Cortical synapse loss in progressive supranuclear palsy

Eileen H. Bigio*, Mary Beth Vono, Sivapong Satumtira, Jennifer Adamson, Estelle Sontag, Linda S. Hynan, Charles L. White, Matt Baker, Mike Hutton

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


Cortical synapse loss, the probable substrate of cognitive impairment in Alzheimer disease (AD), has not previously been evaluated in progressive supranuclear palsy (PSP). Hypothesizing that synapse loss would be greater in demented than non-demented PSP patients, we examined synaptophysin concentrations in 8 cases of PSP (5 demented and 3 non-demented cases). We found a decrease in mean synaptophysin concentration in these 8 cases in frontal, temporal, and parietal lobes, and in cerebellum, compared to the means in corresponding lobes of 16 controls. The decreases were similar to those in 28 cases of AD, but not as great. We determined synaptophysin concentration from motor cortex in only 4 of our PSP cases, 2 demented and 2 non-demented. The average concentrations in these 4 cases were lower than in AD motor cortex; both were lower than controls. When demented and non-demented PSP cases were compared, neocortical synaptophysin concentrations in non-demented PSP cases were lower than in demented cases. There appears to be a link between AD and PSP, in that synapse loss is found in both. However, the basis and significance of the prominent neocortical synapse loss in PSP. especially in non-demented subjects, remain to be explored.

Original languageEnglish (US)
Pages (from-to)403-410
Number of pages8
JournalJournal of neuropathology and experimental neurology
Issue number5
StatePublished - May 2001


  • Cognition
  • Cognitive state
  • Dementia
  • Progressive supranuclear palsy
  • Synapse
  • Synaptophysin
  • Tau

ASJC Scopus subject areas

  • General Medicine


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