B vitamins reduce schizophrenia symptoms, study finds

 

Date:

February 16, 2017

Source:

University of Manchester

Summary:

A review of worldwide studies has found that add-on treatment with high-dose B vitamins -- including B6, B8 and B12 -- can significantly reduce symptoms of schizophrenia more than standard treatments alone.

 

A review of worldwide studies has found that add-on treatment with high-dose b-vitamins -- including B6, B8 and B12 -- can significantly reduce symptoms of schizophrenia more than standard treatments alone.

advertisement

---

The research -- on the effect of vitamin and mineral supplements on symptoms of schizophrenia -- is funded by The Medical Research Council and University of Manchester, and is published in Psychological Medicine, one of the world's leading psychology journals
Lead author Joseph Firth, based at the University's Division of Psychology and Mental Health, said: "Looking at all of the data from clinical trials of vitamin and mineral supplements for schizophrenia to date, we can see that B vitamins effectively improve outcomes for some patients.
"This could be an important advance, given that new treatments for this condition are so desperately needed."
Schizophrenia affects around 1% of the population and is among the most disabling and costly long term conditions worldwide.
Currently, treatment is based around the administration of antipsychotic drugs.

advertisement

---

Although patients typically experience remission of symptoms such as hallucinations and delusions within the first few months of treatment, long-term outcomes are poor; 80% of patients relapse within five years.
The researchers reviewed all randomized clinical trials reporting effects of vitamin or mineral supplements on psychiatric symptoms in people with schizophrenia.
In what is the first meta-analysis carried out on this topic, they identified 18 clinical trials with a combined total of 832 patients receiving antipsychotic treatment for schizophrenia.
B-vitamin interventions which used higher dosages or combined several vitamins were consistently effective for reducing psychiatric symptoms, whereas those which used lower doses were ineffective.
Also, the available evidence also suggests that B-vitamin supplements may be most beneficial when implemented early on, as b-vitamins were most likely to reduce symptoms when used in studies of patients with shorter illness durations.

advertisement

---

Firth added: "High-dose B-vitamins may be useful for reducing residual symptoms in people with schizophrenia, although there were significant differences among the findings of the studies we looked at."
"There is also some indication that these overall effects may be driven by larger benefits among subgroups of patients who have relevant genetic or dietary nutritional deficiencies."
Co-author Jerome Sarris, Professor of Integrative Mental Health at Western Sydney University, added: "This builds on existing evidence of other food-derived supplements, such as certain amino-acids, been beneficial for people with schizophrenia.
"These new findings also fit with our latest research examining how multi-nutrient treatments can reduce depression and other disorders."
The research team say more studies are now needed to discover how nutrients act on the brain to improve mental health, and to measure effects of nutrient-based treatments on other outcomes such as brain functioning and metabolic health.

---

Story Source:
Materials provided by University of Manchester. Note: Content may be edited for style and length.

---

Journal Reference:

1. J. Firth, B. Stubbs, J. Sarris, S. Rosenbaum, S. Teasdale, M. Berk, A. R. Yung. The effects of vitamin and mineral supplementation on symptoms of schizophrenia: a systematic review and meta-analysis. Psychological Medicine, 2017; 1 DOI: 10.1017/S0033291717000022

 

 

Vitamin B And Folic Acid May Reduce Risk Of Age-related Vision Loss

 

 

Date:

March 3, 2009

Source:

JAMA and Archives Journals

Summary:

Taking a combination of vitamins B6 and B12 and folic acid appears to decrease the risk of age-related macular degeneration in women, according to a new report.

 

 

Taking a combination of vitamins B6 and B12 and folic acid appears to decrease the risk of age-related macular degeneration in women, according to a report in the February 23 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

