RxPG News Feed for RxPG News

Medical Research Health Special Topics World
  Home
 
   Health
 Aging
 Asian Health
 Events
 Fitness
 Food & Nutrition
 Happiness
 Men's Health
 Mental Health
 Occupational Health
 Parenting
 Public Health
 Sleep Hygiene
 Women's Health
 
   Healthcare
 Africa
 Australia
 Canada Healthcare
 China Healthcare
 India Healthcare
 New Zealand
 South Africa
 UK
 USA
 World Healthcare
 
   Latest Research
 Aging
  Dementia
   Alzheimer's
  Parkinson's
 Alternative Medicine
 Anaethesia
 Biochemistry
 Biotechnology
 Cancer
 Cardiology
 Clinical Trials
 Cytology
 Dental
 Dermatology
 Embryology
 Endocrinology
 ENT
 Environment
 Epidemiology
 Gastroenterology
 Genetics
 Gynaecology
 Haematology
 Immunology
 Infectious Diseases
 Medicine
 Metabolism
 Microbiology
 Musculoskeletal
 Nephrology
 Neurosciences
 Obstetrics
 Ophthalmology
 Orthopedics
 Paediatrics
 Pathology
 Pharmacology
 Physiology
 Physiotherapy
 Psychiatry
 Radiology
 Rheumatology
 Sports Medicine
 Surgery
 Toxicology
 Urology
 
   Medical News
 Awards & Prizes
 Epidemics
 Launch
 Opinion
 Professionals
 
   Special Topics
 Ethics
 Euthanasia
 Evolution
 Feature
 Odd Medical News
 Climate

Last Updated: Oct 11, 2012 - 10:22:56 PM
Alzheimer's Channel

subscribe to Alzheimer's newsletter
Latest Research : Aging : Dementia : Alzheimer's

   EMAIL   |   PRINT
Different forms of amyloid beta in Alzheimer's disease harm neurons in different ways

Jun 1, 2006 - 1:06:00 PM , Reviewed by: Ankush Vidyarthi
“These findings are quite significant because, although both fibrils and oligomers may contribute to dementia, they do so in very different ways over different time spans,”

 
[RxPG] Researchers at UC Irvine have shown that different forms of amyloid beta lead to neural damage in different ways, leading to an increasingly complex view of amyloid toxicity in the Alzheimer brain. The finding could modify the way therapeutic approaches for the treatment of Alzheimer’s disease are designed.

The researchers studied the effects of different forms of the amyloid beta peptide on human brain cells. Amyloid beta accumulation is one of two hallmarks of Alzheimer’s disease and is considered a major target for researchers looking into therapies for the treatment of the disease. After death, most amyloid beta found in the brains of Alzheimer’s patients is in fibrillar form – long, insoluble fibers bound together in deposits called senile plaques; however, there are also soluble forms of amyloid beta, or oligomers, that may decisively contribute to neural degeneration.

The experiments conducted at UCI showed that the soluble forms of amyloid beta are much more toxic and lead to neuronal death in as little as 12 hours. The fibrillar form, meanwhile, does not actually kill the neurons, but slowly, over a period of 10 or more days, renders them useless.

Not known is whether the soluble amyloid beta in the Alzheimer brain eventually turns into the fibrillar kind, or whether the two are completely different.

“These findings are quite significant because, although both fibrils and oligomers may contribute to dementia, they do so in very different ways over different time spans,” said Jorge Busciglio, an assistant professor of neurobiology and behavior. “This complexity of the amyloid beta species will require more sophisticated therapeutic approaches. For example, it might be dangerous to create compounds that target fibrillar amyloid and try to break them up, because if the fibers dissolve into the soluble form, that could actually speed up cell death and the onset of dementia rather than treat it.”

Atul Deshpande, a graduate student in Busciglio’s laboratory, tested one preparation of fibrillar amyloid beta and two soluble ones, which resemble the types found in the brains of Alzheimer’s patients. In less than 12 hours, the human neurons exposed to one of the two soluble forms started to die. Most of the cells were dead after 24 hours. The cells exposed to the other soluble form took about five times longer to die. In contrast, the brain cells treated with the fibrillar form slowly degenerated. The axons and dendrites in the cells became twisted and rendered the cell functionally useless. For the most part, however, the cells did not die.

According to the scientists, previous research has shown that the brain levels of soluble amyloid beta appear to correlate better with severity of cognitive impairment than the number and density of plaques found in the brain. Then, the more soluble beta amyloid is present, the more severe and rapid the onset of the disease.

Researchers now will have to determine why the soluble form of beta amyloid is so much more toxic. One theory is it binds to neuronal connections, or gateways into the cell, and gives soluble amyloid beta easier, quicker access into the neuron. The UCI research also showed that the soluble form quickly impairs the function of mitochondria, the cells’ energy generators. Brain cells consume more energy than any other cell in the body. If that energy source dies, the cells die as well.

Alzheimer’s disease is a progressive neurodegenerative disorder, affecting 4.5 million to 5 million adults in the United States. If no effective therapies are developed, it is estimated that 13 million Americans will be afflicted with the disease by 2050. It is the third-most-expensive disease to treat and the third-leading cause of death, behind cancer and coronary heart disease.



Publication: The findings were published this week in the Journal of Neuroscience.
On the web: www.uci.edu 

Advertise in this space for $10 per month. Contact us today.


Related Alzheimer's News


Subscribe to Alzheimer's Newsletter

Enter your email address:


 Additional information about the news article
Along with Busciglio and Deshpande, researchers on the study were Charles Glabe, a professor of molecular biology and biochemistry, and graduate researcher Erene Mina. The study was funded by grants from the Alzheimer’s Association, the National Institutes of Health and the Larry L. Hillblom Foundation.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 24,000 undergraduate and graduate students and about 1,400 faculty members. The second-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.3 billion. For more UCI news, visit www.today.uci.edu.
 Feedback
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

 
Contact us

RxPG Online

Nerve

 

    Full Text RSS

© All rights reserved by RxPG Medical Solutions Private Limited (India)