Parkinson's Disease Tulip


advertisement
Reply
 
Thread Tools Display Modes
Old 11-10-2007, 09:49 AM #1
reverett123's Avatar
reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default What really works? A report

OK - OK - I'll put the chips away and take a walk..

Web address:
http://www.sciencedaily.com/releases/2007/11/
071107205759.htm
Antidepressants, Exercise, Age, Even Food Intake, Affect Generation Of New Brain Cells

ScienceDaily (Nov. 9, 2007) — Recent research shows that the production of new brain cells may be crucial for antidepressants to be effective and that the medication's effectiveness is strongly influenced by age. What's more, meal frequency, type of food, and physical exercise affect the brain's ability to manufacture these new cells.

For the first time in nonhuman primate models, scientists have documented the cause-and-effect relationship between antidepressant drugs and neurogenesis. The researchers found that the antidepressant drug fluoxetine improved the behavior of macaque monkeys with depression-like symptoms.

They also discovered that administering the drugs to normally behaving monkeys did not influence their behavior but did alter their brains by boosting neurogenesis in the hippocampus, an area involved in memory and learning.

In one study with macaque monkeys, the stimulation of neurogenesis appeared to be necessary for the treatment of depression, says Tarique Perera, MD, of Columbia University.

"Given the parallels between the monkey behavior model and human clinical depression, and the structural similarities between the macaque and human brains, we expect neurogenesis to play an equally important role in antidepressant mechanisms in humans," he says.

The Columbia University scientists induced the monkeys' depression-like behavior by repeatedly separating the animals from their social groups. In addition, there was a control group of six monkeys that stayed in their social groups. Perera administered the antidepressant fluoxetine to three of the animals in the separated group and three animals in the control group. The remaining separated and control animals were given a placebo.

The placebo-treated separated monkeys progressively lost interest in pleasurable activities, and their social standing dropped. "These behaviors parallel elements of depression in humans," Perera says. In contrast, the control animals' behavior did not change. The scientists identified the reason when they subsequently examined the animals' brain tissue.

In the hippocampus of the fluoxetine-treated monkeys in both the control and separated animals, they found many new cells. However, despite the fact that the rate of neurogenesis in their brains was higher than average, the behavior of the treated control group stayed the same. In fact, it did not differ from the behavior of the placebo-treated animals that remained in social groups.

The scientists next determined the impact of fluoxetine on brain and behavior in the absence of neurogenesis. Four animals underwent two weeks of X-ray radiation directed to the temporal lobe, a brain area that includes the hippocampus. While the dose destroyed new cells, it was low enough to spare mature neurons.

The four separated, X-ray treated animals developed depression-like symptoms despite the fact that they were being treated with fluoxetine. Subsequent analysis of the animals' brain tissue showed that neurogenesis was not increased in these animals despite treatments. The neurogenesis levels in the treated and untreated animals did not differ.

In another animal study, conducted at the University Medical Center in Regensburg, Germany, scientists determined that the action of antidepressant therapy on neurogenesis is highly dependent on the age of the treated individual. Their study suggests that the therapeutic effects of antidepressants in elderly humans may not be mediated by neurogenesis.

The researchers studied mice in three different age groups: 100, 200, and more than 400 days old. These ages correspond roughly to young adult, adult, and elderly individuals in the human population, the scientists say.

"Paradoxically, the stimulatory activity of the antidepressant on neurogenesis was more potent in youngest animals, even if their rate of neurogenesis was already high as compared to the older mice," says Sebastien Couillard-Despres, PhD.

Couillard-Despres and his team also showed that extended treatment with fluoxetine enhanced neurogenesis only in the youngest animals. When the scientists compared the treated and untreated animals in the two youngest age groups, they found that although neurogenesis had occurred in all of these young animals, more newly generated cells survived and developed into specialized types of neurons in the rodents that had received fluoxetine.

To mimic the long-term antidepressant drug therapy that characterizes most people with depression, the scientists treated the lab animals with fluoxetine daily at a clinically relevant dosage over six weeks.

The scientists measured the rate of generation of new brain cells, the survival rate of these cells over time, and the percentage of cells that became mature. In addition to the fluoxetine-treated animals, the study included control animals for every age group. The controls received only a placebo treatment.

Among the other factors that influence neurogenesis in the adult brain is the amount of calories consumed in the diet, according to research of Sandrine Thuret, PhD, at King's College in London.

Her laboratory also discovered that caloric intake affects learning and memory and that, independent of calorie intake, meal frequency and food content both play important roles in neurogenesis in the hippocampus. "Our cell culture data show an impressive increase of 40 percent of adult hippocampal neurogenesis upon addition of omega-3 fatty acids into the cell culture dish," Thuret says.

In laboratory animals, Thuret found that meal frequency is more important than calorie intake in regulating adult hippocampal neurogenesis. "Indeed, adult female mice fed a calorie-restricted diet of 10 percent less than normal-fed mice did have a higher level of newborn cells in the hippocampus," she says. But few of these new cells were neurons. In mice fed every other day-which led to a similar decrease of 10 percent of calories over two days-neurogenesis and learning abilities increased.

"Remarkably, we also showed that diet has an influence on the level of expression of genes in the brain," Thuret says. These genes, which are critical for cognition, are not the same genes that are regulated by intermittent fasting.

