Topic: oAβ1-42

Alzheimer’s disease (AD) early stages are characterized by amyloid beta oligomers (oAβ) toxicity in the hippocampus, leading to its dysfunction. Previously, we characterized a non-transgenic mouse model of early amyloidosis by a single intracerebroventricular (icv.) injection of oAβ1-42, that showed deficient hippocampal-dependent memory and synaptic plasticity impairment in the CA1–CA3 synapse regardless the sex. Social memory impairments have also been described in AD. However, neuronal oscillatory activity in hippocampal CA2 subfield, a region that plays a crucial role in the formation and

The Promyelocytic Leukemia Protein (PML) originally characterized as a tumor suppressor1, regulates various biological processes, such as gene transcription2, cell cycle3,4, DNA damage responses and apoptosis. In the nervous system, PML was shown to balance proliferation vs differentiation of neural progenitors5,6and have a neuroprotective action during early cerebral ischemia7,8. Recently, PML was categorized as a hub gene for AD and complexes9. Although PML protein was reported to regulate neuronal plasticity, misfolded protein degradation, aging and stress10, yet its role in Alzheimer’s dis