Growth factor that may prevent Alzheimer’’s spread identifiedFebruary 9th, 2009 - 1:54 pm ICT by ANI
London, Feb 9 (ANI): In a study on animals, researchers have found that treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF) could potentially provide long-lasting protection by slowing, or even stopping, the progression of Alzheimer’’s disease.
The study by researchers led by University of California, San Diego, showed that Memory loss, cognitive impairment, brain cell degeneration, and cell death were prevented or reversed in several animal models after treatment with BDNF.
“The effects of BDNF were potent. When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease,” Nature magazine quoted Dr. Mark Tuszynski, professor of neurosciences at the UC San Diego School of Medicine and neurologist at the Veterans Affairs San Diego Health System, as saying.
Normally BDNF is produced throughout life in the entorhinal cortex, a portion of the brain that supports memory, and its production decreases in the presence of Alzheimer’’s disease.
For the study, BDNF gene or protein was injected in a series of cell culture and animal models, including transgenic mouse models of Alzheimer’’s disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage.
It was found that in all the above models, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests, as compared to control groups not treated with BDNF.
Particularly, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signalling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals.
One could see the same benefits in the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer’’s disease.
The researchers concluded that the protective and restorative effects of BDNF on damaged neurons and neuronal signalling might offer a new approach to treating Alzheimer’’s disease.
BDNFs protective and restorative effects were independent of the build-up of amyloid, a protein that accumulates in the brain to form plaques in Alzheimer’’s disease.
Tuszynski aid that a large number of current experimental treatments for Alzheimer’’s disease target amyloid production, which makes BDNF a potential alternative protective intervention.
As BDNF targets a different set of disease mechanisms than amyloid modulation, there is also potential to combine BDNF and amyloid-based treatments, theoretically providing a two-pronged attack on the disease.
The study has been published in the journal Nature Medicine. (ANI)
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