Drug Creates New Connections In Brain Restores & Improves Memory

Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience
Article Date: 07 Dec 2007 - 0:00 PDT

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Scientists at the Blanchette Rockefeller Neurosciences Institute (BRNI) have discovered that a cancer drug Bryostatin enhances the formation of new connections in rat brains during memory storage. This drug could potentially increase normal memory capacity in humans as well as repair and restore memory lost from Alzheimer's disease, stroke and head trauma.

In an article to be published in the December 4 issue of the Proceedings of the National Academy of Sciences (PNAS), BRNI Scientific Director Daniel Alkon, M.D., and Jarin Hongpaisan, Ph.D., describe how the cancer drug Bryostatin stimulates the production of connections between neurons in the same structural way that memory storage does naturally. Bryostatin essentially rewires the brain. "There have been no effective drugs to promote brain repair," Dr. Alkon said. "Bryostatin and other BRNI drugs in this class could introduce a whole new era for brain repair. At the same time, we are now closer to understanding what controls the growth of synaptic connections in the adult brain."

The BRNI research shows that a healthy brain normally undergoes some 'rewiring' when it stores memories. Bryostatin enhances this rewiring in normal healthy brains and also creates new connections in brains that have been ravaged by Alzheimer's disease, stroke or head trauma.

Alkon and Hongpaisan used high-powered electron microscopes to directly visualize these synaptic connections between neurons. They also used molecular markers to label these connections to confirm the synaptogenesis induced by memory and Bryostatin.

"Diseases like Alzheimer's actually destroy synapses in the human brain. There is still no recognized cure," said Dr. Alkon. "In our animal studies with Bryostatin, damaged brains repaired synaptic connections of cells that were ruined from disease, giving the brain more capacity for memory. If this result is applicable to humans, this could be life-changing for Alzheimer's patients."

In previous BRNI studies, Bryostatin was found to markedly increase survival of mice with human Alzheimer's genes, decrease the production of the toxic Alzheimer's protein called A Beta, and increase the production of the healthy proteins from human cells.

Bryostatin also shows the ability to accelerate the production of synapses when paired with learning exercises. According to Dr. Alkon, this could eventually lead to new treatment therapies for children with compromised memory activity.

In 2004, BRNI received patent protection for the use of Bryostatin - originally developed as a cancer drug - to treat Alzheimer's disease. BRNI is preparing now for the first clinical trials of Bryostatin for the treatment of neurological disorders. Clinical trials will test whether Bryostatin's promising preclinical results generalize to humans.

BRNI is the world's only non-profit institute dedicated to the study of both human memory and diseases of memory. Its primary mission is to accelerate neurological discoveries from the lab, including diagnostic tools and treatments, to the clinic where it can benefit patients who suffer from neurological and psychiatric diseases.

BRNI is operated in alliance with West Virginia University in Morgantown as well as in collaboration with other academic institutions such as Johns Hopkins University. West Virginia Senator Jay Rockefeller founded the Institute in memory of his mother, Blanchette Hooker Rockefeller, who died of Alzheimer's disease.

West Virginia University Health Sciences Center
PO Box 9083
Morgantown, WV 26506-9083
United States
http://www.hsc.wvu.edu

Article adapted by Medical News Today from original press release.
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Alzheimer's / Dementia

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The word dementia comes from the Latin de meaning "apart" and mens from the genitive mentis meaning "mind". Dementia is the progressive deterioration in cognitive function - the ability to process thought (intelligence). Read more...

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