THURSDAY, March 17 — Cutting-edge gene therapy on Parkinson’s disease patients significantly improved the tremors, rigidity and other motor skill problems that are hallmarks of the illness, a small new study reports.

The phase 2 study enrolled 45 patients with moderate to advanced Parkinson’s disease, with half randomly assigned to receive the gene therapy and half assigned to undergo a “sham” surgery, a mock procedure designed to mimic the experimental approach.

Of the 22 patients who were infused directly into the brain with the glutamic acid decarboxylase (GAD) gene — which prompts the production of a chemical known as GABA that improves motor control — half experienced “clinically meaningful improvements” of their symptoms within six months of surgery, the study authors said.

Although several open-label trials on gene therapy have shown promise in treating neurologic disease, the researchers noted that this is the first of its type to be confirmed in a follow-up randomized double-blind trial, a study in which neither the investigators nor the patients knew which patients were receiving the real or sham treatment.

“It’s a completely novel therapy — unlike anything that’s currently offered,” said co-investigator Dr. Andrew Feigin, an associate investigator at the Center for Neurosciences at Feinstein Institute for Medical Research in Manhasset, N.Y.

“I think we expected to see this effect, but you never know,” Feigin added. “I was gratified.”

The study is published online March 17 in The Lancet Neurology.

Parkinson’s disease affects about one million Americans, most of them over age 50, and is the second most common neurodegenerative disease after Alzheimer’s, according to the National Parkinson Foundation.

In addition to confirming results of earlier clinical trials, the treatment didn’t have any serious adverse effects on the participants, who ranged in age from 30 to 75, according to the study. the most common mild side-effects related to the treatment were headache (affecting seven of the patients in the infusion group versus two in the sham group) and nausea (six versus two).

Phase 3 trials must be conducted before the U.S. Food and Drug Administration decides whether to approve the treatment for general use.

The therapy, which was done with local anesthesia, used a harmless, inactive virus to deliver the GAD gene into each patient’s subthalamic nucleus, a key brain region involving motor function. the gene instructs cells to begin making GABA neurotransmitters to re-establish the normal chemical balance that becomes dysfunctional as the disease progresses.

At the six-month mark, patients in the gene therapy group who had been off their medications for 12 hours showed an average 23.1 percent improvement on a scale used to assess motor function in Parkinson’s patients, while placebo patients had a 12.7 percent improvement.

“For the first time, we’re one step closer to a gene therapy for any neurological disease, because we passed this hurdle,” said study co-author Dr. Michael Kaplitt, vice chairman for research in the department of neurological surgery at Weill Cornell Medical College in New York City.

“I think we’re closer than we’ve ever been to be able to realistically tell patients . . . they can get this done,” said Kaplitt, also a co-founder of Neurologix Inc., the Fort Lee, N.J. company that is developing the GAD therapy and that funded the current study. (Several other researchers also have financial ties to Neurologix and/or a patent related to the GAD product.)

Another surgical procedure, known as deep brain stimulation, which permanently implants a nerve control device in the brain, has helped control Parkinson’s symptoms in thousands of patients over the last decade. Deep brain stimulation is apparently associated with twice the rate of clinical improvement as the gene therapy, according to background information in the study.

Kaplitt and Feigin said it would be difficult to compare the highly effective deep brain stimulation to gene therapy just yet, but that each procedure offers different benefits.

“In practice . . . there are lots of factors,” Feigin said, noting that costs for both may be similar. “Some patients might not want hardware in their brain, or others want tried and true methods. some want state-of-the-art. so a lot will be determined by the patient.”

Dr. Michael S. Okun, national medical director of the National Parkinson Foundation, praised the study, saying it opens the door to “the hope for better symptomatic therapies in Parkinson’s disease, though patients should clearly understand their limitations.”

Okun added, “The gene therapy approach is clever and different. this is an important study, particularly in terms of safety. it will be important to follow these patients longer to look for delayed benefits and potentially delayed risks.”

More information

The U.S. National Institute of Neurological Disorders and Stroke has more on Parkinson’s disease.

Adults With ADHD Symptoms have Tripled Risk of Dementia later, Study Finds

Jan. 20, 2011 — Adults with symptoms of ADHD, or attention deficit hyperactivity disorder, are more than three times as likely as other adults to develop a form of dementia later in life, according to new research from Argentina.

”We found a higher risk of dementia with Lewy bodies in patients with preceding adult ADHD symptoms,” write the researchers from Hospital Italiano Buenos Aires. The study is published in the European Journal of Neurology.

