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2015 ; 10
(9
): e0137357
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Analyzing and Modeling the Kinetics of Amyloid Beta Pores Associated with
Alzheimer s Disease Pathology
#MMPMID26348728
Ullah G
; Demuro A
; Parker I
; Pearson JE
PLoS One
2015[]; 10
(9
): e0137357
PMID26348728
show ga
Amyloid beta (A?) oligomers associated with Alzheimer's disease (AD) form
Ca2+-permeable plasma membrane pores, leading to a disruption of the otherwise
well-controlled intracellular calcium (Ca2+) homeostasis. The resultant
up-regulation of intracellular Ca2+ concentration has detrimental implications
for memory formation and cell survival. The gating kinetics and Ca2+ permeability
of A? pores are not well understood. We have used computational modeling in
conjunction with the ability of optical patch-clamping for massively parallel
imaging of Ca2+ flux through thousands of pores in the cell membrane of Xenopus
oocytes to elucidate the kinetic properties of A? pores. The fluorescence
time-series data from individual pores were idealized and used to develop
data-driven Markov chain models for the kinetics of the A? pore at different
stages of its evolution. Our study provides the first demonstration of developing
Markov chain models for ion channel gating that are driven by optical-patch clamp
data with the advantage of experiments being performed under close to
physiological conditions. Towards the end, we demonstrate the up-regulation of
gating of various Ca2+ release channels due to A? pores and show that the extent
and spatial range of such up-regulation increases as A? pores with low open
probability and Ca2+ permeability transition into those with high open
probability and Ca2+ permeability.
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