Author Topic: Brain Function  (Read 7783 times)

Offline JC Spencer

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Brain Function - the trehalose, glutathione, Candida connection
« Reply #10 on: May 12, 2008, 12:27:48 AM »
Comments by J. C. Spencer
With very little comment, let me simply reference this paper, present the abstract, and call it the trehalose - glutathione - Candida - brain function - connection.  Glutathione - or L-glutathione plays powerful roles in human cells, is a strong antioxidant, effects nutrient metabolism, and regulation of cellular events including gene expression, DNA and protein synthesis, cell growth, and immune response.  It is reported that Parkinson’s patients have a lower level of glutathione in the brain.  I do not believe supplementation of glutathione is a good idea because (1) the supplement may not penetrate the cell membrane and (2) some doctors believe supplementation may inhibit the cellular production of glutathione.  Acetylcysteine is the precursor to glutathione.  A medical doctor instructed me that supplementation with N-acetylcysteine (NAC) is an excellent means of boosting glutathione in the body.  I am told that NAC is rapidly absorbed after oral administration and reaches a maximum plasma level in 2-3 hours, with a half-life of about 6 hours. NAC readily enters the cell and is hydrolyzed to cysteine.

Here is the abstract on the trehalose - glutathione - Candida - brain function - connection.

Disruption of the Candida albicans ATC1 gene encoding a cell-linked acid trehalase decreases hypha formation and infectivity without affecting resistance to oxidative stress

Yolanda Pedreño1,2, Pilar González-Párraga1, María Martínez-Esparza3, Rafael Sentandreu2, Eulogio Valentín2 and Juan-Carlos Argüelles1

1 Área de Microbiología, Facultad de Biología, Universidad de Murcia, E-30071 Murcia, Spain
2 Departamento de Microbiología y Ecología, Universidad de Valencia, E-46100 Burjassot, Valencia, Spain
3 Departamento de Bioquímica y Biología Molecular B e Inmunología, Universidad de Murcia, E-30071 Murcia, Spain

Correspondence Juan-Carlos Argüelles  arguelle@um.es

Abstract
In Candida albicans, the ATC1 gene, encoding a cell wall-associated acid trehalase, has been considered as a potentially interesting target in the search for new antifungal compounds. A phenotypic characterization of the double disruptant  mutant showed that it was unable to grow on exogenous trehalose as sole carbon source. Unlike actively growing cells from the parental strain (CAI4), the null mutant displayed higher resistance to environmental insults, such as heat shock (42 °C) or saline exposure (0.5 M NaCl), and to both mild and severe oxidative stress (5 and 50 mM H2O2), which are relevant during in vivo infections. Parallel measurements of intracellular trehalose and trehalose-metabolizing enzymes revealed that significant amounts of the disaccharide were stored in response to thermal and oxidative challenge in the two cell types. The antioxidant activities of catalase and glutathione reductase were triggered by moderate oxidative exposure (5 mM H2O2), whereas superoxide dismutase was inhibited dramatically by H2O2, where a more marked decrease was observed in  cells. In turn, the mutant exhibited a decreased capacity of hypha and pseudohypha formation tested in different media. Finally, the homozygous null mutant in a mouse model of systemic candidiasis displayed strongly reduced pathogenicity compared with parental or heterozygous strains. These results suggest not only a novel role for the ATC1 gene in dimorphism and infectivity, but also that an interconnection between stress resistance, dimorphic conversion and virulence in C. albicans may be reconsidered. They also support the hypothesis that Atc1p is not involved in the physiological hydrolysis of endogenous trehalose.