advertisement

---

Age-related macular degeneration (AMD) is a leading cause of vision loss in older Americans, according to background information in the article. Treatment options exist for those with severe cases of the disease, but the only known prevention method is to avoid smoking. Recent studies have drawn a connection between AMD and blood levels of homocysteine, an amino acid. High levels of homocysteine are associated with dysfunction of the blood vessel lining, whereas treatment with vitamin B6, vitamin B12 and folic acid appears to reduce homocysteine levels and may reverse this blood vessel dysfunction.
William G. Christen, Sc.D., of Brigham and Women's Hospital and Harvard Medical School, Boston, and colleagues conducted a randomized, double-blind clinical trial involving 5,442 women age 40 and older who already had heart disease or at least three risk factors. Of these, 5,205 did not have AMD at the beginning of the study. In April 1998, these women were randomly assigned to take a placebo or a combination of folic acid (2.5 milligrams per day), pyridoxine hydrochloride (vitamin B6, 50 milligrams per day) and cyanocobalamin (vitamin B12, 1 milligram per day). Participants continued the therapy through July 2005 and were tracked for the development of AMD through November 2005.
Over an average of 7.3 years of treatment and follow-up, 137 new cases of AMD were documented, including 70 cases that were visually significant (resulting in a visual acuity of 20/30 or worse). Of these, 55 AMD cases, 26 visually significant, occurred in the 2,607 women in the active treatment group, whereas 82 of the 2,598 women in the placebo group developed AMD, 44 cases of which were visually significant. Women taking the supplements had a 34 percent lower risk of any AMD and a 41 percent lower risk of visually significant AMD. "The beneficial effect of treatment began to emerge at approximately two years of follow-up and persisted throughout the trial," the authors write.
"The trial findings reported herein are the strongest evidence to date in support of a possible beneficial effect of folic acid and B vitamin supplements in AMD prevention," the authors write. Because they apply to the early stages of disease development, they appear to represent the first identified way—other than not smoking—to reduce the risk of AMD in individuals at an average risk. "From a public health perspective, this is particularly important because persons with early AMD are at increased risk of developing advanced AMD, the leading cause of severe, irreversible vision loss in older Americans."
Beyond lowering homocysteine levels, potential mechanisms for the effectiveness of B vitamins and folic acid in preventing AMD include antioxidant effects and improved function of blood vessels in the eye, they note.
This study was supported by grants from the National Heart, Lung and Blood Institute and from the National Eye Institute. Vitamin E and its placebo were provided by the Cognis Corporation. All other agents and their placebos were provided by BASF corporation.

---

Story Source:
Materials provided by JAMA and Archives Journals. Note: Content may be edited for style and length.

---

Journal Reference:

1. William G. Christen; Robert J. Glynn; Emily Y. Chew; Christine M. Albert; JoAnn E. Manson. Folic Acid, Pyridoxine, and Cyanocobalamin Combination Treatment and Age-Related Macular Degeneration in Women: The Women's Antioxidant and Folic Acid Cardiovascular Study. Archives of Internal Medicine, 2009; 169 (4): 335 DOI: 10.1001/archinternmed.2008.574

 

 

 

B-complex vitamins may help slow progression of dementia

 

 

Date:

October 28, 2010

Source:

Methodist Hospital, Houston

Summary:

Large doses of B-complex vitamins could reduce the rate of brain shrinkage by half in elderly people with memory problems and slow the progression of dementia.

 

 

Large doses of B-complex vitamins could reduce the rate of brain shrinkage by half in elderly people with memory problems and slow the progression of dementia.

advertisement

---

A two-year clinical trial in England has shown that B vitamins, including B-6, B-12 and folic acid, slow down mild cognitive impairment (MCI), a condition which is a major risk factor for Alzheimer disease and other forms of dementia.
Dr. Gustavo C. Román, medical director of the Alzheimer & Dementia Center at the Methodist Neurological Institute in Houston, said that patients who already exhibit signs of dementia and test positive for high levels of homocysteine are more likely to respond well to the large doses of B vitamins. Homocysteine is an amino acid in the blood, and high blood levels are linked to an increased risk of developing Alzheimer disease.
Román has seen the impact of these B vitamins in his patients and found that injections of B-complex vitamins are more effective than oral supplements.
"I'm not saying that everyone who takes B vitamins will prevent dementia," Roman said. "But in the right dosage and for the appropriate patients, the vitamin B-12 treatment could be a step toward modifying disease progression."
Approximately 50 percent of people diagnosed with MCI go on to develop Alzheimer disease within five years. More than five million Americans are estimated to have Alzheimer disease, the most common form of dementia. Román said it is time to seek a medical professional if you notice the following signs that could be symptoms for Alzheimer's:

• Forgetting recently learned information
• Problems with planning and/or solving problems, as working with numbers becoming increasingly difficult
• Great difficulty in completing daily tasks
• Losing track of the time or day; confusion about being in a particular location, like not remembering how they got there
• Difficulty reading and/or judging distances, depth perception, etc.
• Language problems that arise when speaking or writing
• Misplacing items and not being able to retrace steps to recover them
• Loss of skills in judgment making
• Social withdrawal
• Noticeable changes in mood and personality, irritability, aggression

---

Story Source:
Materials provided by Methodist Hospital, Houston. Note: Content may be edited for style and length.

 

Vitamin B: Choline intake improves memory and attention-holding capacity, experts say

 

 

Date:

July 11, 2013

Source:

University of Granada

Summary:

An experimental study in rats has shown that consuming choline, a vitamin B group nutrient found in foodstuffs like eggs and chicken or beef liver, soy and wheat germ, helps improve long-term memory and attention-holding capacity. The study has revealed that choline is directly involved in attention and memory processes and helps modulate them.

