XML Feed for RxPG News   Add RxPG News Headlines to My Yahoo!   Javascript Syndication for RxPG News

Research Health World General
 
  Home
 
 Latest Research
 Cancer
 Psychiatry
 Genetics
 Surgery
 Aging
  Parkinson's
   Rotenone
  Dementia
 Ophthalmology
 Gynaecology
 Neurosciences
 Pharmacology
 Cardiology
 Obstetrics
 Infectious Diseases
 Respiratory Medicine
 Pathology
 Endocrinology
 Immunology
 Nephrology
 Gastroenterology
 Biotechnology
 Radiology
 Dermatology
 Microbiology
 Haematology
 Dental
 ENT
 Environment
 Embryology
 Orthopedics
 Metabolism
 Anaethesia
 Paediatrics
 Public Health
 Urology
 Musculoskeletal
 Clinical Trials
 Physiology
 Biochemistry
 Cytology
 Traumatology
 Rheumatology
 
 Medical News
 Health
 Opinion
 Healthcare
 Professionals
 Launch
 Awards & Prizes
 
 Careers
 Medical
 Nursing
 Dental
 
 Special Topics
 Euthanasia
 Ethics
 Evolution
 Odd Medical News
 Feature
 
 World News
 Tsunami
 Epidemics
 Climate
 Business
 
 India
Search

Last Updated: Nov 18, 2006 - 12:32:53 PM

Parkinson's Channel
subscribe to Parkinson's newsletter

Latest Research : Aging : Parkinson's

   DISCUSS   |   EMAIL   |   PRINT
New genetic model for Parkinson's disease
Jul 31, 2006 - 11:29:00 AM, Reviewed by: Dr. Ankush Vidyarthi

"The course of the disease as well as the brain changes in this mouse are more similar to Parkinson's disease than most other models. This supports the notion that genetic risk factors are important."

 
Researchers at the Karolinska Institute in Sweden are homing in on mechanisms that may explain one set of causes for Parkinson's disease. In mice they have mimicked disturbances of mitochondria thought to be one cause of disease. By genetic means the disturbance of mitochondria - the energy factories of cells - were directed to those nerve cells that produce the transmitter substance dopamine and that die in Parkinson's disease.

"The course of disease in these mice is strikingly similar to human disease", says Dr. Lars Olson.

In the mouse model generated by the research team, a gene called TFAM is automatically deleted from the genome in dopamine nerve cells only. Without TFAM, mitochondria cannot function normally. The so called respiratory chain is compromised and energy production decreases severely in the dopamine cells.

The new mice are born healthy from healthy but genetically modified parents and will develop spontaneous disease. Previous studies in the field have been based on researchers delivering neurotoxic substances to kill the dopamine neurons. In the new mice, however, mice develop disease slowly in adulthood, like humans with Parkinson's disease, which may facilitate research aimed at finding novel medical treatments and other therapies.

"We see that the dopamine producing nerve cells in the brain stem slowly degenerate", says Dr. Nils-G�ran Larsson. "In the microscope we can see that the mitochondria are swollen and that aggregates of a protein, probably alpha-synuclein starts to accumulate in the nerve cell bodies. Inclusions of alpha-synuclein-rich so called Lewy bodies is typical for the human disease."

The causes of Parkinson's disease have long remained a mystery. Genes and environment are both implicated, but recently there has been an increased focus on the roles of genetic factors. It has been found that mutations in a number of genes can lead directly to disease, while other mutations may be susceptibility factors, so that carriers have an increased risk of becoming ill. A common denominator for some of the implicated genes is their suggested role for the normal functioning of mitochondria.

"Like patients, the mice can be treated with levo-Dopa, a precursor of the lost substance dopamine", says Dr. Nils-G�ran Larsson. "The course of the disease as well as the brain changes in this mouse are more similar to Parkinson's disease than most other models. This supports the notion that genetic risk factors are important."

"Like in patients, the dopamine nerve cells in the new mouse model die in a specific order", says Dr. Lars Olson. "We hope the mouse will help us understand why certain dopamine nerve cells are more sensitive than others, so that we can develop drugs that delay, ore even stop the nerve cell death."
 

- "A pathophysiological link between respiratory chain dysfunction and parkinsonism with synuclein inclusions"
 

info.ki.se/ki

 
Subscribe to Parkinson's Newsletter
E-mail Address:

 

The project, which is a collaboration between Dr. Nils-G�ran Larsson's and Dr. Lars Olson's teams and in which Dr. Staffan Cullheim's team has contributed with electron microscopical analysis, is being published this week as an Early edition in Proceedings of the National Academy of Sciences. Collaborations regarding the new Parkinson mouse are also ongoing with Dr. Barry Hoffer's team at NIDA, NIH.

Related Parkinson's News

Laser probe of a brain pigment's anatomy may offer insight into Parkinson's disease
Novel blood test for early detection of Parkinson's, receives national recognition
New genetic model for Parkinson's disease
Expertise In Brain Stimulation Therapy May Improve Outcomes in Parkinson's Disease
Pesticide Dieldrin Linked to Increased Risk of Parkinson's Disease
ER trafficking defect caused by alpha-synuclein accumulation implicated in Parkinson's
Pesticides exposure associated with Parkinson's disease
Tuberculosis drug PAS may cure Parkinson's-like illness
Stabilizing microtubules with L-AP4 reduces rotenone toxicity
New Guidelines Improve Diagnosis and Quality of Life for People with Parkinson Disease


For any corrections of factual information, to contact the editors or to send any medical news or health news press releases, use feedback form

Top of Page

 

© Copyright 2004 onwards by RxPG Medical Solutions Private Limited
Contact Us