Offline JC Spencer

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Brain Function during pregnancy
« Reply #9 on: May 07, 2008, 10:50:28 AM »
Congratulations!  This is the time of LIFE when your baby will get what he or she needs from your body.  If you do not have enough calcium (for an example) in your diet, the baby will still get his from your bones.  Your body was designed to look out for the child.  It is so very important that you feed yourself the super foods of good nutrients including the royal sugars before, during and after these nine months.  Make sure the water you drink if good and clean and the air you breath is smokeless.  I am happy for you.
« Last Edit: June 07, 2008, 06:39:33 PM by JC Spencer »

kendersa

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Brain Function during pregnancy
« Reply #8 on: May 07, 2008, 09:52:30 AM »
I'm pregnant as we speak  (yeah  ;D) and plan on using glyco-nutrients and trehalose my whole pregnancy.  I have been on them since before my pregnancy.  I also plan on continuing to take them as I breast feed in hopes of a very healthy and intelligent baby.   
« Last Edit: May 07, 2008, 10:42:55 AM by JC Spencer »

Offline JC Spencer

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Comments by J. C. Spencer:
Scientists again prove that mother’s breast milk helps children for the next number of years, perhaps for life.  Results of a study of 14,000 children causes doctors to scratch their heads.  Glycomics, the study of sugars, holds the answer to why children who consume the sugars found in mother’s breast milk perform better.  Here at The Endowment for Medical Research, we have learned, and have much supporting evidence, that indeed children make better grades for many years when they have these sugars.  Adults who consume these sugars even in adult life perform better mentally.  We have had two Alzheimer’s papers published from our Alzheimer’s Nutritional Pilot Surveys that showed very positive results.  More research is needed and we are committed to helping improve brain function in children and adults without drugs or harmful side effects by using certain sugars found in nature.

By Will Dunham
May 5, 2008
WASHINGTON (Reuters) - A new study provides some of the best evidence to date that breast-feeding can make children smarter, an international team of researchers said on Monday.
Children whose mothers breast-fed them longer and did not mix in baby formula scored higher on intelligence tests, the researchers in Canada and Belarus reported.

About half the 14,000 babies were randomly assigned to a group in which prolonged and exclusive breast-feeding by the mother was encouraged at Belarussian hospitals and clinics. The mothers of the other babies received no special encouragement.

Those in the breast-feeding encouragement group were, on average, breast-fed longer than the others and were less likely to have been given formula in a bottle.

At 3 months, 73 percent of the babies in the breast-feeding encouragement group were breast-fed, compared to 60 percent of the other group. At 6 months, it was 50 percent versus 36 percent.

In addition, the group given encouragement was far more likely to give their children only breast milk. The rate was seven times higher, for example, at 3 months.

The children were monitored for about 6 1/2 years.

The children in the group where breast-feeding was encouraged scored about 5 percent higher in IQ tests and did better academically, the researchers found.

Previous studies had indicated brain development and intelligence benefits for breast-fed children.

But researchers have sought to determine whether it was the breast-feeding that did it, or that mothers who prefer to breast-feed their babies may differ from those who do not.
The design of the study -- randomly assigning babies to two groups regardless of the mothers' characteristics -- was intended to eliminate the confusion.
'MOTHERS WHO BREAST-FEED ... ARE DIFFERENT'

"Mothers who breast-feed or those who breast-feed longer or most exclusively are different from the mothers who don't," Dr. Michael Kramer of McGill University in Montreal and the Montreal Children's Hospital said in a telephone interview.

"They tend to be smarter. They tend to be more invested in their babies. They tend to interact with them more closely. They may be the kind of mothers who read to their kids more, who spend more time with their kids, who play with them more," added Kramer, who led the study published in the journal Archives of General Psychiatry.

The researchers measured the differences between the two groups using IQ tests administered by the children's pediatricians and by ratings by their teachers of their school performance in reading, writing, math and other subjects.

Both sets of scores were significantly higher in the children from the breast-feeding promotion group.

The study was launched in the mid-1990s. Kramer said the initial idea was to do it in the United States and Canada, but many hospitals in those countries by that time had begun strongly encouraging breast-feeding as a matter of routine.

The situation was different in Belarus at the time, he said, with less routine encouragement for the practice.

Kramer said how breast-feeding may make children more intelligent is unclear.
"It could even be that because breast-feeding takes longer, the mother is interacting more with the baby, talking with the baby, soothing the baby," he said. "It could be an emotional thing. It could be a physical thing. Or it could be a hormone or something else in the milk that's absorbed by the baby."

