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P1‐414: In vivo neuropathology of cortical changes in incipient Alzheimer's disease
Author(s) -
Prestia Annapaola,
Rasser Paul E.,
Bonetti Matteo,
Thompson Paul M.,
Frisoni Giovanni B.
Publication year - 2010
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.2010.05.969
Subject(s) - posterior cingulate , neuropathology , dementia , alzheimer's disease , cardiology , orbitofrontal cortex , psychology , medicine , magnetic resonance imaging , neuroscience , cortex (anatomy) , disease , cognition , prefrontal cortex , radiology
Background: Patients with mild cognitive impairment (MCI) have memory deficits without functional impact on activities of daily living and have a 10-fold greater risk of developing Alzheimer’s dementia (AD) in the following 5 years. Neurodegenerative changes in patients with AD at the dementia stage have been well characterized using structural magnetic resonance imaging (MRI) but earlier changes are still relatively poorly understood. Here we aimed to map the cortical changes in MCI patients, a subgroup of whom later developed AD. Methods: Structural T1-weighted high-resolution MR scans were acquired at baseline (T0) and after 1.4+0.3 (SD) years (T1) from 46 elderly patients with amnestic MCI (age 69+8 years, MMSE 27+2). Twenty cognitively healthy elderly persons were used as controls (age 72+8, MMSE 29+1). Patients were followed for 4 years and assessed yearly with a comprehensive neuropsychological and behavioural battery and 16 converted to AD (cMCI, age 73+5, MMSE 26+2) while 30 remained stable (sMCI, age 67+8, MMSE 28+2). A voxel-based statistical mesh modeling technique (cortical pattern matching) and a related region-of-interest analysis based on Brodmann areas (BAs) were used to map gray matter volume changes between groups and over time. Results: At baseline (T0), cMCI patients had 10-30% lower cortical gray matter volume than healthy controls in regions known to be affected by AD pathology (entorhinal, temporoparietal, posterior cingulate, and orbitofrontal cortex, p<.0001). sMCI patients had on average 10-20% volume deficits confined to the posterior cingulate and orbitofrontal cortex (p<.008). Patients with cMCI were losing 10-15% more gray matter than sMCI during the time interval between T0 and T1 scans, in the posterior cingulate/retrosplenial and frontal, medial temporal and temporal polar cortices (p<.024), with the olfactory network being more involved. Conclusion: Structural gray matter changes in amnestic MCI patients who develop AD in the short term map to cortical areas pertaining to memory networks known to be affected in the earliest stages of the pathology.