Topic: amyloid beta (Aβ)

Galectin-3 is upregulated in Alzheimer's Disease (AD) and has been shown to promote amyloid beta (Aβ) oligomerisation and plaque formation. However, little is known about the effect of galectin-3 on neural cells. Our work aims to determine the effect of galecitn-3 on neurogenesis and on glial clearance of Aβ. Neurospheres generated from primary murine neural stem cells were treated with galectin-3 or the galectin-3 inhibitor TD139. Proliferation, as determined by neurosphere size after 5 days, was decreased in neurospheres treated with galectin-3. Differentiation, as quantified by proportion o

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and inability to perform daily activities. Recent research has implicated tumor necrosis factor-alpha (TNF-α) in the pathogenesis of AD. Elevated levels of TNF-α have been detected in the blood of patients with AD, and TNF-α has been observed in amyloid beta (Aβ) plaques. Despite the promising results from preclinical studies, the efficacy of TNF-α blockade as a therapeutic strategy for AD remains controversial. However, it remains unclear whether and how TNF-α influences the amyloidogenic p

The reduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer’s Disease (AD), but an underlying assumption that neurons are the main source of pathogenic Aβ remains untested. Here we show that oligodendrocytes produce significant amounts of Aβ, which in turn promotes abnormal neuronal hyperactivity in AD. Initially, we assessed publicly available single cell RNA-sequencing and proteomics databases and showed that oligodendrocytes express all the components required to produce Aβ. By employing RNAscope in situ hybridisation we revealed that the brains of AD patients ha