Previous studies have shown babies whose mothers breast-fed them enjoy many health advantages over formula-fed babies.

These include fewer ear, stomach or intestinal infections, digestive problems, skin diseases and allergies, and less risk of developing high blood pressure, diabetes and obesity.
The American Academy of Pediatrics recommends that women who do not have health problems exclusively breast-feed their infants for at least the first six months, with it continuing at least through the first year as other foods are introduced.

(Editing by Maggie Fox and Stacey Joyce)
« Last Edit: May 06, 2008, 09:35:12 PM by JC Spencer »

Offline JC Spencer

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In Chapter 10 "Propensity training can lessen addiction" of my book Expand Your Mind - Improve Your Brain, I allude to fixation.  This loop thinking, fixation, or addiction on a specific subject may be caused by giving into a thought and compounded by a lack of endorphin production in the brain.  Addition of any kind seems to hinder the endorphins.  The bottom line is to have a good chemistry balance of the body and to feed the mind better thoughts on which to focus.  In other words, in the process of improvement, replace bad fixations with more pleasant beneficial thoughts.

Here is a part of Chapter 10 which I hope you find interesting and helpful:

A few years ago, I was teaching a class, and one of my students repeatedly positioned himself in a seat that enabled him to look out the window.  Later, I learned that the reason he chose that seat was so he could view and lust after a liquor ad on a giant billboard across the freeway.

When his eyes contacted the colored picture of liquor in the attractive bottle, the neurons firing in his head lured him into a fantasy for alcohol.  Liquor took him down because that was his propensity and he accepted it.

An addiction is initiated when you first entertain the allurement.  Firing the neurons for the first time felt so good that you allowed them to fire again, and soon they were firing on their own.

There is no choice, no self-control, over the first firing of the neurons; however, you have a choice about future layers of thought put down over the initial thought.

There are two basic ways the neurons continue to fire in their effort to shape a habit that becomes a trait, a lifestyle and then your character.  They are (1) to entertain the feeling repeatedly; or (2) just acquiesce.  Not fighting the destructive impulse allows the neurons to fire at will.  Acquiescence is approval in law and in life.

It is not the freezer that is transmitting a signal to come and eat too much ice cream.  As you pass by the familiar zone, you trigger the latent desire that is imbedded in the neuron(s).  The number of neurons fighting for your desire depends on how many you have trained.

How many times have you experienced a spontaneous desire?  Someone says a word or you see an image which causes you to want something that only a moment ago was not in your thoughts.

You have learned that the power of suggestion fires neurons that, when entertained, fire again and again to form habits, addictions, lifestyles and character.  If those habits are evil desires or addictions, they will continue to grow out of control and can never be satisfied with more of the same.

As additional neurons join the team to grow the addiction, other warriors are called into play.  New signals summon changes in body chemistry; and when drugs or other toxins are added to the equation, they compound the problem.  An example of chemistry change for compounding an addiction is the inhibiting of endorphin production in the brain.

I had the privilege many years ago, to get acquainted and become friends with, the late Dr. Meg Patterson, and her husband, George.  Dr. Patterson, a Scottish surgeon, was a Fellow of the Royal College of Surgeons in Edinburgh, Scotland.  She developed a new technology for stimulating endorphin production after the endorphins had been blocked by heroin, alcohol, cocaine, barbiturates, nicotine, tranquilizers  and other addictive substances.

Dr. Patterson devoted herself to helping many people.  She received wide endorsements from those she helped and friends of those she helped, including Keith Richards, Boy George, Eric Clapton, Pete Townshend, and many others.  Sean Connery stated that her book "Getting Off the Hook" should be standard reading in any modern educational system.

I personally witnessed, first hand, how different  heroin and cocaine addicts had the desire for the drugs completely removed from their systems in ten days, with no withdrawal. This was accomplished by a re-stimulation of endorphin production through an electrical black box programmed for the addict's specific type of addiction.  Electrodes were simply placed behind the ears at the base of the brain.  The addict kept the electrodes on day and night for ten days.

