Topic: APP/PS1 mouse model

Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by a significant decline in episodic memory. More recent research indicates that impairments in spatial navigation may serve as a more sensitive biomarker for AD compared to episodic memory alterations. To study the cellular mechanisms behind spatial memory and navigation deficits in AD we used the APP/PS1 mouse model of amyloidosis. To assess spatial memory updating, a non-stressful paradigm called Objects in Updated Locations (OUL) was employed. This task allows the quantification of the different times of ex

Age and sex are major risk factors in Alzheimer’s disease (AD) with a higher incidence of the disease in females. Chronic microglial activation and dysregulated neuro-inflammation are features of AD and may contribute to disease pathogenesis in a sexually dimorphic manner. We investigated sex differences in microglia in the APP/PS1 mouse model of Alzheimer’s disease and in post mortem brain tissue from patients with Alzheimer’s disease. Here we report elevated levels of activated, iron-laden and dystrophic microglia in the cortex and hippocampus of female APP/PS1 mice, and in post mortem tissu

Soluble amyloid precursor protein-alpha (sAPPα) plays critical roles in healthy brain functions, including cognition, suggesting that it may be a useful therapeutic for the treatment of neurological disorders such as Alzheimer’s disease (AD). Recombinant adeno-associated viruses (AAV) carrying therapeutic transgenes may provide a therapeutically useful delivery strategy. Recently, modified AAV capsids have been designed that cross the blood-brain barrier (BBB) of mice and transduce cells throughout the brain. We investigated if one such capsid, AAV-PHP.eB, could deliver either the human sAPPα