Raquel Sanchez-Varo

TL;DR: Evidence is shown of a switch in the activated microglia phenotype from alternative, at the beginning of Aβ pathology, to a classical at advanced stage of the disease in this model, induced by the age-dependent accumulation of extracellular soluble Aβ oligomers.

TL;DR: These early abnormalities in axonal and presynaptic structures might represent the morphological substrate of hippocampal dysfunction preceding synaptic and neuronal loss and could significantly contribute to AD pathology in the preclinical stages.

TL;DR: The age-dependent appearance of APP-derived soluble factors modulated the PI3K/Akt/GSK-3β signaling pathway through the major neurotrophin receptors and might provide insights into the selective vulnerability of specific neuronal groups in Alzheimer disease.

TL;DR: The data support the view that gal3 inhibition may be a potential pharmacological approach to counteract AD and demonstrate here for the first time a key role of gal3 in AD pathology.

TL;DR: Comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients and patients with Alzheimer’s disease is highlighted.