Topic: Amyloidosis

Alzheimer’s disease (AD) is a neurodegenerative disease and the most common cause of dementia. Amyloidosis mediated by amyloid-beta(1-42) is a key factor in the pathophysiology of the disease. Braak staging of AD proposes that AD begins in the olfactory system, progressing then through the lateral entorhinal cortex to the hippocampus, whereupon symptoms of dementia become apparent. Intracerebral inoculation of healthy rodents with oligomeric amyloid-beta(1-42) results in impairments of hippocampal information processing and storage (doi: 10.3389/fnbeh.2015.00103).To what extent this also affec

Alzheimer’s disease (AD) represents an urgent yet unmet challenge for modern society, calling for exploration of innovative targets and therapeutic approaches. Astrocytes, considering their crucial functions in the CNS, represent promising cell-target.Our aim was to investigate if deletion of the regulatory CaNB1 subunit of calcineurin in astrocytes could mitigate AD-related memory deficits, neuropathology and neuroinflammation.We have generated two, acute and chronic, AD mouse models with astrocytic CaNB1 deletion (ACN-KO). In the acute one we evaluated the ability of β-amyloid oligomers (AβO