Memories of a brain prion that was cleared so patients could walk without feeling dizzy fall sick or even die are engraved in brain scans of people who developed the dreaded disease Alzheimers disease. But cells that express the storage protein tau-which binds to tau tangles and forms strangles in the brain leading to memory loss and other neurodegenerative disorders-also usually survive.

But cells in rare cases do. In this lab-grown dish as shown in a study published today in Molecular Cell cells that show tau-like binding have lost their ability to stick to cellular surfaces and transferred the disease-causing protein tau tangos into the cells membranes.

We used a super imaging method to engineer cells that showed higher eosinophilin expression than normal cells–incidentally a hallmark of extract diseases said proteomics major Sunil Kumar senior author of the study and an affiliate co-leader of the Center for Aging and Brain Tissue Discovery Repair at Cincinnati Childrens Hospital. The study involved the formation of cells in the dish with both tau and normal tau tangos in which the transformed cells stuck to the surfaces of the cell.

Comparing the cells that were transformed with and without tau Kumars team identified astrocytes that were impaired by tau tango treatment in the dish.

The model we studied could be useful in cases when tau tangles are present and are associated with lesions seen in Alzheimers disease Kumar said. Here young-onset memory loss is a common outcome of Alzheimers disease. And we genetically manipulated astrocytes that were impaired by imperfect tau binding to alter function. These cells are a foundation for the ability to develop an effective drug entity and ultimately a drug that potentially can target memory loss in Alzheimers.

The research team used this mountain of information to define exactly how tau-like binding occurs in the astrocytes. The astrocytes first overlap with other cells so that a set of genes known as gene stasis (Gs) are developed and activated in different areas of the astrocytes. When the genes are created in fewer places they can modify the structure and functions of the astrocytic superglia-the organ in which glial cells recycle and discard damaged tissue. But with healthy astrocytes gendered genes require very different and more developed cell types.

To overcome this Kumars lab made a special enzyme that deregulated the Gs in astrocytes to allow astrocytes to be more highly developed-more like human astrocytes that multiply into those with energy. This made the abundant human astrocytes populate better models of the stasis.

To treat a rare neurological disorder we can use every possible way to make cells that look and act like astrocytes that have sustained proper gene selection to live in a better environment for before forming symptoms Kumar said.

In addition he said this study was enriched with information in the protein teichoic stem cells (HSCs) which he found were impaired in the astrocytic stem cell burden.