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Loose Change Forum > Latest News Section > Brain Degeneration And How To Solve It!


Posted by: mynameis Jan 12 2008, 11:43 PM
Study shows marijuana increases brain cell growth

By Juanita King, The Muse (Memorial University of Newfoundland)

ST. JOHN’S, Nfld — Supporters of marijuana may finally have an excuse to smoke weed every day. A recent study in the Journal of Clinical Investigation suggests that smoking pot can make the brain grow.

Though most drugs inhibit the growth of new brain cells, injections of a synthetic cannibinoid have had the opposite effect in mice in a study performed at the University of Saskatchewan. Research on how drugs affect the brain has been critical to addiction treatment, particularly research on the hippocampus.

The hippocampus is an area of the brain essential to memory formation. It is unusual because it grows new neurons over a person’s lifetime. Researchers believe these new cells help to improve memory and fight depression and mood disorders.

Many drugs -— heroin, cocaine, and the more common alcohol and nicotine — inhibit the growth of these new cells. It was thought that marijuana did the same thing, but this new research suggests otherwise.

Neuropsychiatrist Xia Zhang and a team of researchers study how marijuana-like drugs — known collectively as cannabinoids — act on the brain.

The team tested the effects of HU-210, a potent synthetic cannabinoid similar to a group of compounds found in marijuana. The synthetic version is about 100 times as powerful as THC, the high-inducing compound loved by recreational users.

The researchers found that rats treated with HU-210 on a regular basis showed neurogenesis — the growth of new brain cells in the hippocampus. A current hypothesis suggests depression may be triggered when the hippocampus grows insufficient numbers of new brain cells. If true, HU-210 could offer a treatment for such mood disorders by stimulating this growth.

Whether this is true for all cannabinoids remains unclear, as HU-210 is only one of many and the HU-210 in the study is highly purified.

“That does not mean that general use in healthy people is beneficial,” said Memorial psychology professor William McKim. “We need to learn if this happens in humans, whether this is useful in healthy people, and whether THC causes it as well.”

McKim warns that marijuana disrupts memory and cognition. “These effects can be long-lasting after heavy use,” he said. “This makes it difficult to succeed academically if you use it excessively.”

“Occasional light use probably does not have very serious consequences. [But] there is some evidence that marijuana smoke might cause cancer.”

Still, the positive aspects of marijuana are becoming more plentiful as further research is done. McKim says it’s not surprising that THC and compounds like it could have medicinal effects.

“Many have been identified,” he said. “It stimulates appetite in people with AIDS, it is an analgesic, and blocks nausea in cancer patients undergoing chemotherapy. And it treats the symptoms of glaucoma.”

The research group’s next studies will examine the more unpleasant side of the drug.

http://www.peak.sfu.ca/the-peak/2005-3/issue9/ne-mj.html



Reversal Of Alzheimer's Symptoms Within Minutes In Human Study

ScienceDaily (Jan. 9, 2008) — An extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer’s disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation.

This new study highlights the importance of certain soluble proteins, called cytokines, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a critical component of the brain’s immune system. Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimer’s disease interfere with this regulation. To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer’s.

The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used off label in the study.

The use of anti-TNF therapeutics as a new treatment choice for many diseases, such as rheumatoid arthritis and potentially even Alzheimer’s, was recently chosen as one of the top 10 health stories of 2007 by the Harvard Health Letter.

Similarly, the Neurotechnology Industry Organization has recently selected new treatment targets revealed by neuroimmunology (such as excess TNF) as one of the top 10 Neuroscience Trends of 2007. And the Dana Alliance for Brain Initiatives has chosen the pilot study using perispinal etanercept for Alzheimer’s for inclusion and discussion in their 2007 Progress Report on Brain Research.

The lead author of the study, Edward Tobinick M.D., is an assistant clinical professor of medicine at the University of California, Los Angeles and director of the Institute for Neurological Research, a private medical group in Los Angeles. Hyman Gross, M.D., clinical professor of neurology at the University of Southern California, was co-author.

The study is accompanied by an extensive commentary by Sue Griffin, Ph.D., director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who along with Robert Mrak, M.D., chairman of pathology at University of Toledo Medical School, are editors-in-chief of the Journal of Neuroinflammation.

Griffin and Mrak are pioneers in the field of neuroinflammation. Griffin published a landmark study in 1989 describing the association of cytokine overexpression in the brain and Alzheimer’s disease. Her research helped pave the way for the findings of the present study. Griffin has recently been selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit organization of more than 200 leading neuroscientists, including ten Nobel laureates.

“It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention,” said Griffin. “It is imperative that the medical and scientific communities immediately undertake to further investigate and characterize the physiologic mechanisms involved. This gives all of us in Alzheimer’s research a tremendous new clue about new avenues of research, which is so exciting and so needed in the field of Alzheimer’s. Even though this report predominantly discusses a single patient, it is of significant scientific interest because of the potential insight it may give into the processes involved in the brain dysfunction of Alzheimer’s.”

While the article discusses one patient, many other patients with mild to severe Alzheimer’s received the treatment and all have shown sustained and marked improvement.

The new study, entitled “Rapid cognitive improvement in Alzheimer’s disease following perispinal etanercept administration,” and the accompanying commentary, entitled “Perispinal etanercept: Potential as an Alzheimer’s therapeutic,” are available on the Web site of the Journal of Neuroinflammation (http://www.jneuroinflammation.com/content/5/1/2/abstract).

http://www.sciencedaily.com/releases/2008/01/080109091102.htm

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