Additional research on these genes may help identify the cellular and molecular mechanisms underlying the influence of food intake on neurogenesis in the adult brain and in learning and memory.

The search for neurobiological mechanisms that link nutrition, adult neurogenesis, and behavior is a new emphasis in biomedical research, prompted in part by recent findings from laboratory rodent studies indicating that a reduced calorie diet promotes healthy aging.

"It is well recognized that dietary restriction increases life span, reduces neuronal damage, enhances learning abilities, and improves behavioral outcome in experimental animal models of neurodegenerative disorders," Thuret says.

But not well recognized is how these effects are achieved. In her search for the answers, Thuret and her colleagues selected mice as a lab model, since previous research had associated neurogenesis in the hippocampus with improved memory and learning abilities in rodents.

Each of the three groups of mice in the study included 20 adult females, half of which were used for histology and gene expression data. The remainder were used for behavior research. For three months, one group ate at will, the second group ate every other day, and the third were fed a diet in which calories were restricted by 10 percent every day.

The behavioral tests included the Morris water maze (in which scientists measure animals' ability to learn and use visual cues to find a hidden platform) and object recognition tests (in which the ability of the mice to remember their encounter with different objects over time is measured).

"We studied their ability to learn and remember, and we looked at the amount of newborn neurons in their brain upon different diets," Thuret says. "Then we correlated the changes with the regulation of the expression of their genes."

"There is much to learn about the effects of food intake-for example, how much, how often, what, and when-on the cellular and molecular biology of the nervous system and its functional capabilities, reflecting cognitive performance in both normal and ill circumstances," Thuret says.

"This area of investigation needs attention because a better understanding of the neurological mechanisms by which nutrition affects health may lead to novel approaches for disease prevention and treatment."

In another study, frequent physical exercise on activity wheels, which are the rodents' equivalent of a treadmill, was found to stimulate the birth of new brain cells in young laboratory rats with brain damage resembling the prenatal effects of binge drinking by pregnant human females.

William Greenough, PhD, of the University of Illinois at Urbana-Champaign, reports that new brain cells, including neurons as well as supportive glial cells, were generated at much higher rates in the physically active rats than in the rodents whose cages were not connected with activity wheels. "These findings in animals are expected to lead to treatments for humans with brain damage caused by their mother's alcohol consumption," Greenough says.

In the study, newborn rats, 4 to 9 days old, were given alcohol in amounts reflecting prenatal exposure to alcohol caused by human mothers binge drinking while pregnant. At this age, a newborn rat's brain is developing rapidly. In human development, a comparable brain growth spurt occurs during the third trimester of pregnancy.

Twenty days after the young rats were first exposed to alcohol, half of the now adolescent animals were allowed to exercise on activity wheels whenever they wished over a period of 12 days. The home cages of the other half of the rats were not attached to wheels.

In previous studies by this team of researchers, motor skills training helped rats overcome some deficits resulting from alcohol exposure during sensitive periods of brain growth.

"Developmental exposure to alcohol is known to affect coordination and synchronization of paw movements," Greenough says. But after three weeks of daily training on a demanding obstacle course, the rats performed much better than did the untrained, normal rats in the study. The alcohol-exposed, trained rats had learned to maneuver effectively. In addition, as a result of the physical activity, more connections had developed between the neurons in the animals' cerebellum, a brain structure likely to be involved in their improved motor skill.

Prenatal exposure to alcohol resulting from maternal drinking is the most common preventable cause of developmental disability. According to detailed studies of brain structure, heavy prenatal alcohol exposure can destroy cells in many brain regions including the hippocampus, which is crucial to learning, memory, cognition, and emotion.

"Severe impairments in learning and cognition and in emotional regulation are frequently present during development and typically persist into adulthood," Greenough says.

Adapted from materials provided by Society for Neuroscience.
Need to cite this story in your essay, paper, or report? Use one of the following formats:
APA

MLA
Society for Neuroscience (2007, November 9). Antidepressants, Exercise, Age, Even Food Intake, Affect Generation Of New Brain Cells. ScienceDaily. Retrieved November 10, 2007, from http://www.sciencedaily.com* /releases/2007/11/071107205759.htm
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
reverett123 is offline   Reply With QuoteReply With Quote

advertisement
Reply

Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

BB code is On
Smilies are On
[IMG] code is On
HTML code is Off


Similar Threads
Thread Thread Starter Forum Replies Last Post
Anodyne Therapy Works GinaMarie Peripheral Neuropathy 10 06-08-2009 10:24 PM
Laugh if you want, but this seriously works! sjp_fanatic Hydrocephalus 6 08-22-2007 10:12 PM
Something that Works! shari Fibromyalgia and Chronic Fatigue 1 12-05-2006 12:51 AM
Anodyne Therapy Works GinaMarie Multiple Sclerosis 1 10-13-2006 06:12 PM
viagra really works BobbyB ALS 2 10-08-2006 04:57 PM


All times are GMT -5. The time now is 06:41 AM.

Powered by vBulletin • Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.

vBulletin Optimisation provided by vB Optimise v2.7.1 (Lite) - vBulletin Mods & Addons Copyright © 2024 DragonByte Technologies Ltd.
 

NeuroTalk Forums

Helping support those with neurological and related conditions.

 

The material on this site is for informational purposes only,
and is not a substitute for medical advice, diagnosis or treatment
provided by a qualified health care provider.


Always consult your doctor before trying anything you read here.