Correlation between Alteration of Sharp-wave Ripple Coupled Cortical Oscillation and Long-term Memory Deficit in Alzheimer Disease Model Mice

Abstract

Alzheimer' s disease (AD) is the most common cause of dementia and is characterized by a progressive loss of cognitive function and additional neuropsychiatric symptoms. One of the earliest and most prominent symptoms of AD is episodic memory dysfunction [1][2][3][4]. Although the initial episodic memory deficit is well known, the details of amnesia progression with respect to memory storage process remains uncertain because of the variation in disease status of patients and memory tests [5][6][7]. Several human studies have suggested that episodic memory disruption in AD patients is due to ineffective consolidation or storage of new information [8][9][10][11]. These studies showed that AD patients rapidly forget encoded information as the disease progresses. In addition to investigations in humans, studies using AD mice models showed that long-term memory deficits precede short-term memory deficits [12,13]. These results indicate that there might be a sequential mechanism in the episodic memory dysfunction of AD; however, there is still a lack of explanation for these symptoms.Appropriate communication between the hippocampus and cortices is critical for proper future use of encoded information. According to previous studies, this interplay is extensively executed during slow wave sleep (SWS), which is characterized by large-amplitude delta waves [14][15][16][17]. Neural components related to previous events are reactivated, corresponding synaptic connections are strengthened, and irrelevant ones are globally scaled down during the unique oscillations of SWS [18][19][20]. Sharp-wave ripple (SWR) is a principal SWS oscillation generated in the hip-

Interictal epileptiform discharges affect memory in an Alzheimer’s Disease mouse model

“…Mice used in this study, APP/PS1 hemizygotes on a C57BL/6;C3H-congenetic background (JAX Stock No. 004462), have alterations in excitatory/inhibitory (E/I) balance but no known report of IEDs has been documented (Algamal et al, 2021; Algamal et al, 2022; Yang & Jeong 2021). Mice were implanted with a two-shank linear silicon probe in the hippocampus spanning the CA1 layers and the upper blade of the dentate gyrus (Fig.…”

Alzheimer’s disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression

“…Within the APP/PS1 mouse model, PV neuronal projections were increased to CA1 and CA3 pyramidal neurons at an early disease stage, with increased numbers of inhibitory synaptic clusters and synaptic proteins onto pyramidal cells (Hollnagel et al, 2019). There have also been observed differences in SWR coupling with other oscillatory patterns and differences in SWR features in the retrosplenial cortex in the same APP/PS1 mouse model (Yang and Jeong, 2021). Within the APP-KI mouse model, SWR duration was decreased and coordination between the hippocampus and the medial entorhinal cortex was impaired (Funane et al, 2022).…”