Organ transplant drug could stall first stages of Alzheimer’s disease

A class of anti-rejection drugs used after organ transplants may slow the progression of early-stage Alzheimer's disease, a new study has found.

Findings published by UT Southwestern Medical Center suggest that the connections between neurons are lost early in the course of the disease, which most likely causes the behavioral and memory changes that occur as Alzheimer's develops.

It was discovered that nerve cells initially lose dendritic spines, which are described as tiny branch-like extensions at the ends of neurons that receive information across synapses from nearby cells.

Synapses – the junctions where communication between neurons occurs – are also lost and the area of the brain that is most affected governs higher-order functions such as language, spatial reasoning, conscious thinking, sight, hearing and other senses.

Dr. James Malter, chairman of pathology at UT Southwestern and corresponding author of the Science Signaling study, said his team of researchers found that beta-amyloid – which is overproduced in the brains of most people with Alzheimer's – turns on a protein called calcineurin, which then causes the inhibition of a second protein called Pin1, leading to loss of dendritic spines and synapses.

Synapses could be rescued if the neurons received extra Pin1 or were exposed to FK506, a drug that blocks calcineurin and is currently approved by the Food and Drug Administration [FDA] for the prevention of solid organ transplant rejection.

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