Synaptic protein levels altered in vascular dementia

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Abstract

INTRODUCTION: Cerebral ischaemia is the defining pathophysiological abnormality in most forms of vascular dementia (VAD) but the pathogenesis of the dementia remains poorly understood. In Alzheimer's disease (AD), there is early loss of synaptic proteins but these have been little studied in VAD.

MATERIALS & METHODS: We measured synaptophysin, post-synaptic density protein 95 (PSD-95), drebrin, synaptosomal-associated protein 25 (SNAP-25) and vascular endothelial growth factor (VEGF) by ELISA in superior temporal cortex from 11 patients with VAD and, initially, 11 non-dementia controls, and corrected for neuronal content by measurement of neuron-specific enolase. A further 11 controls were subsequently used in a validation study. Simulation of post-mortem delay found that PSD-95 was stable at 4°C but declined slightly at RT. SNAP-25 and drebrin showed good post-mortem stability. Previous studies had shown good post-mortem preservation of synaptophysin and VEGF.

RESULTS: The VAD cases had lower synaptophysin (but p > 0.05 in initial study), significantly lower SNAP-25 (p = 0.024) and significantly higher drebrin (p = 0.020). On comparison with the second control group, the reduction in synaptophysin was significant (p = 0.008) and the other results were confirmed.

CONCLUSION: There is probably a reduction in presynaptic proteins in the temporal cortex in VAD, although not as marked as in AD. In VAD, there is also an increase in drebrin, which may be a response to reduced synaptic input.

Original languageEnglish
Pages (from-to)533-543
Number of pages11
JournalNeuropathology and Applied Neurobiology
Volume41
Issue number4
Early online date5 Jan 2015
DOIs
Publication statusPublished - 1 Jun 2015

Keywords

  • Apolipoproteins E
  • DLG4 protein human
  • Drebrins
  • SNAP 25 protein human
  • Synaptophysin
  • Vascular dementia

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