Topic: Tg2576 mice

We have previously shown a precocious and selective dopamine neurodegeneration in the Ventral Tegmental Area (VTA) of Tg2576 mice, a reliable experimental model of Alzheimer’s Disease (AD). In this model, the VTA neuronal loss causes the decrease of dopamine outflow in the Hippocampus and the Nucleus Accumbens, leading to impaired synaptic plasticity, memory and reward processing. Mesocorticolimbic system deficits are also reported in AD patients. Interestingly, pharmacological interventions aimed at improving DA levels ameliorate AD deficits in mice.However, drug-based treatments might cause

Some individuals with Alzheimer’s disease (AD) pathology exhibit cognitive resilience, offering promising prospects for identifying new therapeutic targets.Aims: Our hypothesis centers around the contribution of resilience to changes in excitatory synapses at the structural and molecular levels, which may underlie healthy cognitive performance in aged AD animals.Methods: We used Morris Water Maze tests, ELISA, western blots, stereological methods and immunoelectron microscopy.Results: Utilizing the Morris Water Maze test, we selected resilient (asymptomatic) and cognitively impaired aged-Tg257

Aim: Decrease in adult neurogenesis has been described to correlate with Alzheimer’s disease (AD) progression, and we have previously demonstrated a causal link between Amyloid-beta oligomers (AβOs) accumulation in adult neural stem cells (NSCs) and reduced subventricular zone (SVZ) neurogenesis in AD Tg2576 mouse model at pre-symptomatic stage. Here we investigated if AβOs targeting in the dentate gyrus of AD mice, both at pre-symptomatic and symptomatic stage, can rescue adult hippocampal neurogenesis (AHN) and recover AD-related memory deficits. Methods: Using a disease modifying gene-thera