Background:
Clinical evidence indicates that patients affected by Alzheimer's Disease (AD)
fail to form new memories although their memories for old events are intact. This amnesic pattern depends
on the selective vulnerability to AD-neurodegeneration of the hippocampus, the brain region that
sustains the formation of new memories, while cortical regions that store remote memories are spared.
Objective:
To identify the cellular mechanisms underlying impaired recent memories and intact remote
memories in a mouse model of AD.
Method:
Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and
anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected
to the Contextual Fear Conditioning (CFC) task or in naïve conditions.
Results:
Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and
anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected
to the Contextual Fear Conditioning (CFC) task or in naïve conditions.
Conclusion:
Our data suggest that in the early AD stages synaptic plasticity of CA1 synapses, crucial
to form new memories, is lost, while plasticity of aCC synapses is intact and contributes to the persistence
of long-term memories.
Deficits in Adult Neurogenesis, Contextual Fear Conditioning, and Spatial Learning in a Gfap Mutant Mouse Model of Alexander Disease