 

 

An experimental study in rats has shown that consuming choline, a vitamin B group nutrient found in foodstuffs like eggs and chicken or beef liver, soy and wheat germ, helps improve long-term memory and attention-holding capacity. The study, conducted by scientists at the University of Granada (Spain) Simón Bolívar University, (Venezuela) and the University of York (United Kingdom), has revealed that choline is directly involved in attention and memory processes and helps modulate them.

advertisement

---

Researchers studied the effects of dietary supplements of choline in rats in two experiments aimed at analysing the influence of vitamin B intake on memory and attention processes during gestation and in adult specimens.
In the first experiment, scientists administered choline to rats during the third term of gestation in order to determine the effect of prenatal choline on the memory processes of their offspring. Three groups of pregnant rats were fed choline-rich, standard or choline-deficient diets. When their offspring had reached adult age, a sample of 30 was selected: 10 were female offspring of dams fed a choline-supplement, 10 had followed a choline-deficient diet and the other 10, a standard diet, acting as a control group.
Long-term memory
This sample of adult offspring underwent an experiment to measure their memory retention: 24 hours after being shown an object all the offspring (whether in the choline-supplement group or not) remembered it and it was familiar to them However, after 48 hours, the rats of dams fed a prenatal choline-rich diet recognized the object better than those in the standard diet group, while the choline-deficient group could not recognize it. Thus, the scientists concluded that prenatal choline intake improves long-term memory in the resulting offspring once they reach adulthood.
In the second experiment, the researchers measured changes in attention that occurred in adult rats fed a choline supplement for 12 weeks, versus those with no choline intake. They found that the rats which had ingested choline maintained better attention that the others when presented with a familiar stimulus. The control group, fed a standard diet, showed the normal learning delay when this familiar stimulus acquired a new meaning. However, the choline-rich intake rats showed a fall in attention to the familiar stimulus, rapidly learning its new meaning.
The study has been undertaken by University of Granada Department of Experimental Psychology researchers Isabel De Brugada-Sauras and Hayarelis Moreno-Gudiño (also on the research staff of Simón Bolívar University together with Diamela Carias); Milagros Gallo-Torre, researcher in the University of Granada Department of Psychobiology and Director of the "Federico Olóriz" University Research Institute for Neuroscience; and Geoffrey Hall, of the Department of Psychology of the University of York. Their study has recently given rise to publications in Nutritional Neuroscience and Behavioural Brain Research.

---

Story Source:
Materials provided by University of Granada. Note: Content may be edited for style and length.

 

Selenium compounds boost immune system to fight against cancer

 

 

Date:

November 24, 2014

Source:

University of Copenhagen - The Faculty of Health and Medical Sciences

Summary:

Cancer types such as melanoma, prostate cancer and certain types of leukemia weaken the body by over-activating the natural immune system. Researchers have now demonstrated that selenium -- naturally found in, e.g., garlic and broccoli -- slows down the immune over-response. In the long term, this may improve cancer treatment.

 

Cancer types such as melanoma, prostate cancer and certain types of leukemia weaken the body by over-activating the natural immune system. Researchers from the University of Copenhagen have now demonstrated that selenium -- naturally found in, e.g., garlic and broccoli -- slows down the immune over-response. In the long term, this may improve cancer treatment. The findings have been published in the Journal of Biological Chemistry.

advertisement

---

The immune system is designed to remove things not normally found in the body. Cells undergoing change, e.g. precursors of cancer cells, are therefore normally recognised and removed by the immune system. Unfortunately, the different cancer cells contain mechanisms that block the immune system's ability to recognise them, allowing them to freely continue cancer development.
Certain cancer cells overexpress immunostimulatory molecules in liquid form. Such over-stimulation has a negative impact on the immune system:
"You can say that the stimulating molecules over-activate the immune system and cause it to collapse, and we are, of course, interested in blocking this mechanism. We have now shown that certain selenium compounds, which are naturally found in, e.g., garlic and broccoli, effectively block the special immunostimulatory molecule that plays a serious role for aggressive cancers such as melanoma, prostate cancer and certain types of leukemia," says Professor Søren Skov, Department of Veterinary Disease Biology, University of Copenhagen.

Dissolved molecules
In this study, the researchers are focusing on the so-called NGK2D ligands. There are eight variants, of which one in particular has caught the researchers' attention, because it assumes liquid form. It is precisely the molecular dissolution that causes serious problems, once the cancer is raging. The entire bloodstream is, so to speak, infected, and the molecule is therefore used as a marker of serious illness:
"Molecules are found both on the surface of the cancer cells and dissolved in the blood of the affected person. We are now able to show that selenium compounds appear to have a very beneficial effect when it comes to neutralising the special variant of the NGK2D ligand -- both in soluble form and when the molecule is placed on the cell surface," says Professor Søren Skov.
Better drugs in future
The researchers are constantly learning more about the disease mechanisms causing aggressive cancers in the skin, blood and reproductive organs:
"The overexpression seen in cancers such as melanoma, prostate cancer and certain types of leukemia significantly impairs the immune system. If we can find ways to slow down the over-stimulation, we are on the right track. The new results are yet another small step towards better cancer drugs with fewer adverse effects," says Søren Skov.

