Alzheimer's Disease And Traumatic Brain Injury Have Same Type Of Cell Destruction

Featured Article
Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience
Article Date: 13 Jul 2009 - 2:00 PDT

email to a friend   printer friendly   opinions  

Researchers in the US found that the destructive cellular pathways that occur following traumatic brain injury are the same as those activated in Alzheimer's Disease, suggesting that both conditions could be treated with new drugs that target these pathways. They said the findings "cement" the relationship beween traumatic brain injury and Alzheimer's Disease.

The research was led by neuroscientist Mark Burns, who is assistant professor at Georgetown University Medical Center (GUMC) in Washington, DC. A paper on their work is being presented at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD 2009) which is taking place from 11 to 16 July in Vienna, Austria.

Burns and colleagues found that deactivating the pathways using a gamma secretase inhibitor reduced neuron loss and protected against loss of cognitive and motor function in animals with traumatic brain injury. Gamma secretase inhibitor is a class of drug currently being tested as a therapy for Alzheimer's Disease.

Burns said this study showed that the same drug might work to prevent loss of neurons in both traumatic brain injury and Alzheimer's Disease.

The brains of elderly patients who died from Alzheimer's Disease often show a build up of a toxic peptide called beta amyloid. The same substance is also found in the brains of around one third of people who have suffered traumatic brain injury, including children. said Burns, who explained in a media statement that people who have suffered such a brain injury are at 400 per cent higher risk of developing Alzheimer's.

When a traumatic injury occurs to the brain, a mass of brain cells or neurons dies, and this is then followed by a second "wave" of beta amyloid build up. This secondary damage can last several months or even years and leaves big holes inside the brain.

Amyloid peptides are chains of amino acids made when a longer chain called amyloid precursor protein (APP) is chopped up by enzymes. This is done in two stages: the first stage of cleavage is controlled by the enzyme beta secretase and the second stage is controlled by gamma secretase. Scientists have hypothesized that inhibiting gamma secretase might be a way to treat Alzheimer's, thus trials are under way for drugs designed to do this.

One such gamma secretase inhibitor is DAPT, and in this study Burns and colleagues experimented with DAPT in mice. One group of mice was treated with the drug while another group was bred so they could not produce beta secretase in the first place. They also had a third group of mice who had not been altered or treated, the "normal" controls.

Brain injury in the unaltered mice was followed by a rapid accumulation of beta amyloid, and the expected deficits in motor and cognitive function. But mice treated with DAPT and mice that could not produce beta secretase had brain lesions that were up to 70 per cent smaller and suffered less impairment.

Burns said they concluded that:

"Modulation of beta and gamma secretase may provide novel therapeutic targets for the treatment of traumatic brain injury."

According to the Alzheimer's Association, there are around 5.3 million Americans living with Alzheimer's disease, which together with dementia triples health care costs of those aged 65 and over in the US.

The study was sponsored by the National Institutes of Health and the Klingel Family Foundation.

-- Alzheimer's Association.

Sources: Georgetown University Medical Center, Alzheimer's Association.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

• Additional
• References
• Citations