3-rx.comCustomer Support3-rx.com
Find a product
    HomeAbout UsFAQContactHelp
 
   
 
News Center
Health Centers
Medical Encyclopedia
Drugs & Medications
Diseases & Conditions
Medical Symptoms
Med. Tests & Exams
Surgery & Procedures
Injuries & Wounds
Diet & Nutrition
Special Topics
Online Pharmacy



Type 2 diabetes mellitus, more often known as type 2 diabetes, is the most common type of diabetes


Join our Mailing List





Syndicate

You are here : 3-RX.com > Home > Brain - Neurology -

Meth abuse may speed age-related brain degeneration

Brain • • NeurologyAug 28, 07

Young people who abuse methamphetamines may put themselves at risk of parkinson-like movement disorders later in life, a new animal study suggests.

In experiments with mice, scientists found that animals deficient in a protein called glial cell line-derived neurotrophic factor (GDNF) were especially vulnerable to long-term movement problems after being exposed to the neurotoxic effects of a methamphetamine “binge.”

GDNF is needed for the proper functioning of dopamine, a brain chemical involved in regulating movement. Both GDNF and dopamine are depleted in the brains of people with Parkinson’s disease.

Because methamphetamines can damage dopamine-producing cells in the brain, researchers have speculated that young meth users may be at elevated risk of parkinson-like movement disorders as they age.

The new findings, reported in The Journal of Neuroscience, support that theory.

“The study in mice tells us that people who make less GDNF protein may be more vulnerable to the motor deficits caused by methamphetamine and that those effects may not be revealed until we get older,” explained principal author Dr. Jacqueline McGinty, a professor in the department of neurosciences at the Medical University of South Carolina in Charleston.

For their study, McGinty and her colleagues used both normal mice and mice missing one of their genes for GDNF. Two weeks after being exposed to a meth binge, the animals tended to show dopamine depletion and other signs of brain damage, with the GDNF-deficient mice being especially vulnerable.

Similarly, these mice were more likely to have movement impairments when they were 12 months old—old age for rodents.

No one knows what percentage of the population has an abnormal GDNF gene, McGinty told Reuters Health, but individuals certainly vary in how much GDNF protein their genes make.

It’s possible, she and her colleagues say, that young people with naturally lower levels of the protein may be susceptible to long-term brain damage and Parkinson-like symptoms at an older age.

“Motor deficits during aging may be accelerated if young adults are exposed to an environmental toxin like methamphetamine,” McGinty said.

SOURCE: The Journal of Neuroscience, August 15, 2007. 



Print Version
Tell-a-Friend

RELATED ARTICLES:
  High-Fat Ketogenic Diet to Control Seizures Is Safe Over Long Term
  Parkinson’s disease research uncovers social barrier
  Special suit helps kids with cerebral palsy
  Genetic Risk Factor Identified for Parkinson’s Disease: Gene Variant Influences Vitamin B6 Met
  Gene variant protects against Alzheimer’s
  Why some brains are more vulnerable to stress and resistant to antidepressants
  New approach to fighting Alzheimer’s shows potential in clinical trial
  Alzheimer’s protein may be early risk factor
  Surgery Not Linked to Memory Problems in Older Patients
  Researchers to Test First Gene Therapy For Alzheimer’s Patients
  ‘Scaffolding’ Protein Changes in Heart Strengthen Link Between Alzheimer’s Disease
  Hybrid molecules show promise for exploring, treating Alzheimer’s

 


Advertisement
















Home | About Us | FAQ | Contact | Advertising Policy | Privacy Policy | Bookmark Site