18% in the VaD group). Thus, anxiety symptoms appear greater in VaD than in AD. Compared to AD, rates of anxiety symptoms may be greater in fronto-temporal dementia (Porter et al., 2003) and similar in dementia associated with Parkinson’s disease (Aarsland et al., 2001).
Anxiety and dementia severity
Five studies examined the relationship between anxiety symptoms and dementia severity (see Table 3). Two studies (Chen et al., 2000; Sclan et al., 1996) found lower anxiety at the profound/terminal stages of dementia, and two others (Lyketsos et al., 2000; Shankar et al., 1999) found no significant effect of dementia severity. The latter two studies, however, did not distinguish between severe and profound/terminal dementia. A fifth study (Forsell & Winblad, 1997) found lower anxiety at the moderate/severe stages. Results of this study are questionable, however, because dementia type was not reported and the instrument used to assess anxiety, the Comprehensive Psychopathological Rating Scale (Asberg, Montgomery, Perris, Schalling, & Sedvall, 1978), has not been validated in dementia. Thus, findings suggest that anxiety is relatively stable across the range of dementia severity, until the profound/terminal stage, where it decreases.
Inflammation , brain and your health
Inflammation , brain and your health
Inflammation , brain and your health
————–
For AGELOC quality supplements that are anti-inflammatory and resets your gene expression to a younger you, visit:
Connie is giving a seminar for health centers and companies about aging hacks, inflammation, brain and senior care. Email motherhealth@gmail.com
We are inviting all health care reps and pros to our nutrition testing business. See Dr Oz Pharmanex scanner in YouTube.
$300 million no-bid contract for Puerto Rico forbids any government audit
- GOP judge resigns after prohibiting mom from seeing infant for 14 months over unpaid court fees
- Trump lawyer Michael Cohen sold buildings to mystery buyers for millions in cash
- Trump increasingly frustrated his greatness isn’t being recognized
- Daily Kos fell short of our fundraising goal last month, and is $82,113 away from our October goal . Can you chip in to support independent, progressive media?
- HUD again blocks request, says Ben Carson’s taxpayer-funded travel records aren’t ‘public interest’
- Denver Indivisible greets Mike Pence in a very special way
- Federal court signals it could deal a huge victory against GOP gerrymandering in North Carolina
- Cambridge Analytica was ‘instrumental’ in Trump’s campaign—until yesterday
- FEMA had a plan for responding to a hurricane in Puerto Rico—but it doesn’t want you to see it
- Fox News is scaring off advertisers with their relentless Trump-fluffing, lies, and racism
- Sign if you agree: The U.S. needs to stop supporting Big Polluters in international climate discussions—sign the petition now.
- Movie review: ‘The Brainwashing of My Dad’
- New US ambassador to Canada and coal billionaire says she believes ‘both sides’ of climate change
- Immigration agents take 10-year-old girl with cerebral palsy into custody after emergency surgery
- CNN gives congressman a chance to walk back his anti-Semitic conspiracy, but he digs even deeper
- After fighting for her right to an abortion, immigrant teen finally gets one
- That $300 million no-bid contract for Puerto Rico forbids any government audit or review
Researchers Link Regular Marijuana Use to More Sex
Summary: Contrary to popular conceptions that marijuana may impair sexual desire and performance, a new study reveals frequent marijuana use is associated with increased coital frequency.
Source: Stanford.
The first study to examine the relationship between marijuana use and frequency of sexual intercourse at the population level in the United States shows a positive correlation between the two.
The jury’s still out on rock ’n’ roll. But the link between sex and at least one drug, marijuana, has been confirmed.
A study by investigators at the Stanford University School of Medicine indicates that, despite concerns among physicians and scientists that frequent marijuana use may impair sexual desire or performance, the opposite appears more likely to be the case.
The findings, published online Oct. 27 in the Journal of Sexual Medicine, are based on an analysis of more than 50,000 Americans ages 25-45. And they’re unambiguous.
“Frequent marijuana use doesn’t seem to impair sexual motivation or performance. If anything, it’s associated with increased coital frequency,” said the study’s senior author, Michael Eisenberg, MD, assistant professor of urology. The lead author is Andrew Sun, MD, a resident in urology.
Hint of a causal connection
The study does not establish a causal connection between marijuana use and sexual activity, Eisenberg noted. But the results hint at it, he added. “The overall trend we saw applied to people of both sexes and all races, ages, education levels, income groups and religions, every health status, whether they were married or single and whether or not they had kids.”
The study is the first to examine the relationship between marijuana use and frequency of sexual intercourse at the population level in the United States.
“Marijuana use is very common, but its large-scale use and association with sexual frequency hasn’t been studied much in a scientific way,” Eisenberg said.
According to the National Institute on Drug Abuse, more than 20 million adult Americans are current marijuana users. With the drug’s legalization for medical or recreational use in 29 states, that number is climbing. But despite marijuana’s growing status as a recreational drug, its status as a procreational drug remains ambiguous: On one hand, there are reports of erectile dysfunction in heavy users, and rigorous studies have found reduced sperm counts in men who smoke it; on the other hand, experiments conducted in animal models and humans indicate that marijuana stimulates activity in brain regions involved in sexual arousal and activity.
