ArticleAlzheimer's research & therapy2024
Cholecystokinin B receptor agonists alleviates anterograde amnesia in cholecystokinin-deficient and aged Alzheimer's disease mice.
Article in Alzheimer's research & therapy, 2024. 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.
- Excitatory cholecystokinin neurons in the CA3 area regulate the navigation learning and neuroplasticity.eLife · 2026Article
- NLP-12/Cholecystokinin signaling stabilizes sensory dendritic structure and protects neuronal healthspan inbioRxiv : the preprint server for biology · 2026Article
- Entorhinal Cholecystokinin in Alzheimer's Disease: Its Earliest Vulnerability and Rescue Effects Across Different Disease Stages in a Mouse Model.Cellular and molecular neurobiology · 2026Article
- Discovery of a β-arrestin-biased CCKBR agonist that blocks CCKBR-dependent long-term potentiation.Nature communications · 2025Article
- Cell Type Specific Inference of Perturbations in Synaptic Communication with MultiNeuronChat.bioRxiv : the preprint server for biology · 2025Article
- Central neuropeptides as key modulators of astrocyte function in neurodegenerative and neuropsychiatric disorders.Psychopharmacology · 2025Review
- Cholecystokinin facilitates the formation of long-term heterosynaptic plasticity in the distal subiculum.Communications biology · 2025Article
- A review on recent advances in Alzheimer's disease: The role of synaptic plasticity.AIMS neuroscience · 2025Review
- Cholecystokinin neurotransmission in the central nervous system: Insights into its role in health and disease.BioFactors (Oxford, England)Review
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12 authors.
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Abstract
backgroundAs one major symptom of Alzheimer's disease (AD), anterograde amnesia describes patients with an inability in new memory formation. The crucial role of the entorhinal cortex in forming new memories has been well established, and the neuropeptide cholecystokinin (CCK) is reported to be released from the entorhinal cortex to enable neocortical associated memory and long-term potentiation. Though several studies reveal that the entorhinal cortex and CCK are related to AD, it is less well studied. It is unclear whether CCK is a good biomarker or further a great drug candidate for AD.
methodsmRNA expressions of CCK and CCK-B receptor (CCKBR) were examined in two mouse models, 3xTg AD and CCK knock-out (CCK
resultsAged 3xTg AD mice exhibited reduced CCK mRNA expression in the entorhinal cortex but reduced CCKBR expression in the neocortex and hippocampus, and impaired cognition and neuroplasticity comparable with CCK
conclusionsHere we provide more evidence to support the role of CCK in learning and memory and its potential to treat AD. We elaborated on the rescue effect of a promising novel drug, HT-267, on aged 3xTg AD mice. Although the physiological etiology of CCK in AD still needs to be further investigated, this study sheds light on a potential pharmaceutical candidate for AD and dementia.
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