Lewy body dementia (LBD) affects about 1.3 million people in the U.S., according to the Lewy Body Dementia Association. Lewy bodies is the name given to the abnormal protein deposits that disrupt the brain’s normal functioning.

The symptoms include cognitive impairment, like the more well-known dementia, Alzheimer’s disease. however, in the Lewy body form, patients can also have visual hallucinations, fluctuation in cognition — sometimes appearing fine, other times not — and motor abnormalities similar to those in Parkinson’s disease patients.

But a U.S.-based expert cautions that the study found an association between ADHD symptoms and the dementia, not cause and effect. “It may be that both of these disorders are linked to some other risk factor that is common for both,” says James B. Leverenz, MD, chair of the Lewy Body Dementia Association’s scientific advisory council and professor of neurology and psychiatry and behavioral sciences at the University of Washington, Seattle. He reviewed the study for WebMD.

ADHD and Dementia: The Study

Led by Angel Golimstok at the Hospital Italiano Buenos Aires, researchers evaluated 360 patients with dementia — 109 had LBD and 251 had Alzheimer’s — comparing them with 149 healthy people matched by sex, education, and age.

Then they looked at how often ADHD symptoms had been reported earlier. in patients who were too impaired to answer, they got information from an informant who had known the patient for at least 10 years and had information from a close relative who knew the patient in childhood. The researchers say that since this method has not been validated, they refer to the patients as having ADHD symptoms, rather than being diagnosed with ADHD.

•  47.8% of those with LBD had previous ADHD symptoms.
• 15.2% of those with Alzheimer’s disease had previous ADHD symptoms.
• 15.1% of those in the healthy group did.

Why the link? “It is believed that the same neurotransmitter pathway problems are involved in the development of both conditions, so our research set out to test the theory that adult ADHD often precedes [Lewy body dementia],” Golimstok says in a news release.

The researchers believe their study is the first to look at the link between ADHD symptoms and dementia.

In ADHD, often diagnosed in childhood, people have problems paying attention and can act impulsively. Symptoms can persist into adulthood.

“Our hypothesis is that ADHD could be the clinical result of the first step in these pathway disorders, and after a long time, this problem degenerates to a more severe pathology with structural changes in the brain, as Lewy Body Dementia is,” Golimstok writes in an email interview with WebMD.

“A question to answer in the very near future is, Could available ADHD treatment prevent the conversion to a degenerative disease such as Lewy Body Dementia?” Golimstok writes.

For people with recurring yeast infections by Greg Lee

When I was a kid, my mother would pour weed killer on dandelions to try to grow more grass in our yard. somehow, other weeds like crabgrass, plantain, and buttercups would spring up in their place despite repeated use of harsh herbicides. These other weeds were more persistent in taking over the lawn than dandelions.

How are stubborn weeds like a recurring yeast infection?

Just like weeds that keep coming back, yeast can return over and over again in Lyme disease patients Yeast infections, also known as Candidiasis, is an overgrowth of the Candida species of yeast in the body. Candida albicans is the most common species and it can infect the mouth, genitals, or the entire body. Immune compromised patients, like people with Lyme disease, are more susceptible to yeast infections. in addition, antibiotic treatment for Lyme disease kills off beneficial bacteria, which increases the areas for yeast to grow in the body. Medications can help reduce a yeast infection.

Anti-fungal medications reduce yeast infections in the body Symptoms of a yeast infection are: itching, redness, inflammation, cottage cheese-like discharge with a foul odor, white coating on the tongue and throat, asthma, psoriasis, or multiple sclerosis1. Some symptoms may be triggered by eating products containing refined sugars, wheat, or dairy. These symptoms include: fatigue, irritability, mood swings, bloating, or cramping pain. many Lyme disease patients with yeast get relief from anti-fungal medications like Diflucan (fluconazole) or Nystatin. Unfortunately, yeast infections often return.

Supplements can also help reduce a yeast infection Taking probiotics helps to resupply your system with healthy bacteria that prevent yeast from taking over. Garlic and grapefruit seed extract are also effective anti-yeast supplements. However, some patients have reactions to garlic or they dislike having garlic body odor. and some people are on medications which interact with grapefruit. Other herbs like lavender, echinachea, and tea tree can reduce yeast.

Are there other ways to help eliminate a recurring yeast infection?

There are three herbs that help to significantly reduce the recurring symptoms of a yeast infection These anti-yeast herbs not only eliminate Candida, but also many other infectious germs.

