Interactions of Npc1 and amyloid accumulation/deposition in the APP/PS1 mouse model of Alzheimer's

Although Niemann-Pick C1 disease has frequently been called "juvenile Alzheimer's", the effects of introducing Npc1 mutations into a mouse model of Alzheimer's have not previously been performed. We have crossed Npc1 (+/-) mice with APP/PS1 "Alzheimer's" mice and studied A beta 42 accumulation and amyloid plaque formation. Mice heterozygous for Npc1 and positive for the APP and PS1 transgenes accumulated A beta 42 more rapidly than the APP/PS1 controls and this correlated, as expected, with the area of amyloid plaques. We conclude that the alterations of intracellular cholesterol present in Npc1 (+/-) mice can influence the progress of Alzheimer's disease in the APP/PS1 mouse model.