Sep 10, 2010 15:01 GMT  ·  By

Alzheimer's disease is largely believed to be caused by amyloid beta ( Αβ) proteins, that are also blocking the transport of important cargoes between brain cells.

Researchers from the Gladstone Institute of Neurological Disease (GIND) have figured out a way of preventing such traffic jams, by reducing the level of another protein called tau, that regulates Αβ.

Aβ proteins build up to toxic levels within the brains of Alzheimer's patients and block the axonal transport of the cargoes.

The axons are the long processes that connect neurons in the brain to many other neurons, and are extremely important for the transport of different cargoes on which depend the neurons' functions.

The most important cargoes that need to be transported are mitochondria, which are basically the energy factories of the cells, and also proteins that are necessary to the growth and survival of brain cells.

Lennart Mucke, MD, GIND director and senior author of the study explained that scientists “previously showed that suppressing the protein tau can prevent Aβ from causing memory deficits and other abnormalities in mouse models of AD.”

“We wondered whether this striking rescue might be caused, at least in part, by improvements in axonal transport,” he added.

So as all scientists do, they experimented on mouse neurons grown in culture dishes, Science Daily reports.

They took neurons from normal mice or from mice that lacked one or both tau genes, and exposed them to human Aβ proteins.

The results showed that the Aβ slowed down the axonal transport of mitochondria and growth factors, but this happened only in neurons that had the tau genes.

Keith Vossel, MD, lead author of the study said that these results caused a large excitement among scientists.

“Whether tau affects axonal transport or not has been a controversial issue, and nobody knew how to prevent Aβ from impairing this important function of neurons.

“Our study shows that tau reduction accomplishes this feat very effectively.”

Dr Mucke reminded that “some treatments based on attacking Aβ have recently failed in clinical trials, and so, it is important to develop new strategies that could make the brain more resistant to Aβ and other AD-causing factors.”

“Tau reduction looks promising in this regard, although a lot more work needs to be done before such approaches can be explored in humans.”

Other scientists part of the team include Gladstone's Jens Brodbeck, Aaron Daub, Punita Sharma, and Steven Finkbeiner, as well as Kai Zhang and Bianxiao Cui of Stanford's chemistry department.

This work was published online in Science Express and was supported by the NIH and the McBean Family Foundation.