---

Story Source:
Materials provided by University of Copenhagen - The Faculty of Health and Medical Sciences. Note: Content may be edited for style and length.

---

Journal Reference:

1. M. Hagemann-Jensen, F. Uhlenbrock, S. Kehlet, L. Andresen, C. Gabel-Jensen, L. Ellgaard, B. Gammelgaard, S. Skov. The Selenium Metabolite Methylselenol Regulates the Expression of Ligands That Trigger Immune Activation through the Lymphocyte Receptor NKG2D. Journal of Biological Chemistry, 2014; 289 (45): 31576 DOI: 10.1074/jbc.M114.591537

Why you should be taking Zinc today?

 

 

Zinc supply affects cardiac health

Study shows link between zinc levels and cardiac health

 

    Why you should be taking Zinc today?

---

Oxidative stress occurs when more free radicals are generated in the cell than can be intercepted by antioxidants such as vitamin E. It has already been proven that a severe lack of zinc, which promotes obvious clinical symptoms is also associated with increased cellular stress. However, such an extreme shortage is very rare. Short-term and latent shortages of zinc occur much more frequently. So far, research is sparse on whether this is also linked to oxidative stress.
Due to its high metabolic activity, the researchers have focused on studying the heart muscle. A particularly high number of free radicals occurs here relative to the amount of tissue mass. Furthermore, the heart muscle also has a lower antioxidative capacity than other tissues. Therefore, it is particularly susceptible to oxidative stress.
For the study published in the Journal of Nutrition, this has been investigated by monitoring two antioxidants: glutathione and vitamin E (?-Tocopherol). Both disable free radicals, wherein vitamin E in particular is responsible for the integrity of the cell membrane. The cell membrane shields the cell contents from the environment.
Why you should be taking Zinc today?
Oxidative stress is regulated by the zinc status
Young piglets were deprived of nutritional zinc to different extents for a few days. Thereby, the scientists were able to determine how a declining amount of zinc in the body affected the animals' heart muscles. They noticed that the concentration of glutathione and vitamin E in the heart muscle declined alongside the bodies´ zinc status. Hence, the body's zinc supply already affects the heart's ability to deal with oxidative stress at this early stage. According to current research, oxidative stress is a predisposing factor for heart diseases.
Why you should be taking Zinc today?
Furthermore, it was observed that genes responsible for programmed cell death (apoptosis) are upregulated in this phase of cell stress accompanied by declining zinc supply levels. "The body was no longer able to compensate for the resulting shortage of zinc, even though our tests only ran for a few days," said lead author Daniel Brugger from the Chair of Animal Nutrition at TUM.
As the situation progressed, it was observed that the heart attempted to compensate: "After the first phase, during which a reduction in tissue zinc concentration was observed, the heart muscle intervened and increased the amount of zinc back to the basal (control) level. However, this increase took place at the expense of the zinc content of other organs -- above all the liver, kidneys, and the pancreas."
Why you should be taking Zinc today?
Further yet unpublished liver data also indicates that this decline in tissue zinc is accompanied by events of subclinical inflammation. This seems to also apply to other organs, above all the primary immune tissues. Additional studies will be necessary in order to confirm these findings.

Why you should be taking Zinc today?

---

Story Source:
Materials provided by Technical University of Munich (TUM). Note: Content may be edited for style and length.

---

Journal Reference:

1. Daniel Brugger, Wilhelm M Windisch. Short-Term Subclinical Zinc Deficiency in Weaned Piglets Affects Cardiac Redox Metabolism and Zinc Concentration. The Journal of Nutrition, 2017; 147 (4): 521 DOI: 10.3945/jn.116.240804

 

Selenium effective treatment against breast cancer, study suggests

 

Date:

October 20, 2014

Source:

Texas Tech University

Summary:

Selenium, when attached to a monoclonal antibody presently used to treat breast cancer, has shown greater success in destroying cancer cells in a patient who has developed resistance to the chemotherapy, research demonstrates. Almost a quarter of a million people were diagnosed with breast cancer this year, while another 3 million are living with the disease.

