The official MedZine Blog

Also this week MedZine brings you the latest medical news on various medical specialisms. In this editorial some striking studies are highlighted. This week we have selected two studies, both concerning neurological breakthroughs. The first describes the development of a process that renders a whole brain transparent. The second study sheds light on one of the major toxic mechanisms of Alzheimer's disease.

Creating a transparent brain

To study the brain until now the best option was to study thin slices of brain. A new process developed by researchers at Stanford University, called CLARITY, makes the brain permeable and transparent. In this approach, published online on April 10th in Nature, the fat that normally holds the brain's working components in place is replaces by a clear gel. This keeps the intact brain three-dimensional complexity of fine wiring and molecular structures intact and accessible to visible light and chemicals. "Studying intact systems with this sort of molecular resolution and global scope — to be able to see the fine detail and the big picture at the same time — has been a major unmet goal in biology, and a goal that CLARITY begins to address," says Deisseroth, one of the authors and leader of the project. This method may be the key to unraveling the wiring of the brain.

Unraveling the mystery of Alzheimer’s disease

A study in Neuron by scientists from The Scripps Research Institute uncovers how brain damage in Alzheimer's disease arises. People in the earliest stages of Alzheimer's disease begin to lose synapses in certain memory-related brain areas. Small aggregates of the protein amyloid beta can cause this loss of synapses, but how they do so has been a mystery. Polleux and colleagues showed that a loss of synapses is linked to the overactivation of an enzyme called AMPK. Blocking the enzyme in a mouse model for Alzheimer’s disease prevented synapse loss. Amyloid beta oligomers trigger certain neuronal receptors, which leads to calcium influx and subsequent activation of the enzyme CAMKK2. This CAMKK2 activates AMPK and the protein tau is phosphorylated. Hyperphosphorylated tau is found in the tangled plaques in Alzheimer’s disease. In addition to having implications for Alzheimer's drug discovery, the findings suggest the need for further safety studies on an existing drug for Type 2 Diabetes, metformin, that causes AMPK activation.  

Source: Eurekalert, Nature and Neuron