Gui-Qiu Yu

TL;DR: It is concluded that Aβ is synaptotoxic even in the absence of plaques and that high levels of Aβ1–42 are insufficient to induce plaque formation in mice expressing wild-type hAPP, supporting the emerging view that plaque-independent Aβ toxicity plays an important role in the development of synaptic deficits in AD and related conditions.

TL;DR: It is reported that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus.

TL;DR: The results indicate that Aβ, tau, and Fyn jointly impair synaptic and network function and suggest that disrupting the copathogenic relationship between these factors could be of therapeutic benefit.

TL;DR: It is shown that a modest increase in astroglial TGF-β1 production in aged transgenic mice expressing the human β-amyloid precursor protein results in a three-fold reduction in the number of parenchymal amyloid plaques, and indicates that TGF -β1 might promote microglial processes that inhibit the accumulation of Aβ in the brain parenchyma.

TL;DR: It is demonstrated that CatB actually reduces levels of Abeta peptides, especially the aggregation-prone species Abeta1-42, through proteolytic cleavage, and likely fulfills antiamyloidogenic and neuroprotective functions.