Simon Gengler

TL;DR: A novel transgenic mouse model on a C57BL/6J genetic background that coexpresses KM670/671NL mutated amyloid precursor protein and L166P mutated presenilin 1 under the control of a neuron‐specific Thy1 promoter element (APPPS1 mice) is generated, well suited for studying therapeutic strategies and the pathomechanism of amyloidsosis by cross‐breeding to other genetically engineered mouse models.

TL;DR: Val(8)GLP-1 protected LTP in 9- and 18-month-old Alzheimer's disease mice when given for 3 weeks at 25 nmol/kg intraperitoneal injection, and LTP was enhanced in 18- month-old wild type mice, indicating that Val(8), an enzyme-resistant analogue of the incretin hormone glucagon-like peptide 1 also ameliorates age-related synaptic degenerative processes.

TL;DR: The results suggest that increased formation and aggregation of beta amyloid with aging is responsible for the impaired LTP with aging in this mouse model, while the transient increase of PPF at 6 months of age is caused by some other mechanism.

TL;DR: It is shown that injection of 3x10 nmol amyloid i.c.v. transiently impairs learning of a radial arm maze and the induction of hippocampal long-term potentiation and that these effects are reversible and therefore most likely do not involve neuronal death.

TL;DR: It is demonstrated that DA‐JC1 is neuroprotective in the 6‐OHDA brain lesion rat model of PD, and dual GLP‐1/GIP receptor agonists show promise as a novel treatment for PD.