TY - JOUR
T1 - Neuroimaging as a marker of the onset and progression of Alzheimer's disease
AU - Masdeu, Jose C.
AU - Zubieta, Jose L.
AU - Arbizu, Javier
N1 - Funding Information:
Dr. Juan Pablo Cabello helped provide the illustrations for Figs. 1 and 2 . This study was supported by the UTE “Fundación para la Investigación Médica Aplicada” (“Foundation for Applied Medical Research”), Pamplona, Spain.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/9/15
Y1 - 2005/9/15
N2 - Several neuroimaging techniques are promising tools as early markers of brain pathology in Alzheimer's disease (AD). On structural MRI, atrophy of the entorhinal cortex is present already in mild cognitive impairment (MCI). In the autosomal dominant forms of AD, the rate of atrophy of medial temporal structures separates affected from control persons even 3 years before the clinical onset of cognitive impairment. The elevated annual rate of brain atrophy offers a surrogate tool for the evaluation of newer therapies using smaller samples, thereby saving time and resources. On functional MRI, activation paradigms activate a larger area of parieto-temporal association cortex in persons at higher risk for AD, whereas the entorhinal cortex activation is lesser in MCI. Similar findings have been detected with activation procedures and water (H2
15O) PET. Regional metabolism in the entorhinal cortex, studied with FDG PET, seems to predict normal elderly who will deteriorate to MCI or AD. SPECT shows decreased regional perfusion in limbic areas, both in MCI and AD, but with a lower likelihood ratio than PET. Newer PET compounds allow for the determination in AD of microglial activation, regional deposition of amyloid and the evaluation of enzymatic activity in the brain of AD patients.
AB - Several neuroimaging techniques are promising tools as early markers of brain pathology in Alzheimer's disease (AD). On structural MRI, atrophy of the entorhinal cortex is present already in mild cognitive impairment (MCI). In the autosomal dominant forms of AD, the rate of atrophy of medial temporal structures separates affected from control persons even 3 years before the clinical onset of cognitive impairment. The elevated annual rate of brain atrophy offers a surrogate tool for the evaluation of newer therapies using smaller samples, thereby saving time and resources. On functional MRI, activation paradigms activate a larger area of parieto-temporal association cortex in persons at higher risk for AD, whereas the entorhinal cortex activation is lesser in MCI. Similar findings have been detected with activation procedures and water (H2
15O) PET. Regional metabolism in the entorhinal cortex, studied with FDG PET, seems to predict normal elderly who will deteriorate to MCI or AD. SPECT shows decreased regional perfusion in limbic areas, both in MCI and AD, but with a lower likelihood ratio than PET. Newer PET compounds allow for the determination in AD of microglial activation, regional deposition of amyloid and the evaluation of enzymatic activity in the brain of AD patients.
KW - Alzheimer
KW - Early marker
KW - fMRI
KW - Functional brain imaging
KW - Molecular brain imaging
KW - MRI
KW - Neuroimaging
KW - PET
KW - SPECT
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U2 - 10.1016/j.jns.2005.05.001
DO - 10.1016/j.jns.2005.05.001
M3 - Article
C2 - 15961110
AN - SCOPUS:24044478786
SN - 0022-510X
VL - 236
SP - 55
EP - 64
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
IS - 1-2
ER -