Topic: amyloid-beta peptide

Alzheimer’s disease (AD) is characterized by a long asymptomatic phase associated with the toxic accumulation of oligomeric form of amyloid-beta peptide (Aβo). One of the first event reported in this phase seems to be a specific hippocampal hyperactivity in both humans and AD mouse model. We highlighted that this early hyperactivity starts with an abnormal increase of calcium activity in astrocytes which affects neighbouring neurons in the hippocampus. We identified an astrocytic calcium channel, transient receptor potential ankyrin-1 (TRPA1), implicated in the Aβo-induced hippocampal hyperact

Alzheimer's disease (AD), the leading cause of dementia, has traditionally been described as a pathology primarily affecting cognitive function with impaired neuronal and glial functioning. However, recent studies suggest that more than 75% of patients exhibit early emotional perturbations and that cerebrovascular remodeling could underlie these cognitive and emotional impairments. The aim of this study was to characterize the time of onset of anxio-depressive-like phenotype in a mouse model of AD and their potential correlation with blood-brain barrier (BBB) dysfunctions already described by