 

 

Almost a quarter of a million people were diagnosed with breast cancer this year, while another 3 million are living with the disease. Although the cure rate for breast cancer is high -- it has an 89 percent 5-year survival rate -- a large number of patients have a recurrence of their cancer. Breast Cancer Awareness Month highlights the continuing research on this type of cancer, the second most common cancer in the United States.

advertisement

---

Julian Spallholz, a professor of nutritional sciences at Texas Tech University, has studied the effects of selenium on several types of cancer. His research on attaching selenium to the leading clinical chemotherapeutic monoclonal antibody for a type of breast cancer shows it can more effectively kill the cancer cells, he reports.
About 20 percent of breast cancer patients have overexpressed growth receptors, known as Her2+ receptors, on the cancer cells, which cause uncontrolled tumor growth. The clinical treatment options on the market today focus on those receptors.
This treatment consists of monoclonal antibodies, which scientists have developed to target cancer cells such as Her2+. This has proven to be effective, but a patient's cancer can often develop resistance to the drug.
Selenium, when attached to a monoclonal antibody presently used to treat breast cancer, has shown greater success in destroying cancer cells in a patient who has developed resistance to the chemotherapy.
"The selenium research conducted by students and colleagues over the years and with the data from this commercial monoclonal antibody leads one to the longer term view that the redox technology produced by selenium and employed here is applicable to many medical applications. Additional applications include other clinical cancer monoclonal antibodies, targeting polypeptides, aptamers and possibly antibiotics. The attached selenium chemistry has the effect of changing the pharmacologic profile of a targeting drug," Spalholz notes.

---

Story Source:
Materials provided by Texas Tech University. Note: Content may be edited for style and length.

Prof. Tim Noakes - 'Medical aspects of the low carbohydrate lifestyle'

When to Take Your Vitamins and Supplements

Rhonda Patrick: Nutrigenomics, Epigenetics, and Stress Tolerance

How Diet & Lifestyle Influence Aging & Brain Function [UCSF Healthy Hear...

Bruce Ames: Vitamin and Mineral Inadequacy Accelerates Aging-associated ...

Molecular 'switch' reverses chronic inflammation and aging

Date:

February 6, 2020

Source:

University of California - Berkeley

Summary:

Scientists have identified a molecular 'switch' that controls the immune machinery responsible for chronic inflammation in the body. The finding could lead to new ways to halt or even reverse many age-related conditions, from from Alzheimer's and Parkinson's to diabetes and cancer.

---

 

Hourglass, aging concept (stock image).

Credit: © photosaint / Adobe Stock

Chronic inflammation, which results when old age, stress or environmental toxins keep the body's immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer's and Parkinson's to diabetes and cancer.

advertisement

---

Now, scientists at the University of California, Berkeley, have identified a molecular "switch" that controls the immune machinery responsible for chronic inflammation in the body. The finding, which appears online Feb. 6 in the journal Cell Metabolism, could lead to new ways to halt or even reverse many of these age-related conditions.
"My lab is very interested in understanding the reversibility of aging," said senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. "In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases."
In the study, Chen and her team show that a bulky collection of immune proteins called the NLRP3 inflammasome -- responsible for sensing potential threats to the body and launching an inflammation response -- can be essentially switched off by removing a small bit of molecular matter in a process called deacetylation.
Overactivation of the NLRP3 inflammasome has been linked to a variety of chronic conditions, including multiple sclerosis, cancer, diabetes and dementia. Chen's results suggest that drugs targeted toward deacetylating, or switching off, this NLRP3 inflammasome might help prevent or treat these conditions and possibly age-related degeneration in general.
"This acetylation can serve as a switch," Chen said. "So, when it is acetylated, this inflammasome is on. When it is deacetylated, the inflammasome is off."
By studying mice and immune cells called macrophages, the team found that a protein called SIRT2 is responsible for deacetylating the NLRP3 inflammasome. Mice that were bred with a genetic mutation that prevented them from producing SIRT2 showed more signs of inflammation at the ripe old age of two than their normal counterparts. These mice also exhibited higher insulin resistance, a condition associated with type 2 diabetes and metabolic syndrome.
The team also studied older mice whose immune systems had been destroyed with radiation and then reconstituted with blood stem cells that produced either the deacetylated or the acetylated version of the NLRP3 inflammasome. Those who were given the deacetylated, or "off," version of the inflammasome had improved insulin resistance after six weeks, indicating that switching off this immune machinery might actually reverse the course of metabolic disease.
"I think this finding has very important implications in treating major human chronic diseases," Chen said. "It's also a timely question to ask, because in the past year, many promising Alzheimer's disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return. So, I think it's more urgent than ever to understand the reversibility of aging-related conditions and use that knowledge to aid a drug development for aging-related diseases."
Co-authors of the study include Ming He, Hou-Hsien Chiang and Hanzhi Luo, previously at UC Berkeley where the research was carried out; Zhifang Zheng, Mingdian Tan, Rika Ohkubo and Wei-Chieh Mu at UC Berkeley; Qi Qiao, Li Wang and Hao Wu at Harvard Medical School; and Shimin Zhao at Fudan University.
This research was supported in part by the National Institutes of Health under grants R01DK117481, R01DK101885, R01AG063404, R01AG 063389, DP1HD087988 and R01Al124491; the National Institute of Food and Agriculture; the France-Berkeley Fund, a Glenn/AFAR Scholarship; the Dr. and Mrs. James C.Y. Soong Fellowship; the Government Scholarship for Study Abroad (GSSA) from Taiwan; the ITO Foundation Scholarship and the Honjo International Scholarship.

