作者: Jorge J. Palop , Lennart Mucke , Erik D. Roberson
DOI: 10.1007/978-1-60761-744-0_17
关键词:
摘要: High levels of Aβ impair neuronal function at least in part by disrupting normal synaptic transmission and causing dysfunction neural networks. This network includes abnormal synchronization activity resulting epileptiform activity. Over time, this aberrant can lead to the depletion calcium-dependent proteins, such as calbindin, Fos, Arc, compensatory inhibitory remodeling hippocampal circuits, including GABAergic sprouting ectopic expression neuropeptide Y (NPY) dentate granule cells. Here we present detailed protocols for detecting quantifying these alterations mouse models Alzheimer's disease (AD) immunohistochemistry. These methods are useful surrogate measures chronic AD epilepsy. In addition, since have found that severity changes relates degree Aβ-dependent cognitive impairments, biomarkers impairment AD.