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• W1569894857 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 A lzheimer's disease ( AD ), there is early loss of synaptic proteins, but these have been little studied in VAD . Materials and Methods We measured synaptophysin, postsynaptic density protein 95 ( PSD ‐95), drebrin, synaptosomal‐associated protein 25 ( SNAP ‐25) and vascular endothelial growth factor ( VEGF ) by enzyme‐linked immunosorbent assays in superior temporal cortex from 11 patients with VAD and, initially, 11 non‐dementia controls. We 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." @default.
• W1569894857 created "2016-06-24" @default.
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• W1569894857 date "2015-04-23" @default.
• W1569894857 modified "2023-10-03" @default.
• W1569894857 title "Synaptic protein levels altered in vascular dementia" @default.
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• W1569894857 doi "https://doi.org/10.1111/nan.12215" @default.
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