---

Story Source:
Materials provided by University of California - Berkeley. Original written by Kara Manke. Note: Content may be edited for style and length.

---

Journal Reference:

1. Ming He, Hou-Hsien Chiang, Hanzhi Luo, Zhifang Zheng, Qi Qiao, Li Wang, Mingdian Tan, Rika Ohkubo, Wei-Chieh Mu, Shimin Zhao, Hao Wu, Danica Chen. An Acetylation Switch of the NLRP3 Inflammasome Regulates Aging-Associated Chronic Inflammation and Insulin Resistance. Cell Metabolism, 2020; DOI: 10.1016/j.cmet.2020.01.009

vitamins and minerals power.

vitamins and minerals power.

Origins of immune system mapped, opening doors for new cancer immunotherapies

Cell atlas of human thymus could help engineer improved therapeutic T cells

 

 

 

 

Date:

February 20, 2020

Source:

Wellcome Trust Sanger Institute

Summary:

A first cell atlas of the human thymus gland could lead to new immune therapies to treat cancer and autoimmune diseases. Researchers mapped thymus tissue through the human lifespan to understand how it develops and makes vital immune cells called T cells. In the future, this information could help researchers to generate an artificial thymus and engineer improved therapeutic T cells.

 

 

A first cell atlas of the human thymus gland could lead to new immune therapies to treat cancer and autoimmune diseases. Researchers from the Wellcome Sanger Institute, Newcastle University and Ghent University, Belgium, mapped thymus tissue through the human lifespan to understand how it develops and makes vital immune cells called T cells. In the future, this information could help researchers to generate an artificial thymus and engineer improved therapeutic T cells.

advertisement

---

Published today (20 February) in Science, this human thymus atlas has revealed new cell types and identified signals that tell immature immune cells how to develop into T cells. The atlas could also help scientists understand diseases that affect T cell development such as severe combined immunodeficiency (SCID), and adds to the Human Cell Atlas initiative which is creating a Google map of the entire human body.
The thymus gland is located in the chest and produces T cells, key white blood cells that fight infection and disease. These T cells then leave the thymus to enter the blood and other parts of the body to mature further. T cells seek out and destroy invading bacteria and viruses, and also recognise cancer cells and kill them.
Problems in thymus development causes defective T cell generation. This can result in severe immune deficiencies such as SCID, leaving people susceptible to infections. Alternatively, it can affect T cell regulation resulting in autoimmune diseases such as Type 1 diabetes. While mature T cells have been well studied, the development of the human thymus and T cells within it is not fully understood.
Researchers used single cell technology to isolate and analyse around 200,000 individual cells from the developing thymus, and child and adult thymus tissue. They looked at which genes were active in each individual cell to identify the cells, discovering new cell types, and used those genes as tags to map each cell to its exact location in the thymus.
Dr Jongeun Park, the first author on the study from the Wellcome Sanger Institute, said: "We have produced a first human thymus cell atlas to understand what is happening in the healthy thymus across our lifespan, from development to adulthood, and how it provides the ideal environment to support the formation of T cells. This openly available resource will allow researchers worldwide to understand how the immune system develops to protect our body."
Therapeutic T cells are currently being used in the clinic to treat B-cell lymphoma and leukaemia cancers, however a major drawback to these treatments is creating the right subtype of T cells.
Professor Muzlifah Haniffa, a senior author of the study from Newcastle University and Senior Clinical Fellow at the Wellcome Sanger Institute, said: "With this thymus cell atlas, we are unravelling the cellular signals of the developing thymus, and revealing which genes need to be switched on to convert early immune precursor cells into specific T cells. This is really exciting as in the future, this atlas could be used as a reference map to engineer T cells outside the body with exactly the right properties to attack and kill a specific cancer -- creating tailored treatments for tumours."
Professor Tom Taghon, a senior author of the study from Ghent University, Belgium, said: "We now have a very detailed understanding of how T cells form in healthy tissue. We have been able to identify a similar population of precursor cells in the developing thymus and liver, and we believe that these precursors are important for initiating T cell development in the fetus, and for the establishment of a fully competent thymus organ. This is helping us put jigsaw pieces together to get a bigger picture of how immunity develops."
The thymus is unusual in that it is largest and most active in childhood and shrinks after puberty. The thymus has been called the 'pacemaker of life' and by age 35 has almost disappeared. Understanding how the thymus develops and then withers could cast light on aging and how the immune system changes through life.
Dr Sarah Teichmann, a senior author from the Wellcome Sanger Institute and co-chair of the Human Cell Atlas Organising Committee, said: "This map of the thymus is an important part of the Human Cell Atlas mission to chart every cell type in the human body. It is helping us learn about developmental pathways within the body, and the age-associated decline of the immune system. This has applications in cellular engineering, including the possibility of creating an artificial thymus for regenerative medicine."

