Targeting Dementia by Tackling Synaptic Tau
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Patrik Verstreken, Ph.D.
Scientific Director & Group Leader
VIB-KU Leuven Center for Neuroscience, Belgium
Patrik Verstreken, Ph.D., is a distinguished neuroscientist and Director of the VIB-KU Leuven Center for Brain & Disease Research whose work has advanced understanding of synaptic function in health and neurodegenerative disease. His laboratory investigates the proteins, lipids, mitochondria, and cellular pathways that sustain neuronal communication and how their disruption contributes to Parkinson’s disease and tauopathies. Using fruit flies, mice, and human stem cell-derived neurons, Dr. Verstreken has identified key synaptic and organelle defects associated with neurodegeneration and strategies to counter them. His research is revealing fundamental mechanisms of brain disease and potential avenues for therapeutic intervention.
Summary
Synaptic dysfunction is an early pathological feature of Tau-associated neurodegenerative diseases, including Alzheimer’s disease. Targeting early synaptic dysfunction may offer therapeutic benefits by helping to prevent cognitive decline and disease progression; however, the mechanisms underlying Tau-associated synaptic defects remain unclear. Under disease conditions in patients and animal models of Tau-related disease, Tau becomes mislocalized to pre- and postsynaptic compartments. Recent work demonstrates that presynaptic Tau contributes to synaptic defects.
The presentation will highlight research showing that disrupting this synaptic function of Tau can prevent Tau-induced synaptic loss and cognitive decline. It will also discuss future studies examining how this same process may function under normal physiological conditions to sculpt and protect the brain. This work not only identifies new presynaptic roles for Tau but also points to a potential therapeutic opportunity for addressing early synaptic dysfunction and cognitive decline in neurodegenerative disease.
Learning Objectives:
- That Tau-induced synaptic dysfunction is an early feature in the course of dementia.
- That it is possible to interfere with Tau-induced synaptic decline and rescue cognitive decline in animal models, i.e. recognise the therapeutic potential of targeting early synaptic dysfunction in Tau-associated disorders.
- Discuss emerging insights into the physiological roles of Tau at the synapse (and beyond), and that these functions may teach us about Tau-induced disease.
This page was last updated on Wednesday, August 26, 2026