Dr. Patterson proved that it is possible for the brain to change its propensity.  When the addiction is strong, help is required to change for the better.

« Last Edit: May 06, 2008, 03:52:22 PM by JC Spencer »

Offline JC Spencer

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New Findings about Huntington's / Why Help may be near
« Reply #5 on: April 30, 2008, 08:18:58 PM »
Commentary by J. C. Spencer

Researchers in neurodegenerative diseases at Howard Hughes Medical Institute have linked toxic RNA with Huntington's disease.  This significant discovery reveals the importance for improving the function of the mitochondria where the RNA is manufactured as well as correcting the altered gene expression that causes Huntington's.  After reading this report, connect the dots to the published Huntington's paper entitled, Trehalose alleviates polyglutamine-mediated pathology in mouse model of Huntington disease.  Please understand, these two papers are dealing with mice and fruitflies.  Further research is needed in the human population with Huntington's.  This new information may give us an indication as to why we are having positive results in those participating in our self funding, self evaluation Trehalose Nutritional Pilot Survey.  All that is required to participate in this Huntington study is for the individual or family to complete a self evaluation form each month while using trehalose over time.  The longer a Huntington's patient is in the study the more data can be gathered.  The Forms can be downloaded from the Home Page at www.endowmentmed.org

APRIL 30, 2008
Toxic RNA Contributes to Neurodegeneration
In studies with fruitflies, researchers have discovered that a mutant RNA may be partially to blame for the neurodegeneration associated with spinocerebellar ataxia type 3 (SCA3). The toxic RNA may exacerbate the disease, which causes loss of muscle coordination and paralysis of the eye muscles and is known to be caused by the buildup of an aberrant protein inside neurons.

The scientists said their findings suggest that treatments that target the abnormal RNA might offer double benefits by alleviating both the protein as well as RNA toxicity.
 
"One possibility our findings suggest is that treatments that seek to alleviate Huntington's and other polyglutamine diseases by knocking down the RNA could offer two-pronged benefits."
Nancy M. Bonini

Howard Hughes Medical Institute investigator Nancy M. Bonini and her colleagues published their findings April 30, 2008, in an advance online publication in the journal Nature. Co-authors include Lin-Bo Li, Zhenming Yu and Xiuyin Teng, who were all members of Bonini's laboratory at the University of Pennsylvania.

Over the last decade, Bonini and her colleagues have painstakingly recreated models of human neurodegenerative disease in the fruit fly. Their work involves introducing the gene for the human neurodegenerative disease into the fly, recreating the effects of the disease so that it can be studied in a highly manipulable system.

In the studies reported in Nature, the researchers used a strain of the fruitfly Drosophila that had a mutation in the gene that is altered in human patients with SCA3. This fruitfly strain exhibits neural degeneration and is a useful laboratory model for human SCA3.

SCA3 is one of a class of diseases known as polyglutamine repeat diseases. SCA3 and the other polyglutamine diseases, like Huntington's disease and SCA1, are caused by genetic mutations consisting of an abnormally long number of repeats of three nucleotides, also known as triplet repeats. The length of the "genetic stutter" of nucleotides can vary in each disease. For this set of diseases, the repeated nucleotide triplet is CAG, which encodes an amino acid called glutamine. The mutant version associated with human disease thus leads to a protein with an abnormally long glutamine string. The malformed protein is toxic to cells and causes neurological degeneration.

In SCA3 and similar diseases, the length of this glutamine string can grow as it is passed down from one generation to the next. This feature of the disease, called repeat instability, has important clinical implications because expansion of repeats causes the disease to arise earlier and with greater severity in successive generations of people who carry the mutation, Bonini explained.

When the genetic causes of polyglutamine diseases were first identified, researchers found that the aberrant proteins were toxic, but they did not look closely at whether the RNA could be toxic as well, Bonini said. To convert a gene into protein, cells begin by copying DNA into RNA. The RNA molecule serves as the template the cell uses to build a protein.