Herb #1: Radix Gentianae, Chinese name: Long Dan Cao2 The properties of this herb are bitter, cold, clears heat, and reduces infection. this is used to treat jaundice, eczema, lack of appetite, abdominal fullness, genital itching, foul smelling yellow vaginal discharge, and yellow scanty urine. this herb is also used to treat stomach pain, headache, deafness, bitter taste in the mouth, red eyes, sexually transmitted diseases, seizures and convulsions, and infectious hepatitis. The ability of this herb to clear heat reduces symptoms of high fever, burning stomach pain, dry throat, severe tinnitus, ear pain or discharge, irritability, short temper, insomnia or nightmares, and constipation with yellow urine.

Long Dan Cao is contraindicated in patients with coldness in the stomach, anemia, and severe fatigue. Small doses of this herb before meals stimulate gastric acid production and enhance absorption. People with sensitive stomachs are encouraged to take this herb with food. this herb may be associated with drowsiness and sedation. People who take this herb should exercise caution while driving or operating machinery. this herb has a diuretic effect, so use with diuretic drugs may increase the elimination of water and electrolytes. this herb potentiates the effects of barbiturates.

Long Dan Cao has demonstrated liver protecting properties in mice studies. this herb is also effective in inhibiting Pseudomonas aeruginosa, Bacillus proteus, Salmonella typhi, Diplococcus meningitidis, Staphylococcus aureus (staph), and some dermaphytes. One extract of this herb, Gentiopicrin demonstrated toxicity for malaria parasites.

Herb #2: Herba Lysimachiae or gold money grass, Chinese name: Jin Qian Cao3 The properties of this herb are sweet, salty, cool, clears heat, and eliminates toxins. it is used to clear infections, reduce painful urination, clear kidney and gallbladder stones. it also treats stomach pain, distention, chest fullness, emotional instability, and frequent sighing. it is used to treat jaundice, skin sores, lesions, and snake bites. this herb can be applied topically or taken internally.

Research shows that it increases the production of bile in rats. in another study, it doubled the blood perfusion in the heart and kidneys of dogs. this herb inhibits the growth of Corynebacterium diphtheriae (diphtheria), Staphylococcus aureus (staph), Bacillus subtilis, Candida albicans, and E. coli. this herb has a diuretic effect, so use with diuretic drugs may increase the elimination of water and electrolytes.

Herb #3: Caulis Lonicerae or honeysuckle stem, Chinese name: Ren Dong Teng4 The properties of this herb are sweet, cold, clears heat, eliminates toxins, and dispels infection. it is used to treat itching, swelling, redness, and burning pain. it also helps to relieve spasms and cramps in the intestines and the respitory tract. this herb inhibits the growth of Staphylococcus aureus (staph), Bacillus subtilis, Candida albicans, Salmonella typhi, Bacillus proteus, Bacillus dysenteriae, and H. suis. it is also used to treat a spirochete infection called leptospirosis. There are no known drug interactions at the time of publication.

How do you know that these herbs are working to kill off your yeast infection?

Patients report a significant reduction of yeast symptoms After adding the above herbs to their anti-Lyme herbs, several patients have reported a decrease in vaginal discharge, increased energy, stamina and decreased brain fog in as little as one week. Several of these patients were also taking antibiotic medications. The right combination can help reduce persistent yeast infection symptoms.

The right herb combination can help you to stop a recurring yeast infection just like eliminating pesky weeds from your lawn, the proper combination of herbs helps you to stop a returning yeast infection. since some of these herbs come with cautions on their use, work with a Lyme literate herbalist to develop a safe and effective herbal strategy for your condition.

1. Crook, William G. 1986. The yeast connection: a medical breakthrough. New York: Vintage Books. 2. Chen, John K., and Tina T. Chen. 2004. Chinese Medical Herbology and Pharmacology. City of Industry CA: Art of Medicine Press, Inc., pp. 148 – 150. 3. Chen, John K., and Tina T. Chen. 2004. Chinese Medical Herbology and Pharmacology. City of Industry CA: Art of Medicine Press, Inc., pp. 413 – 414. 4. Chen, John K., and Tina T. Chen. 2004. Chinese Medical Herbology and Pharmacology. City of Industry CA: Art of Medicine Press, Inc., pp. 173 – 174.

Note: this information has not been evaluated by the FDA. it is generic and for general information purposes only, and is not meant to prevent, diagnose, treat or cure any condition, illness, or disease. it is very important that you make no change in your health care plan or  regimen without researching and discussing it in collaboration with your  professional health care team.

Next Step: Internet Radio Interview with Greg Lee this Sunday evening on the “in Short Order” Talk ShowA live interview on alternative treatments for healing Lyme diseasewith Greg Lee co-founder of the two Frogs Healing Center.Hosted by: Sue Vogan and Dr. Warren LevinSunday January 16th, 7:00 pm – 9:00 pm

Click here for more information:blogtalkradio.com/in-short-order

Parkinson’s disease patients have not benefited from any new type of standard treatment in decades. even so, there have been important discoveries about the disease that may lead to whole new treatment strategies.

