Brains from non-Alzheimer's individuals containing amyloid deposits accelerate Aβ deposition in vivo

Background: One of the main features of Alzheimer's disease (AD) is the presence of A beta deposits, which accumulate in the brain years before the onset of symptoms. We and others have demonstrated that cerebral A beta-amyloidosis can be induced in vivo by administration of AD-brain extracts into transgenic mice. However, it is currently unknown whether amyloid formation can be induced using extracts from individuals harboring A beta deposits, but not clinical disease. Results: In this study we analyzed the amyloid-inducing capability of samples from individuals affected by mild cognitive impairment (MCI) and Non-Demented persons with Alzheimer's disease Neuropathology (NDAN). Our results show that inoculation of transgenic mice with MCI and NDAN brain samples accelerated A beta pathology in a similar way as extracts from confirmed AD. Conclusions: This data demonstrate that the sole presence of A beta aggregates in a given sample, regardless of the clinical condition, is capable to accelerate A beta deposition in vivo. These findings indicate that the amyloid-inducing activity may be present in the brain of people during pre-symptomatic or a-symptomatic stages of AD.