Beta-amyloid induced increase in choline flux across PC12 cell membranes
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Acknowledgements
This work was supported by the NIA Intramural Program. The authors would like to thank Dr. Gerald Ehrenstein for inspiration and insightful discussions and Dr. Kishena Wadhwani for his help at the beginning of the project.
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Compartmental modeling and analysis of the effect of β-amyloid on acetylcholine neurocycle via choline leakage hypothesis
2021, Computers and Chemical EngineeringCitation Excerpt :Furthermore, soluble Aβ oligomer aggregates are rarely targeted by therapeutics due to their very low concentrations in AD brains compared to the insoluble oligomers (Atwood et al., 2003). Aβ oligomers prevent glutamate to transport in cultured astrocytes and could alter the concentration of salts and nutrients through cellular membrane as well (Allen et al., 1997). The aggregation of Aβ peptides and their plaques deposition in the central nervous system (CNS) cause a loss of neurons and a lack of acetylcholine (ACh) which is considered the main symptoms of AD (Contestabile, 2011; Davies and Maloney, 1976).
Altered gene expression and neuropathology in Alzheimer's disease
2006, Neurobiology of AgingGlycerophosphocholine is elevated in cerebrospinal fluid of Alzheimer patients
2004, Neurobiology of AgingAmyloid β peptides and central cholinergic neurons: Functional interrelationship and relevance to Alzheimer's disease pathology
2004, Progress in Brain ResearchCitation Excerpt :Whether Aβ peptides induce toxicity in cholinergic neurons by interacting with any of these receptor subtypes remain to be established. However, it has been demonstrated that 24 h exposure to μM Aβ1–40 can increase choline fluxes from PC12 cells (Allen et al., 1997). If μM Aβ peptide does so in cholinergic neurons, it is likely that the observed vulnerability could partly be the consequence of a concomitant decrease in the uptake and an increase leakage of choline from the neurons.
6β-Acetoxy nortropane regulated processing of amyloid precursor protein in CHOm<inf>1</inf> cells and rat brain
2003, European Journal of Pharmacology
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Present address: Department of Dynamic Pathology, Research Institute of Neurological Diseases and Geriatrics, Kyoto Prefectural University of Medicine, 465 Kajii, Hirokoji, Kawaramachi, Kyoto, 602 Japan.