Researchers at UCSF, working with nerve cells grown in the lab and with mice, now have discovered an important role for the protein that was first found to be associated with Parkinson’s disease more than a decade ago. Researchers had not previously identified a functional role for the protein, called synuclein.

Parkinson’s disease runs in families with extra copies of the synuclein gene, and autopsy studies indicate that levels of the protein in brain tissue are elevated in all forms of Parkinson’s.

The new research reveals that abnormally high levels of synuclein in the brain impair the firing of synapses — the transmission of signals between one nerve cell and the next. this happens long before typical disease symptoms appear. The discovery may lead to new drug development aimed at halting the relentless progression of the disease. Current therapy only treats symptoms.

The lead scientist behind the new discovery is UCSF neurologist Robert Edwards, MD, who studies the molecular basis for signaling at synapses and who also treats patients with Parkinson’s disease.

“Synuclein is the central protein in Parkinson’s,” Edwards says. “The reason why we think it’s important is because synuclein deposits in the brains of everyone who has Parkinson’s disease.” Synuclein is made by nerve cells – called neurons by scientists – and normally is found at synapses.

But synuclein also deposits in the brain of Parkinson’s patients, suggesting that these aggregates may cause the disease.

“we know that the simple increase in synuclein causes degeneration—the question is whether the aggregates are responsible,” Edwards says. “It now appears that the degenerative process involving synuclein may begin long before the protein forms clumps in the brain.”

“this finding shifts the focus in Parkinson’s from cell loss to the much earlier phenomenon of synaptic dysfunction — something that will be much more amenable to treatment,” Edwards says.

UCSF researcher Robert Edwards, MD, has found that release of signaling neurotransmitters at the junction between two nerve cells – called a synapse — is hindered in a mouse model for Parkinson’s disease.

When a nerve cell “fires,” neurotransmitters are released on one side of the synapse from tiny sacs called synaptic vesicles. after release the neurotransmitters bind to receptors on the other side of the synapse. A resultant change in the electrical potential across the cell membrane in the post-synaptic nerve cell determines whether it will fire in turn, propagating the signal through the nerve pathway. In mice with extra copies of genes for the protein called synuclein, fewer vesicles in the pre-synaptic nerve cell release their neurotransmitters when the cell fires. this hinders transmission of the chemical signal across synapses in the nerve pathway.

Here the ends of the pre-synaptic cells are shown in green, and the synaptic vesicles that release neurotransmitters are pink. The tips of post-synaptic cells that respond to the neurotransmitters are shown in blue. Credit: Farrukh Chaudhry,Victoria Berge

The most familiar symptoms of Parkinson’s disease – tremors, rigidity and a general lack of movement – are considered to result from the gradual loss of brain cells that make the neurotransmitter dopamine. currently, the mainstay of treatment is dopamine replacement with L-dopa or other drugs that mimic dopamine.

Treatment can for a time compensate for the loss of naturally produced dopamine and alleviate symptoms. However, these drugs eventually fail to work, due to progression of the disease.

“we have no treatment for the underlying degeneration, because it remains poorly understood,” Edwards says.

Because increases in synuclein have been shown to cause Parkinson’s, synuclein provides a crucial entry point for understanding the degenerative process, according to Edwards, including the loss of neurons.

The loss of function n Parkinson’s disease that is attributed to loss of neurons in the brain may in part be due to impaired signaling, Edwards suggests.

“even people with advanced Parkinson’s still have a substantial number of dopamine-producing neurons that remain. our prediction is that even the neurons that survive don’t work very well, due to functional impairment at synapses.”

Less well-recognized symptoms of Parkinson’s disease do not involve the loss of dopamine-producing neurons, but almost certainly reflect an increase in synuclein within other cells, according to Edwards.

Late in the disease, these symptoms include dementia, low blood pressure and incontinence, which do not respond to dopamine replacement. However, symptoms that can precede the typical motor problems by two decades or more include depression, constipation, and an unusual sleep problem called REM (rapid eye movement) behavior disorder. These symptoms most likely reflect the increased production of synuclein by neurons that do not make dopamine, and impaired neurotransmitter release from these neurons, Edwards says.

Another UCSF Parkinson’s disease researcher, Robert Nussbaum, MD, earlier directed research teams that identified mutations or extra copies of the synuclein gene as the cause of rare, inherited forms of the disease.

