RESEARCH ARTICLE Non-neuronal and neuron t h

is available at the end of the articleBackground β-Amyloid (Aβ) peptide deposition in the brain is com-monly associated with aging and age-related neurological diseases. Extracellular Aβ deposition in brain parenchyma, especially in the form of neuritic plaques, serves as one of the definitive diagnostic criteria for Alzheimer’s disease (AD) [1,2]. Aβ deposition can also occur in the wall of blood vessels, referred to as cerebral amyloid angiopathy (CAA). Further, β-amyloidosis may present on the pial surface, which is also considered a part of CAA. Overall, CAA coexists frequently with plaque lesions in AD brains [3]. Also of note, postmortem studies show that vascular amyloidosis can occur in the brains of non-demented elderly or patients with vascular dementia and other neu-rological conditions [4-9]. While CAA may be regarded as a pathological rather than disease entity, its clinical impact is increasingly recognized. CAA is frequently associate