ArticleCerebral cortex (New York, N.Y. : 1991)2020
Preserved Calretinin Interneurons in an App Model of Alzheimer's Disease Disrupt Hippocampal Inhibition via Upregulated P2Y1 Purinoreceptors.
Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Methodology for human-induced pluripotent stem cell-derived excitatory and inhibitory neuron coculture with astrocytes for Alzheimer's disease modelling.Brain communications · 2026Article
- Hippocampal Interneurons Shape Spatial Coding Alterations in Neurological Disorders.Molecular neurobiology · 2025Review
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Quantification and correlation of amyloid-β plaque load, glial activation, GABAergic interneuron numbers, and cognitive decline in the young TgF344-AD rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Astrocytes Lingering at a Crossroads: Neuroprotection and Neurodegeneration in Neurocognitive Dysfunction.International journal of biological sciences · 2025Review
- Bats as instructive animal models for studying longevity and aging.Annals of the New York Academy of Sciences · 2024Review
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
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- P2Y1R silencing in Astrocytes Protected Neuroinflammation and Cognitive Decline in a Mouse Model of Alzheimer's Disease.Aging and disease · 2024Article
- Advances in Therapeutics to Alleviate Cognitive Decline and Neuropsychiatric Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Review
- Age-Dependent Sex Differences in Perineuronal Nets in anInternational journal of molecular sciences · 2023Article
- Presubiculum principal cells are preserved from degeneration in knock-in APP/TAU mouse models of Alzheimer's disease.Seminars in cell & developmental biology · 2023Article
- The fate of interneurons, GABABrain pathology (Zurich, Switzerland) · 2023Review
- Local and long-range GABAergic circuits in hippocampal area CA1 and their link to Alzheimer's disease.Frontiers in neural circuits · 2023Review
- P2Y1 Receptor as a Catalyst of Brain Neurodegeneration.NeuroSci · 2022Review
- Delineating selective vulnerability of inhibitory interneurons in Alpers' syndrome.Neuropathology and applied neurobiology · 2022Article
- Alzheimer's Disease Enhanced Tonic Inhibition is Correlated With Upregulated Astrocyte GABA Transporter-3/4 in a Knock-InFrontiers in pharmacology · 2022Article
- Mutual Interactions between Brain States and Alzheimer's Disease Pathology: A Focus on Gamma and Slow Oscillations.Biology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
To understand the pathogenesis of specific neuronal circuit dysfunction in Alzheimer's disease (AD), we investigated the fate of three subclasses of "modulatory interneurons" in hippocampal CA1 using the AppNL-F/NL-F knock-in mouse model of AD. Cholecystokinin- and somatostatin-expressing interneurons were aberrantly hyperactive preceding the presence of the typical AD hallmarks: neuroinflammation and amyloid-β (Aβ) accumulation. These interneurons showed an age-dependent vulnerability to Aβ penetration and a reduction in density and coexpression of the inhibitory neurotransmitter GABA synthesis enzyme, glutamic acid decarboxylase 67 (GAD67), suggesting a loss in their inhibitory function. However, calretinin (CR) interneurons-specialized to govern only inhibition, showed resilience to Aβ accumulation, preservation of structure, and displayed synaptic hyperinhibition, despite the lack of inhibitory control of CA1 excitatory pyramidal cells from midstages of the disease. This aberrant inhibitory homeostasis observed in CA1 CR cells and pyramidal cells was "normalized" by blocking P2Y1 purinoreceptors, which were "upregulated" and strongly expressed in CR cells and astrocytes in AppNL-F/NL-F mice in the later stages of AD. In summary, AD-associated cell-type selective destruction of inhibitory interneurons and disrupted inhibitory homeostasis rectified by modulation of the upregulated purinoreceptor system may serve as a novel therapeutic strategy to normalize selective dysfunctional synaptic homeostasis during pathogenesis of AD.
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