Yoon Cho, Cayzac S et al. in Neurobiol. Aging

Altered hippocampal information coding and network synchrony in APP-PS1 mice. Cayzac S, Mons N, Ginguay A, Allinquant B, Jeantet Y, Cho YH. Neurobiol Aging. 2015 Sep 1. pii: S0197-4580(15)00440-6. doi: 10.1016/j.neurobiolaging.2015.08.023

Yoon H Cho / Team leader: Neurobiology of behavior / INCIA

Alzheimer’s disease mice lost in space!

β-Amyloid peptide of different forms, the hallmark of Alzheimer’s disease (AD), is recognized as very harmful for synaptic transmission and function well before neuronal loss and therefore responsible for early cognitive and behavioral changes in AD.

In our recent paper, we described how the hippocampal single cell and population activity supporting spatial and memory representations might be altered in a mouse model expressing mutated human amyloid precursor protein and presenilin 1 genes. Adult AD mice with significant β-Amyloid were recorded for CA1 hippocampal cell activity while they learn a behavioral task in an operant chamber with nose-poke operanda.

We found that during the task learning the well known place cell activity in the hippocampus was less specific to animal’s location in AD mice as compared to those observed in normal mice. However, the hippocampal activity associated with other tasks and behaviors remained relatively unchanged in these transgenic mice. In addition, the two human mutations also were associated with a significant slowdown of hippocampal local oscillatory activity in the theta and ultra-fast ripple frequencies.

Our data enhance our understanding of how the AD related mutations may perturb in vivo cellular and network function to produce cognitive and other behavioral changes in early AD.
 

Schema: Altered place cell fring in a mouse model of Alzheimer’s disease mice