---

Story Source:
Materials provided by Wellcome Trust Sanger Institute. Note: Content may be edited for style and length.

---

Journal Reference:

1. Jong-Eun Park, Rachel A. Botting, Cecilia Domínguez Conde, Dorin-Mirel Popescu, Marieke Lavaert, Daniel J. Kunz, Issac Goh, Emily Stephenson, Roberta Ragazzini, Elizabeth Tuck, Anna Wilbrey-Clark, Kenny Roberts, Veronika R. Kedlian, John R. Ferdinand, Xiaoling He, Simone Webb, Daniel Maunder, Niels Vandamme, Krishnaa T. Mahbubani, Krzysztof Polanski, Lira Mamanova, Liam Bolt, David Crossland, Fabrizio de Rita, Andrew Fuller, Andrew Filby, Gary Reynolds, David Dixon, Kourosh Saeb-Parsy, Steven Lisgo, Deborah Henderson, Roser Vento-Tormo, Omer A. Bayraktar, Roger A. Barker, Kerstin B. Meyer, Yvan Saeys, Paola Bonfanti, Sam Behjati, Menna R. Clatworthy, Tom Taghon, Muzlifah Haniffa, Sarah A. Teichmann. A cell atlas of human thymic development defines T cell repertoire formation. Science, 2020; 367 (6480): eaay3224 DOI: 10.1126/science.aay3224

Molecular 'switch' reverses chronic inflammation and aging

Date:

February 6, 2020

Source:

University of California - Berkeley

Summary:

Scientists have identified a molecular 'switch' that controls the immune machinery responsible for chronic inflammation in the body. The finding could lead to new ways to halt or even reverse many age-related conditions, from from Alzheimer's and Parkinson's to diabetes and cancer.

Share:

FULL STORY

---

Hourglass, aging concept (stock image).

Credit: © photosaint / Adobe Stock

  

Chronic inflammation, which results when old age, stress or environmental toxins keep the body's immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer's and Parkinson's to diabetes and cancer.

advertisement

---

Now, scientists at the University of California, Berkeley, have identified a molecular "switch" that controls the immune machinery responsible for chronic inflammation in the body. The finding, which appears online Feb. 6 in the journal Cell Metabolism, could lead to new ways to halt or even reverse many of these age-related conditions.
"My lab is very interested in understanding the reversibility of aging," said senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. "In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases."
In the study, Chen and her team show that a bulky collection of immune proteins called the NLRP3 inflammasome -- responsible for sensing potential threats to the body and launching an inflammation response -- can be essentially switched off by removing a small bit of molecular matter in a process called deacetylation.
Overactivation of the NLRP3 inflammasome has been linked to a variety of chronic conditions, including multiple sclerosis, cancer, diabetes and dementia. Chen's results suggest that drugs targeted toward deacetylating, or switching off, this NLRP3 inflammasome might help prevent or treat these conditions and possibly age-related degeneration in general.
"This acetylation can serve as a switch," Chen said. "So, when it is acetylated, this inflammasome is on. When it is deacetylated, the inflammasome is off."
By studying mice and immune cells called macrophages, the team found that a protein called SIRT2 is responsible for deacetylating the NLRP3 inflammasome. Mice that were bred with a genetic mutation that prevented them from producing SIRT2 showed more signs of inflammation at the ripe old age of two than their normal counterparts. These mice also exhibited higher insulin resistance, a condition associated with type 2 diabetes and metabolic syndrome.
The team also studied older mice whose immune systems had been destroyed with radiation and then reconstituted with blood stem cells that produced either the deacetylated or the acetylated version of the NLRP3 inflammasome. Those who were given the deacetylated, or "off," version of the inflammasome had improved insulin resistance after six weeks, indicating that switching off this immune machinery might actually reverse the course of metabolic disease.
"I think this finding has very important implications in treating major human chronic diseases," Chen said. "It's also a timely question to ask, because in the past year, many promising Alzheimer's disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return. So, I think it's more urgent than ever to understand the reversibility of aging-related conditions and use that knowledge to aid a drug development for aging-related diseases."
Co-authors of the study include Ming He, Hou-Hsien Chiang and Hanzhi Luo, previously at UC Berkeley where the research was carried out; Zhifang Zheng, Mingdian Tan, Rika Ohkubo and Wei-Chieh Mu at UC Berkeley; Qi Qiao, Li Wang and Hao Wu at Harvard Medical School; and Shimin Zhao at Fudan University.
This research was supported in part by the National Institutes of Health under grants R01DK117481, R01DK101885, R01AG063404, R01AG 063389, DP1HD087988 and R01Al124491; the National Institute of Food and Agriculture; the France-Berkeley Fund, a Glenn/AFAR Scholarship; the Dr. and Mrs. James C.Y. Soong Fellowship; the Government Scholarship for Study Abroad (GSSA) from Taiwan; the ITO Foundation Scholarship and the Honjo International Scholarship.