Bonini and her colleagues did not set out to use their fruitfly model of SCA3 to search for signs of RNA toxicity. Rather, they let the fly tell them in an unbiased way about genes that could improve or worsen symptoms of the disease. During these studies, the researchers discovered that activating the muscleblind (mbl) gene in the flies dramatically increased neural degeneration.

Further analyses suggested that the mbl gene exacerbated the disease by interacting with RNA. And when the researchers inserted the human version of the mbl gene into the fly, they saw that the neurodegeneration also worsened, providing a hint that mbl might also play a role in human polyglutamine diseases.

Intrigued by the possibility that the RNA itself was toxic, Bonini and her colleagues next molecularly interrupted the repetitive RNA sequence. Normally, the RNA has a long series of CAG repeats; the researchers interrupted the sequence so that it now had CAA and CAG repeats This RNA sequence encodes the same mutant protein, but the RNA was not predicted to fold in the same toxic manner. When they introduced this interrupted RNA back into their fruitflies, significantly less neurodegeneration occurred, further indicating that the RNA itself might be toxic.

Then the researchers genetically engineered mutant flies that produced only the repetitive RNA but no aberrant protein. Those flies showed significant neural degeneration. "That finding suggested that the RNA on its own contributes to the pathology," said Bonini.

She said the new results reveal that polyglutamine diseases like SCA3 and Huntington's disease may share the property of RNA toxicity with a different class of triplet repeat diseases, which includes myotonic dystrophy type 1 and fragile X-associated ataxia. Those diseases also arise from genetic mutations that produce a stuttering RNA. That RNA does not, however, produce an abnormal, toxic protein; the pathology of those diseases is thought to arise only from the toxicity of the RNA.

Although the new studies suggest that the two classes of triplet repeat diseases are caused in part by RNA toxicity, Bonini said their analyses indicate that the mechanism of RNA toxicity appears to be different for each class of disease. In future studies, the researchers will concentrate on determining the mechanisms of RNA toxicity in the polyglutamine disease fly model, she said.

Bonini said the new findings could offer the promise of more effective treatments for polyglutamine diseases. "One possibility our findings suggest is that treatments that seek to alleviate Huntington's and other polyglutamine diseases by knocking down the RNA could offer two-pronged benefits," she said. "They would not only reduce the level of the toxic protein, but also knock down the toxic RNA. Thus, such treatments might be more effective than those directed only at the protein," she said.

Ling-Bo Li is now a postdoc in a Hughes Lab at Utah (with Brenda Bass).


http://www.hhmi.org/news/bonini20080430.html


« Last Edit: May 06, 2008, 08:28:37 PM by JC Spencer »

Offline JC Spencer

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Can the Huntington Gene be turned off?
« Reply #4 on: April 12, 2008, 09:06:43 AM »
This week a blog out of Seattle caught my interest.  You can read the whole article in our NEWS section under Huntington's.

A Seattle Firm takes a stab at turning off Huntington Gene  - Trehalose may be doing the same thing  - More research is needed  -  Using drugs to turn off genes can get sticky.  - JCS

Here is the article:

In Huntington's disease, which afflicts about one in 10,000 Americans, one gene is defective --making it difficult for patients to walk, talk or swallow.

So, if there was a way to "silence" that one gene there could potentially be a cure.
That's the promise of RNA interference technology, and it has three Seattle-area companies trying to find a way to make it deliver.

"There has been no other technology that has been capable of shutting off aberrant genes," said H. Stewart Parker, the chief executive of Seattle-based Targeted Genetics.

On Monday, her company said it would accelerate its work on RNA interference -- or RNAi -- by acquiring partner Sirna Therapeutics' rights to a pre-clinical RNAi program targeting the Huntington's disease gene. No cash exchanged hands, although Targeted Genetics will pay Sirna Therapeutics royalties on sales if it commercializes a product targeting Huntington's disease.

The two companies had been working together on the program since 2005.

