Teacher: Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.
Teacher: Now, understand the problem? If you are still confused, see the following example:
Context: Architecturally, the school has a Catholic character. Atop the Main Building's gold dome is a golden statue of the Virgin Mary. Immediately in front of the Main Building and facing it, is a copper statue of Christ with arms upraised with the legend 'Venite Ad Me Omnes'. Next to the Main Building is the Basilica of the Sacred Heart. Immediately behind the basilica is the Grotto, a Marian place of prayer and reflection. It is a replica of the grotto at Lourdes, France where the Virgin Mary reputedly appeared to Saint Bernadette Soubirous in 1858. At the end of the main drive (and in a direct line that connects through 3 statues and the Gold Dome), is a simple, modern stone statue of Mary.
Question: To whom did the Virgin Mary allegedly appear in 1858 in Lourdes France?
Solution: Saint Bernadette Soubirous
Reason: This is the correct answer. Because the question is asking for the name of the person and following sentence from the passage answers it: It is a replica of the grotto at Lourdes, France where the Virgin Mary reputedly appeared to Saint Bernadette Soubirous in 1858.

Now, solve this instance: Context: One of the major histopathological hallmarks of Alzheimer's disease (AD) is cerebral deposits of extracellular -amyloid peptides. Preclinical studies have pointed to glucagon-like peptide 1 (GLP-1) receptors as a potential novel target in the treatment of AD. GLP-1 receptor agonists, including exendin-4 and liraglutide, have been shown to promote plaque-lowering and mnemonic effects of in a number of experimental models of AD. Transgenic mouse models carrying genetic mutations of amyloid protein precursor (APP) and presenilin-1 (PS1) are commonly used to assess the pharmacodynamics of potential amyloidosis-lowering and pro-cognitive compounds. In this study, effects of long-term liraglutide treatment were therefore determined in two double APP/PS1 transgenic mouse models of Alzheimer's disease carrying different clinical APP/PS1 mutations, i.e. the 'London' (hAPPLon/PS1A246E) and 'Swedish' mutation variant (hAPPSwe/PS1E9) of APP, with co-expression of distinct PS1 variants. Liraglutide was administered in 5 month-old hAPPLon/PS1A246E mice for 3 months (100 or 500 ng/kg/day, s.c.), or 7 month-old hAPPSwe/PS1E9 mice for 5 months (500 ng/kg/day, s.c.). In both models, regional plaque load was quantified throughout the brain using stereological methods. Vehicle-dosed hAPPSwe/PS1E9 mice exhibited considerably higher cerebral plaque load than hAPPLon/PS1A246E control mice. Compared to vehicle-dosed transgenic controls, liraglutide treatment had no effect on the plaque levels in hAPPLon/PS1A246E and hAPPSwe/PS1E9 mice. In conclusion, long-term liraglutide treatment exhibited no effect on cerebral plaque load in two transgenic mouse models of low- and high-grade amyloidosis, which suggests differential sensitivity to long-term liraglutide treatment in various transgenic mouse models mimicking distinct pathological hallmarks of AD.
Question: Which disease the London mutation involved in?
Student:
alzheimer's disease