ArticleNeurobiology of disease2018
Behavioral and SCN neurophysiological disruption in the Tg-SwDI mouse model of Alzheimer's disease.
Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The Neuroimmune Duality of CD4⁺ T Cells: Drivers of Damage and Repair in the Brain.Molecular neurobiology · 2026Review
- The sleep-wake cycle: molecular mechanisms, disorders, and therapeutic targets in the context of energy metabolism.Signal transduction and targeted therapy · 2026Review
- Neuronal microscale biophysical instability mediates macroscale network dynamics shaping pathological manifestations.bioRxiv : the preprint server for biology · 2026Article
- Exercise and neural circuit stability in early Alzheimer's disease: evidence across memory, executive, cholinergic, and circadian systems.Frontiers in aging neuroscience · 2026Review
- Glial cells are involved in day-night protein dysregulation in the hippocampus of a mouse model of Alzheimer's disease.Scientific reports · 2025Article
- Chronic Treatment of a Mouse Model of Cerebral Amyloid Angiopathy and Brain ATbioRxiv : the preprint server for biology · 2025Article
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Neuronal and glial vulnerability of the suprachiasmatic nucleus in tauopathies: evidence from human studies and animal models.Molecular neurodegeneration · 2024Review
- Dysregulated clock gene expression and abnormal diurnal regulation of hippocampal inhibitory transmission and spatial memory in amyloid precursor protein transgenic mice.Neurobiology of disease · 2021Article
- Defining circadian disruption in neurodegenerative disorders.The Journal of clinical investigation · 2021Review
- Evaluating Circadian Dysfunction in Mouse Models of Alzheimer's Disease: Where Do We Stand?Frontiers in neuroscience · 2020Review
- Disorders of Body Weight, Sleep and Circadian Rhythm as Manifestations of Hypothalamic Dysfunction in Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Disruption of circadian rhythms is commonly reported in individuals with Alzheimer's disease (AD). Neurons in the primary circadian pacemaker, the suprachiasmatic nucleus (SCN), exhibit daily rhythms in spontaneous neuronal activity which are important for maintaining circadian behavioral rhythms. Disruption of SCN neuronal activity has been reported in animal models of other neurodegenerative disorders; however, the effect of AD on SCN neurophysiology remains unknown. In this study we examined circadian behavioral and electrophysiological changes in a mouse model of AD, using male mice from the Tg-SwDI line which expresses human amyloid precursor protein with the familial Swedish (K670N/M671L), Dutch (E693Q), Iowa (D694N) mutations. The free-running period of wheel-running behavior was significantly shorter in Tg-SwDI mice compared to wild-type (WT) controls at all ages examined (3, 6, and 10 months). At the SCN level, the day/night difference in spike rate was significantly dampened in 6-8 month-old Tg-SwDI mice, with decreased AP firing during the day and an increase in neuronal activity at night. The dampening of SCN excitability rhythms in Tg-SwDI mice was not associated with changes in input resistance, resting membrane potential, or action potential afterhyperpolarization amplitude; however, SCN neurons from Tg-SwDI mice had significantly reduced A-type potassium current (I
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