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P3‐155: Early striatal amyloid deposition distinguishes down syndrome and autosomal dominant Alzheimer's disease from late‐onset amyloid deposition
Author(s) -
McDade Eric,
Cohen Ann D.,
Christian Bradley T.,
Price Julie,
Mathis Chester,
Klunk William,
Handen Ben
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.1526
Subject(s) - amyloid (mycology) , pittsburgh compound b , amyloidosis , alzheimer's disease , medicine , pathology , disease , endocrinology
(DTI). Methods: DTI was implemented on 192 participants who were cognitively normal, determined by a clinical dementia rating (CDR) of 0. Fractional anisotropy (FA), radial diffusivity (DR), axial diffusivity (DA) and mean diffusivity (MD) were derived from DTI. Total tau, tau phosphorylated at threonine-181 (ptau181), and Ab1-42 levels were determined in CSF. Participants were divided into normal, preclinical but asymptomatic (stage1 [amyloid+, neuronal injury-] and stage2 [amyloid+, neuronal injury+] according to the definition of preclinical stages from NIA and Alzheimer’s Association. Monte Carlo (MC) simulation was employed to evaluate the effect of different pathologies in preclinical AD, such as neuroinflammatory cell infiltration,WM injury and vasogenic edema, on DTI indices in a computer generated geometric model (Figure 2). Simulation protocol is same as our previous study. Results: In preclinical stage 1, DR, DA and MD significantly decreased compared to normal group in a wide spread WM regions (Figure 1). Those results may suggest early inflammatory cell infiltration (Table 1). MC simulation confirmed that slightly increased amount of microglia cell activated after blood-