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Shared Transcriptomic Signatures Reveal Synaptic Pruning as a Link Between Alzheimer's Disease and Epilepsy
Abstract Alzheimer's disease (AD) and epilepsy (EP) exhibit a complex, bidirectional relationship, however, the molecular mechanisms underlying their comorbidity remain poorly understood. To address this gap, we analyzed large-scale transcriptomic datasets from pilocarpine-induced EP mouse models (n = 200), two AD mouse models expressing human tau (rTg4510) or amyloid precursor protein (J20) (n = 141), and transcriptomic profiles from AD and EP patient cohorts.
Shared Transcriptomic Signatures Reveal Synaptic Pruning as a Link Between Alzheimer's Disease and Epilepsy
Abstract Alzheimer's disease (AD) and epilepsy (EP) exhibit a complex, bidirectional relationship, however, the molecular mechanisms underlying their comorbidity remain poorly understood. To address this gap, we analyzed large-scale transcriptomic datasets from pilocarpine-induced EP mouse models (n = 200), two AD mouse models expressing human tau (rTg4510) or amyloid precursor protein (J20) (n = 141), and transcriptomic profiles from AD and EP patient cohorts.
Shared Transcriptomic Signatures Reveal Synaptic Pruning as a Link Between Alzheimer's Disease and Epilepsy
Abstract Alzheimer's disease (AD) and epilepsy (EP) share a complex, bidirectional relationship, yet the molecular basis of their comorbidity remains unclear. To address this, we analyzed publicly available large-scale transcriptomic datasets from pilocarpine-induced EP mouse models (n = 200), two AD mouse models expressing human tau (rTg4510) or amyloid precursor protein (J20) (n = 141), and transcriptomic profiles from AD and EP patient cohorts.
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