In Edwards’ recent studies of synuclein, published this year in a leading neuroscience journal, Neuron, his group used both laboratory-grown neurons and a mouse model for the disease. The neurons and mice have both of their two normal synuclein genes, plus additional copies of the normal human gene. this results in the production of abnormally large amounts of the protein.

Synuclein inhibits the transmission of signals within nerve pathways, Edwards found. but there was not yet any evidence of typical Parkinson’s symptoms in the young mice. “In addition, there was no obvious pathology in their brains – basically they look okay,” Edwards says.

On a molecular level there is still more to learn about how synuclein inhibits neurotransmitter release. Edwards’ lab group also found that the increase in synuclein triggers a reduction in the amount of other proteins normally found at the synapse, especially a class of proteins called synapsins, which also remain poorly understood.

“We’re trying to look at the earliest steps in Parkinson’s disease,” Edwards says. “The earliest event is that synuclein goes up. we think that this leads directly to the inhibition of neurotransmitter release, before aggregation of the protein or cell death. once we understand more about how synuclein inhibits neurotransmitter release, we should be able to develop a simple assay to screen potential drugs.

“my hypothesis is that the activity of this gene is normally going up and down in all of our neurons in response to signals we don’t understand. I think that this fluctuation is a normal process, and what triggers Parkinson’s disease is when synuclein goes up too much, for too long.

“Others are trying to make synuclein levels go down using drugs. I would like to understand when and how the protein goes up under normal circumstances, and then avoid these conditions – that might be a lot easier.”

In another recent UCSF study, Nussbaum found that increased levels of synuclein cause constipation in a mouse model, due to accumulation of the protein in nerves of the gut. Importantly, no other signs of Parkinson’s — such as the loss of dopamine-making cells or the deposition of synuclein – were apparent in these animals, suggesting that they represent an early stage of Parkinson’s.

Constipation may develop a decade or more before other Parkinson’s symptoms, many clinicians have found. Edwards suggests that the effects of excess synuclein on nerve pathways in the gut may play a role.

“we found that synuclein inhibits the release of neurotransmitter, before there is any actual injury to the cell,” Edwards says. “this probably explains the early symptoms in Parkinson’s, such as constipation, which Bob also reported in mice.”

Edwards’ work on synuclein has been funded by the National Institutes of Health, the Michael J. Fox Foundation and the Wayne and Gladys Valley Foundation.

Genes and Environment in Parkinson’s Disease: A Conversation with Robert NussbaumUCSF Science Café, November 6, 2008

Stopping Parkinson’s: A Conversation with Rob EdwardsUCSF Science Café, November 17, 2006

World of Chronic Pain Suddenly looks different to ResearchersUCSF Science Café, November 16, 2009

UCSF Parkinson’s Disease Clinic and Research Center

The Michael J. Fox Foundation for Parkinson’s Research

Last modified: October 15, 2010

“This is so far the largest genetic study of the inflammatory bowel diseases (IBD), which include Crohns disease,” says Dr Mauro D’Amato, associate professor at Karolinska Institutet’s Department of Bioscience and Nutrition and leader of the Swedish part of the study. “Based on the new results, we can now explain 23 per cent of the genetic predisposition to Crohn’s disease.”

The study, which is published in the scientific journal Nature Genetics, is based on a genetic survey of over 22,000 Crohn’s disease patients and 29,000 controls from Europe, North America, New Zealand, and Australia. an estimated 25,000-plus people in Sweden have Crohn’s disease, and over 500 new cases are diagnosed every year. Crohns disease is a chronic inflammation of the bowels; it is intermittent and commonly manifests with symptoms such as diarrhoea and abdominal pain, but also fever, rectal bleeding, weight loss, fatigue, joint pain, and skin disorders can be part of the clinical picture. Crohn’s disease is treated with anti-inflammatory drugs and/or surgery.

Earlier twin studies have shown that Crohn’s disease is caused by the interaction of genetic and environmental factors, and people with affected relatives are at higher risk of developing the disease. in the present study, researchers have identified a total of 71 genes associated with Crohn’s disease. in line with previous results, most of these genes are involved in the control of the interactions between the intestinal bacterial flora and local immune cells in the mucosa, and in the activation of what is known as the adaptive immune response.

“The most exciting findings may come now from the identification of the biological role of those genes for which we know very little or nothing at all,” says Dr D’Amato.

The study is one of several projects being conducted within the frame of the International IBD Genetic Consortium (IIBDGC), and has been coordinated by the corresponding author Dr Miles Park from the University of Cambridge. The researchers hope that future large-scale studies will provide clues as to why inflammatory bowel diseases occur. This will ease diagnosis and enable doctors to design improved therapeutic strategies.