ArticleFrontiers in molecular neuroscience2017
Amino-Terminal β-Amyloid Antibody Blocks β-Amyloid-Mediated Inhibition of the High-Affinity Choline Transporter CHT.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- A lifespan staging model of basal forebrain cholinergic vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Cholinergic Reinforcement Signaling Is Impaired by Amyloidosis Prior to Its Synaptic Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Personalized Management and Treatment of Alzheimer's Disease.Life (Basel, Switzerland) · 2022Review
- Pharmacogenomics of Alzheimer's Disease: Novel Strategies for Drug Utilization and Development.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Serum unsaturated phosphatidylcholines predict longitudinal basal forebrain degeneration in Alzheimer's disease.Brain communications · 2022Article
- Fas Apoptosis Inhibitory Molecule Blocks and Dissolves Pathological Amyloid-β Species.Frontiers in molecular neuroscience · 2021Article
- Relationships between Mitochondrial Dysfunction and Neurotransmission Failure in Alzheimer's Disease.Aging and disease · 2020Review
- Homomeric and Heteromeric Aβ Species Exist in Human Brain and CSF Regardless of Alzheimer's Disease Status and Risk Genotype.Frontiers in molecular neuroscience · 2019Article
- Soluble Aβ42 Acts as Allosteric Activator of the Core Cholinergic Enzyme Choline Acetyltransferase.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a common age-related neurodegenerative disorder that is characterized by progressive cognitive decline. The deficits in cognition and attentional processing that are observed clinically in AD are linked to impaired function of cholinergic neurons that release the neurotransmitter acetylcholine (ACh). The high-affinity choline transporter (CHT) is present at the presynaptic cholinergic nerve terminal and is responsible for the reuptake of choline produced by hydrolysis of ACh following its release. Disruption of CHT function leads to decreased choline uptake and ACh synthesis, leading to impaired cholinergic neurotransmission. We report here that cell-derived β-amyloid peptides (Aβ) decrease choline uptake activity and cell surface CHT protein levels in SH-SY5Y neural cells. Moreover, we make the novel observation that the amount of CHT protein localizing to early endosomes and lysosomes is decreased significantly in cells that have been treated with cell culture medium that contains Aβ peptides released from neural cells. The Aβ-mediated loss of CHT proteins from lysosomes is prevented by blocking lysosomal degradation of CHT with the lysosome inhibitor bafilomycin A1 (BafA
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.