Thorsten Pflanzner

TL;DR: Genetic evidence that LRP1 modulates the pathogenic actions of soluble Aβ in the brain by clearing Aβ across the blood-brain barrier is presented for the first time.

TL;DR: The data identify a previously unrecognized mechanism linking CRP and brain edema formation and present a signaling pathway that offers new sites of therapeutic intervention.

TL;DR: It is shown that LeX‐glycosylated LRP1 is also expressed in the stem cell compartment of the developing spinal cord and has broader functions in the developing CNS, suggesting that LRP 1 facilitates NSPCs differentiation via interaction with apolipoprotein E (ApoE).

TL;DR: Current knowledge and views on the major pathogenetic mechanisms of Alzheimer's disease, including modulation of γ-secretase activity, the activation of the peroxisome proliferator- activated receptor-γ, binding to prostaglandin receptors or interactions at the blood-brain barrier, and the potential as future AD therapeutics are reviewed.

TL;DR: It is found that the cellular prion protein (PrPc), a putative receptor implicated in mediating Aβ neurotoxicity in Alzheimer's disease (AD), participates in Aβ transcytosis across the blood—brain barrier.