Looking at survey responses
To arrive at an accurate determination of marijuana’s effect on intercourse frequency, Eisenberg and Sun turned to the National Survey of Family Growth, sponsored by the federal Centers for Disease Control and Prevention. The survey, which provides data pertaining to family structures, sexual practices and childbearing, reflects the overall demographic features of the U.S. population. Originally conducted at regular intervals, the survey is now carried out on an annual basis. It explicitly queries respondents on how many times they’ve had intercourse with a member of the opposite sex in the past four weeks, and how frequently they’ve smoked marijuana over the past 12 months.
The investigators compiled answers to those questions for all years since 2002, when the survey first began collecting data on men as well as women. They included data from respondents ages 25-45 and excluded a small percentage (fewer than 3 percent) of respondents who had failed to answer one or more relevant questions.
In all, Eisenberg and Sun obtained data on 28,176 women averaging 29.9 years of age and 22,943 men whose average age was 29.5. They assessed these individuals’ self-reported patterns of marijuana use over the previous year and their self-reported frequency of heterosexual intercourse over the previous four weeks.
Some 24.5 percent of men and 14.5 percent of women in the analysis reported having used marijuana, and there was a positive association between the frequency of marijuana use and the frequency of sexual intercourse. This relationship applied to both sexes: Women denying marijuana use in the past year, for example, had sex on average 6.0 times during the previous four weeks, whereas that number was 7.1 for daily pot users. Among men, the corresponding figure was 5.6 for nonusers and 6.9 for daily users.
In other words, pot users are having about 20 percent more sex than pot abstainers, Eisenberg noted.
Positive association is universal
Moreover, Eisenberg said, the positive association between marijuana use and coital frequency was independent of demographic, health, marital or parental status.
In addition, the trend remained even after accounting for subjects’ use of other drugs, such as cocaine or alcohol. This, Eisenberg said, suggests that marijuana’s positive correlation with sexual activity doesn’t merely reflect some general tendency of less-inhibited types, who may be more inclined to use drugs, to also be more likely to have sex. In addition, coital frequency rose steadily with increasing marijuana use, a dose-dependent relationship supporting a possible active role for marijuana in fostering sexual activity.
Nevertheless, Eisenberg cautioned, the study shouldn’t be misinterpreted as having proven a causal link. “It doesn’t say if you smoke more marijuana, you’ll have more sex,” he said.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Stanford’s Department of Urology supported the work.
Source: Bruce Goldman – Stanford
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Journal of Sexual Medicine.
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Stanford “Researchers Link Regular Marijuana Use to More Sex.” NeuroscienceNews. NeuroscienceNews, 27 October 2017.
<http://neurosciencenews.com/marijuana-sex-life-7824/>.
<http://neurosciencenews.com/marijuana-sex-life-7824/>.
Soaring rents, falling wages in the bay area
As the tech boom has driven rents sky-high, renting families and seniors in San Jose have actually seen their incomes go down.
That’s one of the key findings from “Soaring Rents, Falling Wages,” our new research brief we released today at City Hall. We revealed that the gap between wages and what it takes to afford an apartment has grown 3 times since 2009. And while tenants are stretched to the breaking point, big landlords and absentee corporations are making millions off our housing crisis.
Email Connie at motherhealth@gmail.com to turn your house into senior care homes.
Donate your real estate to Green Research Institute 501c3, motherhealth@gmail.com 1708 Hallmark Lane San Jose CA 95124
New classes for families on estate planning and immune system, aging hacks & senior care coming soon. Email motherhealth@gmail.com to sign up.
Measure your nutrition with nutrition tester. All doctors and health care pros are welcome to integrate this tester. See Dr Oz Pharmanex scanner at YouTube. We are looking for business owners, working from home and medical/pharma sales reps to do this nutrition test business. Email motherhealth@gmail.com
Male and female caregivers are available live in in the greater bay area. 408-854-1883
Reset your gene expression to a younger you with AGELOC supplements at :
http://www.clubalthea.pxproducts.com
Transplanted Hematopoietic Stem Cells Reverse Damage Caused By Friedreich’s Ataxia
Summary: According to researchers, a single infusion of HSPCs may halt cellular damage caused by Friedreich’s ataxia.
Source: UCSD.
Researchers at University of California San Diego School of Medicine report that a single infusion of wildtype hematopoietic stem and progenitor cells (HSPCs) into a mouse model of Friedreich’s ataxia (FA) measurably halted cellular damage caused by the degenerative disease.
The findings, published online in the October 25 issue of Science Translational Medicine, suggest a potential therapeutic approach for a disease that currently is considered incurable.
Friedreich’s ataxia is an inherited, degenerative neuromuscular disorder that initially impairs motor function, such as gait and coordination, but can lead to scoliosis, heart disease, vision loss and diabetes. Cognitive function is not affected. The disease is progressively debilitating, and ultimately requires full-time use of a wheelchair. One in 50,000 Americans has FA.
