Topic: hippocampal neuroinflammation

Recent preclinical and clinical observations identified alterations in the midbrain along the prodromal phase of Alzheimer’s disease (AD). These alterations include degeneration of monoamine neurons, resulting in deficits in ascending monoaminergic pathways in target areas related to AD, as the hippocampus. Incidentally, recent findings link the role of monoamines in the modulation of neuroinflammation.Here we sought to prove how the degeneration of the midbrain, leading to monoamine loss in the hippocampus, activates a neuroinflammatory response, in addition to alterations of synaptic plastic

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