Cerebrospinal fluid cyclase-associated protein 2 is increased in Alzheimer’s disease and correlates with tau pathology

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Synaptic dysfunction represents an early pathological event that precedes neurodegeneration in Alzheimer's disease (AD), even though the molecular mechanisms that underlie synaptic dysfunction remain to be completely understood [1,2].Nonetheless, in vivo synaptic biomarkers are highly relevant as they have the potential to reveal early-stage changes and to track target engagement of specific disease-modifying strategies.A range of cerebrospinal fluid (CSF) synapse-related biomarkers including neurogranin, GAP43, SNAP25, neuregulin-1, PSD-95 and neuronal pentraxin have indeed been reported in AD at variance with other dementing illnesses [1-3].This work focused on the cyclase-associated protein 2 (CAP2), a postsynaptic actin-binding protein that governs actin cytoskeleton dynamics in dendritic spines.CAP2 is expressed in the brain and in a limited range of tissues.CAP2 downregulation differently affects neuronal and dendritic spine morphology in cerebral cortex and hippocampus [4,5].In excitatory neurons, CAP2 regulates cofilin activity and actin cytoskeleton dynamics in spines.CAP2 dimerization is crucial for the long-term potentiation-induced cofilin translocation into spines and structural spine remodelling.This mechanism has

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