FA is caused by reduced expression of a mitochondrial protein called frataxin (FXN) due to a two mutated or abnormal copies of the FXN gene. In their study, Stephanie Cherqui, PhD, associate professor in the UC San Diego School of Medicine Department of Pediatrics, and colleagues used a transgenic mouse model that expresses two mutant human FXN transgenes, and exhibits the resulting progressive neurological degeneration and muscle weakness.
Human hematopoietic stem and progenitor cells (HSPCs), derived from bone marrow, have become a primary vehicle for efforts to replace or regenerate cells destroyed by a variety of diseases. Previous research by Cherqui and colleagues had shown that transplanting wildtype or normal mouse HSPCs resulted in long-term kidney, eye and thyroid preservation in a mouse model of cystinosis, another genetic disorder.
In this study, Cherqui’s team transplanted wildtype HSPCs into an FA mouse model, reporting that the HSPCs engrafted and soon differentiated into macrophages in key regions of the mice’s brain and spinal cord where they appeared to transfer wildtype FXN into deficient neurons and muscle cells.
“Transplantation of wildtype mouse HSPCs essentially rescued FA-impacted cells,” said Cherqui, “Frataxin expression was restored. Mitochondrial function in the brains of the transgenic mice normalized, as did in the heart. There was also decreased skeletal muscle atrophy.”
The scientists note that the mouse model is not perfect mirror of human FA. Disease progression is somewhat different and the precise pathology in mice is not fully known. However, Cherqui said the findings are encouraging and point toward a potential treatment for a disease that currently has none.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Co-authors include: Celine J. Rocca, Spencer M. Goodman, Jennifer N. Dulin, Joseph H. Haquang, Hya Gertsman, Jordan Blondelle, Janell L.M. Smith, and Charles J. Heyser, all at UC San Diego.
Disclosure: Stephanie Cherqui is cofounder, shareholder and a member of both the scientific board and board of directors of GenStem Therapeutics Inc. The terms of this arrangement have been reviewed and approved by the University of California San Diego in accordance with its conflict of interest policies.
Funding: Funding provided by National Institutes of Health the Cystinosis Research Foundation the Sanford Stem Cell Clinical Center and the California Institute of Regenerative Medicine..
Source: Scott LaFee – UCSD
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Stephanie Cherqui, UC San Diego School of Medicine.
Original Research:Abstract for “Transplantation of wild-type mouse hematopoietic stem and progenitor cells ameliorates deficits in a mouse model of Friedreich’s ataxia” by Celine J. Rocca, Spencer M. Goodman, Jennifer N. Dulin, Joseph H. Haquang, Ilya Gertsman, Jordan Blondelle, Janell L. M. Smith, Charles J. Heyser and Stephanie Cherqui in Science Translational Medicine. Published online October 25 2017 doi:10.1126/scitranslmed.aaj2347
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
UCSD “Transplanted Hematopoietic Stem Cells Reverse Damage Caused By Friedreich’s Ataxia.” NeuroscienceNews. NeuroscienceNews, 26 October 2017.
<http://neurosciencenews.com/friedreichs-ataxia-stem-cells-7820/>.
<http://neurosciencenews.com/friedreichs-ataxia-stem-cells-7820/>.
Abstract
Transplantation of wild-type mouse hematopoietic stem and progenitor cells ameliorates deficits in a mouse model of Friedreich’s ataxia
Friedreich’s ataxia (FRDA) is an incurable autosomal recessive neurodegenerative disease caused by reduced expression of the mitochondrial protein frataxin due to an intronic GAA-repeat expansion in the FXN gene. We report the therapeutic efficacy of transplanting wild-type mouse hematopoietic stem and progenitor cells (HSPCs) into the YG8R mouse model of FRDA. In the HSPC-transplanted YG8R mice, development of muscle weakness and locomotor deficits was abrogated as was degeneration of large sensory neurons in the dorsal root ganglia (DRGs) and mitochondrial capacity was improved in brain, skeletal muscle, and heart. Transplanted HSPCs engrafted and then differentiated into microglia in the brain and spinal cord and into macrophages in the DRGs, heart, and muscle of YG8R FRDA mice. We observed the transfer of wild-type frataxin and Cox8 mitochondrial proteins from HSPC-derived microglia/macrophages to FRDA mouse neurons and muscle myocytes in vivo. Our results show the HSPC-mediated phenotypic rescue of FRDA in YG8R mice and suggest that this approach should be investigated further as a strategy for treating FRDA.
“Transplantation of wild-type mouse hematopoietic stem and progenitor cells ameliorates deficits in a mouse model of Friedreich’s ataxia” by Celine J. Rocca, Spencer M. Goodman, Jennifer N. Dulin, Joseph H. Haquang, Ilya Gertsman, Jordan Blondelle, Janell L. M. Smith, Charles J. Heyser and Stephanie Cherqui in Science Translational Medicine. Published online October 25 2017 doi:10.1126/scitranslmed.aaj2347
Comparative analysis of gait in Parkinson’s disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy.
Abstract
Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson’s disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson’s disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson’s disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.
