Functional compensation in incipient Alzheimer's disease

• Published in: Neurobiology of aging Vol. 31; no. 3; pp. 387 - 397
• Main Authors: Caroli, A, Geroldi, C, Nobili, F, Barnden, L.R, Guerra, U.P, Bonetti, M, Frisoni, G.B
• Format: Journal Article
• Language: English
• Published: London Elsevier Inc 01.03.2010; Elsevier
• Subjects: Aged; Alzheimer Disease - diagnostic imaging; Alzheimer Disease - pathology; Biological and medical sciences; Brain - diagnostic imaging; Brain - pathology; Cognition Disorders - diagnostic imaging; Cognition Disorders - pathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Development. Senescence. Regeneration. Transplantation; Female; Follow-Up Studies; Functional compensation; Fundamental and applied biological sciences. Psychology; Humans; Incipient AD; Internal Medicine; Magnetic Resonance Imaging; Male; Medical sciences; MRI; Neurology; Neuropsychological Tests; Prospective Studies; SPECT; Tomography, Emission-Computed, Single-Photon; Vertebrates: nervous system and sense organs; Voxel-based analysis; Voxel-based analysis; MRI; Functional compensation; SPECT; Incipient AD; Nervous system diseases; Senescence; Alzheimer disease; Nuclear magnetic resonance imaging; Photon; Cerebral disorder; Central nervous system disease; Degenerative disease; Emission tomography
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2008.05.001

Abstract Aim of this study was to investigate the functional compensation mechanism in incipient Alzheimer's disease (AD). Seventeen elderly healthy subjects and nine amnestic MCI patients with incipient AD underwent brain MR scan and 99mTc ECD SPECT. We processed all images with SPM2, we created t maps, showing the wholebrain GM atrophy and functional changes, and we properly masked them with each other in order to assess relatively preserved perfusion or depression. Incipient AD showed GM atrophy in the medial temporal and temporoparietal lobes, in the insula and in the retrosplenial cortex, and GM hypoperfusion in the medial temporal and temporoparietal lobes. Relatively preserved perfusion, we could hypothesize to be compensatory in the setting of neuronal loss, was found in the posterior cingulate, in the head of the hippocampus, in the amigdala, and in the insula bilaterally, while functional depression occurred in bilateral parahippocampal gyri. In AD, a perfusional compensatory mechanism takes place in the neocortex, while perfusional depression occurs in the medial temporal lobe. These results help understand the reactive phenomena induced by the brain to try and counteract the pathological changes of AD.