CSF levels of synaptosomal-associated protein 25 and synaptotagmin-1 in first-episode psychosis subjects

Chengai Xu, Carl M. Sellgren, Helena Fatouros-Bergman, Fredrik Piehl, Kaj Blennow, Henrik Zetterberg, Ann Brinkmalm, Alexander Frizell Santillo, Sofia Lundgren, Simon Cervenka, Göran Engberg, Sophie Erhardt, Karolinska Schizophrenia Project (KaSP) Consortium

Research output: Contribution to journalArticlepeer-review

1 Citation (SciVal)


Post-mortem studies consistently show evidence of reduced synaptic protein levels in patients with schizophrenia. Clinically high-risk subjects show a steeper decrease in grey matter thickness and in vitro modeling using patient-derived cells implicate excessive synaptic pruning during neurodevelopment as a part of the schizophrenia pathophysiology. However, it is unclear to what extent synapse elimination is present during various stages of the disease, which is of clinical importance as in a real-world setting most subjects received their first-episode psychosis (FEP) diagnosis not until their mid-twenties. In the present study, we measured cerebrospinal fluid (CSF) concentrations of the two pre-synaptic proteins synaptosomal-associated protein 25 (SNAP-25) and synaptotagmin-1 (SYT-1), both of which are increased in conditions of ongoing synaptic degeneration, in 44 FEP subjects (mean age 29.9 years) and 21 healthy controls (25.9 years) using immunoprecipitation mass spectrometry. Neither protein was found to differ between healthy controls and patients, and they showed no correlation with symptom ratings, cognitive performance or antipsychotic medication. Additional studies in high-risk subjects in the early prodromal phase will be needed to address if excessive synapse destruction occurs before the development of overt psychotic symptoms.

Original languageEnglish
Pages (from-to)136-142
Number of pages7
JournalIBRO Reports
Publication statusPublished - 2020 Jun

Subject classification (UKÄ)

  • Neurology
  • Psychiatry


  • Schizophrenia
  • SNAP-25
  • Synapse pruning
  • SYT-1


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