UCSB Scientists Make Important Alzheimer’s Discovery

Scientists at UC Santa Barbara have uncovered a recent finding that may lead those studying Alzheimer’s disease and the drugs that help fight it in a new direction. 

Scientists looked at what effect amyloid beta, a cause of Alzheimer’s among other diseases, has on a protein called tau.  The team used test tube biochemistry along with a number of cultured cells as models to examine how amyloid beta effects tau. 

Stuart Feinstein, a professor of molecular, cellular and developmental biology as well as a senior author and co-director of UCSB’s Neuroscience Research Institute explained that he and his student’s research aimed to help pharmaceutical companies create effective Alzheimer’s medication.  Feinstein explained, “The more precisely they understand the biochemistry of the target, the better attack a pharmaceutical company can make on a problem."

The research team expected to find that amyloid beta led to extensive abnormal tau phosphorylation because this was the consensus in the medical community.  However, the team found that when amyloid beta was added to neuronal cells, the tau in those cells became completely fragmented.  Within a day, the cells were dead.  Tau has many jobs, but it mainly functions to regulate the cellular cytoskeleton, which is constantly changing.  When it does not function properly, the cell dies. 

Feinstein explained, “If you destroy tau, which is an important regulator of the microtubules, one could easily see how that could also cause cell death.” 

The team is now focusing on the implications of these experiments with the hope that these findings can lead to a much better understanding of the causes of Alzheimer’s disease among the medical community.

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