Topic: amyloid-beta (Aβ)

Aggregation of amyloid-beta (Aβ) is among the earliest pathological changes in Alzheimer's disease (AD, Kamenetz et al., 2003). In some individuals, however, memory and other cognitive functions remain intact, despite the presence of abundant Aβ pathology (Stern, 2012). This suggests that neurons and networks can recruit mechanisms that protect against Aβ pathology, a concept known as cognitive resilience (CR). Notably, this occurs in a sex-dependent manner, with greater CR in females (Buckley et al., 2019, Ossenkoppele et al., 2020).The underlying mechanisms of resilience to AD pathology rema

Background: Alzheimer's disease (AD) is a neurological disease characterised pathologically by loss of synapses and neurones, accumulation of amyloid-beta (Aβ) deposits and formation of neurofibrillary tangles. This results in progressive cognitive impairment as people age. Ganaxolone, a synthetic analogue of allopregnanolone, has shown a protective effect on gliosis associated with demyelination. However, its effect on Aβ deposits and neuronal loss associated with AD is still unknown. Additionally, its effect on liver x receptors (LXR) has not yet been reported. In this study, we investigated