Amyloid-β Peptides Disrupt Interactions Between VAMP-2 and SNAP-25 in Neuronal Cells as Determined by FRET/FLIM.

Journal of Alzheimer's Disease : JAD
Nidhi ShardaKarunya K Kandimalla

Abstract

Synaptic dysfunction prevalent in Alzheimer's disease (AD) brain is closely associated with increased accumulation of amyloid-β (Aβ) peptides in the brain parenchyma. It is widely believed that Aβ peptides trigger synaptic dysfunction by interfering with the synaptic vesicular fusion and the release of neurotransmitters, primarily facilitated by the SNARE protein complexes formed by VAMP-2, SNAP-25, and syntaxin-1. However, Aβ interactions with SNARE proteins to ultimately disrupt synaptic vesicular fusion are not well understood. Our objective is to elucidate mechanisms by which Aβ peptides perturb SNARE complexes. Intensity (qualitative) and lifetime (quantitative) based measurements involving Forster (fluorescence) resonance energy transfer (FRET) followed by fluorescence lifetime imaging microscopy (FLIM) were employed to investigate the effect of Aβ peptides on dynamic interactions between VAMP-2, labeled with cerulean (Cer) at the N-terminus (FRET donor), and SNAP-25 labeled with citrine (Cit) on the N-terminus (FRET acceptor). The FRET and FLIM interactions at the exocytosis locations on the pre-synaptic membrane were recorded under spontaneous and high potassium evoked conditions. Moreover, cellular accumulation of fluo...Continue Reading

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Citations

Feb 2, 2021·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Feng ChenYan Wang
Dec 12, 2020·The Journal of Pharmacology and Experimental Therapeutics·Nidhi ShardaKarunya K Kandimalla
Mar 24, 2021·Chemical Reviews·Christian WernerChristian Geis

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