---

Story Source:
Materials provided by University of California - Berkeley. Original written by Kara Manke. Note: Content may be edited for style and length.

---

Journal Reference:

1. Ming He, Hou-Hsien Chiang, Hanzhi Luo, Zhifang Zheng, Qi Qiao, Li Wang, Mingdian Tan, Rika Ohkubo, Wei-Chieh Mu, Shimin Zhao, Hao Wu, Danica Chen. An Acetylation Switch of the NLRP3 Inflammasome Regulates Aging-Associated Chronic Inflammation and Insulin Resistance. Cell Metabolism, 2020; DOI: 10.1016/j.cmet.2020.01.009

How I Reversed My Parkinson’s Disease Symptoms

How I Reversed My Parkinson’s Disease Symptoms: There is hope that you can reverse your Parkinson's disease symptoms by natural means. Discover what you need to start doing today.

What Is Parkinson’s Disease?

Parkinson’s disease is a neurological condition afflicting about one percent of men and women over the age of seventy years old.
Individuals with Parkinson’s disease have tremor of the hands, rigidity, poor balance, and mild intellectual deterioration. The tremor is most apparent at rest and is less severe with movement. Shaking or tremors are an early symptom of Parkinson’s disease. Progression leads to trembling in arms, legs, jaw, and rigidity or stiffness of the limbs.
Research has shown that Parkinson’s disease occurs when a small region in the brain, called the substantia nigra, begins to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine. Tremors begin to happen and movement slows when you have inhibited dopamine function.
Dopamine is broken down in the brain by an enzyme called monoamine oxidase (MAO). When the activity of MAO is inhibited, dopamine stays around longer, and this is beneficial to those with Parkinson’s disease.

What Helps Parkinson’s Disease?

There is no official cure for Parkinson’s Disease.
As the disease progresses, patients often suffer from cognitive decline. Existing treatments can help ease symptoms, but over time, the drugs themselves can cause debilitating side effects.
Carbidopa is most commonly used for Parkinson’s disease. However, there can be a number of negative side effects and problems associated with the administration of carbidopa during treatment of Parkinson’s disease. This is thought to be because the administration of carbidopa will deplete the body of vitamin B-6, l-tyrosine, l-tryptophan, 5-hydroxytryptophan (5-HTP), serotonin, and sulfur amino acids.
The properly balanced administration of Mucuna pruriens (a natural form of l-dopa), and not carbidopa, in conjunction with 5-HTP, l-tyrosine, l-cysteine, and other supportive nutritional supplements can improve symptoms.
A research study, led by Dr. Marty Hinz and printed in the International Journal of Internal Medicine, was done with 254 Parkinson’s patients who were newly diagnosed with no previous treatment and those who were diagnosed more than 20 years before and had tried many other medical treatment options. It showed that these supplements were helpful in the treatment of Parkinson’s Disease.
In additional studies, Dr. Hinz has pioneered new research showing that replacing carbidopa with mucuna pruriens can arrest symptoms of Parkinson’s at any stage, and in many cases, reverse it. Without carbidopa, he recommends a specific protocol of natural supplements similar to the protocol that I used to reverse my Parkinson’s. However, my personal protocol should not be attempted if one is taking carbidopa.
The Buck Institute for Research on Aging has been investigating Parkinson’s Disease for years. Their research has shown that low doses of lithium administered to laboratory mice reduced involuntary motor movements, a troubling side effect of the medication most commonly used to treat Parkinson’s disease.
A clinical study of 885 Parkinson’s patients validated that in 78% of the cases, patients taking 10mg per day of NADH reported positive improvements in their condition. Some doctors recommend 40mg/day to experience more benefits. This can be expensive, but if your budget allows, it would be a great addition.

What to Do

Dr. Hinz has passed on his amino acid IV treatment to doctors and is available around the country. Research “neurotransmitter restoration therapy” for more information.
From my personal experience and in helping hundreds of people at my wellness retreats in Northern California, my natural solutions and protocols have helped all brain disorders.
These suggestions for optimal brain function should not be followed if you are currently taking prescribed drugs for Parkinson’s. Taking tyrosine and 5-HTP with certain medications, particularly for Parkinson’s, can produce negative side effects and be dangerous.
If you are currently taking prescribed drugs or carbidopa, collaborate with a Dr. Hinz trained doctor before going off your dependence on Parkinson’s drugs. You can find a doctor that Dr. Hinz has trained in his system by calling NeuroResearch Clinics at 877-626-2220. This number cannot help you directly but they can recommend and refer you to a doctor who can.