How does tau pathology affect the function of the
ventral visual stream?
Elise H. Thompson (Postdoctoral Fellow, Fyhn Group, FYSCELL, IBV)
Pathological tau protein is one of the hallmarks of dementia. Tau proteins are microtubule associated proteins, and they contribute to stabilizing the cell skeleton. In the diseased state, tau proteins become hyperphosphorylated and detach from the microtubule, thus destabilizing the skeleton. We study the pathology by introducing a human tau mutation, termed P301S, into mouse neurons in vivo. The gene is packed in a virus vector and injected directly into the lateromedial part of the secondary visual cortex (LM). After allowing time for the pathology to develop, we test the animals in a visual association task. This task is believed to rely on the function of LM and the ventral visual stream. In a separate experiment, we studied whether activity LM really is crucial for mice to complete this visual association task. To achieve this we used DREADD, Designer Receptor Exclusively Activated by Designer Drugs, which is a method of increasing or decreasing the neuronal activity in a brain area of choice for a limited amount of time. We used it to decrease the activity in LM during learning of the visual association task. We found that the mice can still learn the task, but the latency to execute a decision is reduced. Preliminary results from mice with tau pathology in LM showed that their behavior is affected in a similar manner. These results suggest that the tau mutation causes a reduction in the neuronal activity; we plan to verify this using imaging to record activity in vivo.