Like other Seattle-area companies working on RNAi, Targeted Genetics is confronting one of the barriers challenging RNAi's promise: how to efficiently and safely deliver RNAi molecules to cells.

Targeted Genetics is trying to deliver RNA molecules by linking them to the adeno-associated virus, a naturally occurring virus that the company is also using to develop treatments for inflammatory arthritis and HIV/AIDS.

Targeted Genetics' Parker said that method was advantageous because it essentially created "a little factory" ensuring that the RNAi molecules do not have to be repeatedly redosed and have a longer effect.

"We think for diseases in the brain (such as Huntington's disease), it's the best alternative," she said. "When you're going to introduce drugs to the brain you don't want to do that very often."

Parker said that Targeted Genetics is conducting long-term studies of the treatment in animals and that it could enter clinical trials in late 2009.

PhaseRX, a Seattle-based startup that in February landed commitments for up to $19 million in venture capital funding, is developing synthetic polymers to move RNAi molecules across cell membranes.

"These polymers actually mimic some of the viral (proteins) and the way they get into cells," said founder Robert Overell in an interview when PhaseRX announced its funding. He declined to elaborate Monday.

A third company, Nastech Pharmaceutical of Bothell, is developing lipid formulations of RNAi molecules. The company says that properly designed lipid formulations can interact with cell membranes and gain access to a cell's interior. The company is also developing peptides to "drag RNAi molecules across," said President Gordon Brandt.

"We believe our delivery approach is the best one out there," Brandt said. In addition, the company has developed a new set of RNAi molecules that the company says do not overlap with the intellectual property of the field's two major players -- Sirna Therapeutics and Alnylam Pharmaceuticals.

Nastech has identified four therapeutic targets for its RNAi technology -- two against rheumatoid arthritis and influenza and two, in an earlier stage, targeting cardiovascular disease and cancer.

No clinical trials have started.

"It's a new scientific area," Brandt staid. "There won't be any shortcuts. This is going to be a long process."

The company hopes RNAi will boost its faltering stock price and business -- which suffered in the wake of the loss of a partnership last fall with Procter & Gamble to develop a nasal spray to treat osteoporosis.

During a March 3 conference call, Nastech CEO Steven Quay said that the company hoped to partner its RNAi technology with a large pharmaceutical company.

"One of the remarkable things in this area was that Sirna Therapeutics, which was acquired at an early stage by Merck for $1.1 billion, and Alnylam with a market capital of $1.2 billion, each inked $700 million-plus deals with big pharma partners for their preclinical programs," Quay said, according to a transcript.

It was Merck's acquisition of Sirna in 2006 that eventually led to Monday's announcement that Targeted Genetics would buy Sirna's portion of the Huntington's disease partnership, Parker said.

"For simplicity purposes, from their standpoint, it was beyond the focus of what they wanted to do," she said.

http://blog.seattlepi.nwsource.com/thelifesciencesblog/archives/136036.asp
« Last Edit: April 13, 2008, 10:35:49 AM by JC Spencer »

Offline JC Spencer

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« Last Edit: April 11, 2008, 08:14:45 PM by JC Spencer »

Offline JC Spencer

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Brain Function
« Reply #2 on: March 13, 2008, 10:49:29 AM »
I am told that over 600 diseases are directly controlled by the brain and EVERY disease is influenced by proper function or malfunction of the brain.  The ability to safely improve brain function is the ROSETTA STONE of medical science.
« Last Edit: May 05, 2008, 03:40:58 PM by JC Spencer »

Offline JC Spencer

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Brain Function
« Reply #1 on: March 12, 2008, 11:54:51 PM »
I am opening up a new category in our Sugar Science Forum: Brain Function.
A lot of research for the last few years have brought us to a new era of understanding more about brain function than any time in history.  It is exciting to see what we are learning and what is ahead.  I welcome discussion from the general public and the most learned professors and scientists.  I am looking forward to your comments and questions.

Click on the Brain Function Topic area and let us open our minds together.  Give us your thoughts!
« Last Edit: April 28, 2008, 11:53:29 PM by JC Spencer »