Aurélien M. Badina

Introduction Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease, affecting 3–4% of people over 60 years old in Europe, Asia and America,1 with ageing populations driving increasing global incidence. Brain glucose hypometabolism is a well-described characteristic of AD.

Abstract Multiple lines of evidence point to peripheral immune alterations in bipolar disorder (BD) although the activity of brain immune mechanisms remain largely unexplored. To identify the cell type-specific immune alterations in the BD brain, we performed a proteomic and single nuclear transcriptomic analysis of postmortem cingulate cortex samples from BD and control subjects. Our results showed that genes associated to the genetic risk for BD are enriched in microglia and astrocytes.

Abstract Clinical and translational research has identified deficits in the dopaminergic neurotransmission in the striatum in Alzheimer's disease (AD) and this could be related to the pathophysiology of psychiatric symptoms appearing even at early stages of the pathology. We hypothesized that AD pathology in the hippocampus may influence dopaminergic neurotransmission even in the absence of AD-related lesion in the mesostriatal circuit.