부산대학교 도서관

It is becoming increasingly clear that dysfunction of the EC may play a role in the early stages of AD. Evidence for this notion comes from studies using in vivo electrophysiological recordings in mouse models of AD and brain imaging of AD patients. Deficits of memory and spatial navigation related to EC dysfunction are also being elucidated. Such deficits, for instance in path integration, have potential to be used as early behavioral biomarkers for the detection of AD, even at the early period currently defined as the 'preclinical stage'. Layer 2 neurons in the EC are one of the candidate neuron types causing EC dysfunction, and studies are underway to clarify their exact roles in the pathogenesis of EC dysfunction. Studies to elucidate the molecular pathways causing EC dysfunction are also currently underway. High-throughput sequencing techniques are starting to pinpoint candidate genes. Better understanding of the network, cellular, and molecular mechanisms of EC dysfunction may lead to future prevention of disease progression at the early stage of AD. The entorhinal cortex (EC) is the brain region that often exhibits the earliest histological alterations in Alzheimer's disease (AD), including the formation of neurofibrillary tangles and cell death. Recently, brain imaging studies from preclinical AD patients and electrophysiological recordings from AD animal models have shown that impaired neuronal activity in the EC precedes neurodegeneration. This implies that memory impairments and spatial navigation deficits at the initial stage of AD are likely caused by activity dysfunction rather than by cell death. This review focuses on recent findings on EC dysfunction in AD, and discusses the potential pathways for mitigating AD progression by protecting the EC. [ABSTRACT FROM AUTHOR]