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DOI: 10.1148/radiol.2411050628
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Quantitative MR Imaging in Alzheimer Disease1

Anita Ramani, PhD, Jens H. Jensen, PhD and Joseph A. Helpern, PhD

1 From the Center for Biomedical Imaging, Department of Radiology, New York University School of Medicine, KIP-600-F, 660 First Ave, New York, NY 10016-3240 (A.R., J.H.J., J.A.H.); and Departments of Psychiatry (J.A.H.) and Physiology and Neuroscience (J.H.J., J.A.H.), New York University School of Medicine, New York, NY. Received April 15, 2005; revision requested June 14; revision received July 25; accepted September 8; final review and update by A.R. April 17, 2006. J.A.H. supported by grants from the Werner Dannheisser Trust and the Institute for the Study of Aging. Address correspondence to A.R. (e-mail: anita.ramani{at}med.nyu.edu).


Figure 1
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  		Figure 1a: Diagrams show that (a) in normal aging, ß-amyloid peptides are produced by brain cells and are soluble, but (b) in abnormal conditions, these peptides become insoluble and can be clustered together by chaperone proteins, resulting in the formation of plaques.

 

Figure 1
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  		Figure 1b: Diagrams show that (a) in normal aging, ß-amyloid peptides are produced by brain cells and are soluble, but (b) in abnormal conditions, these peptides become insoluble and can be clustered together by chaperone proteins, resulting in the formation of plaques.

 

Figure 2
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  		Figure 2: A–D, Definition of auxiliary guideline traces on selected sagittal T1-weighted three-dimensional spoiled gradient-echo MR sections (repetition time msec/echo time msec, 24/5; section thickness, 1.5 mm; flip angle, 40°; two signals acquired; field of view, 26 x 26 x 18.6 cm; matrix, 256 x 192 x 124). E–N, Definition of hippocampal traces on selected coronal MR sections from most rostral (E) to most caudal (N) aspects of the structure (right hemisphere). O, Three-dimensional reconstruction of hippocampal shape based on coronal traces. (Reprinted, with permission, from reference 218.)

 

Figure 3
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  		Figure 3: Coronal unenhanced baseline (left) and coregistered year 2 follow-up (middle) T1-weighted MR images (35/9; flip angle, 60°; matrix, 256 x 192; thickness, 1.2 mm) and normalized difference displayed with narrower 20% signal intensity window to enable visualization of brain tissue loss within the boundary region (right). Rectangles are location of the medial temporal lobe (MTL) region. Coronal sections through foot of the hippocampus are shown for three representative study participants. Top: Images in a 72-year-old man who remained healthy at year 6.4 after baseline; annual MTL atrophy rate was 0.2%. Middle: Images in a 70-year-old woman who remained healthy at year 2 and declined to mild cognitive impairment (MCI) by year 6; annual MTL atrophy rate was 0.8%. Bottom: Images in a 77-year-old man with normal findings at baseline who declined to AD by year 2; annual MTL atrophy rate was 1.3%. (Reprinted, with permission, from reference 95.)

 

Figure 4
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  		Figure 4: Scatterplots show strong correlations between Mini-Mental State Examination (MMSE) scores and mean diffusivity (left: ADC, expressed as micrometers squared per millisecond) and fractional anisotropy values (right) in WM of patients with AD. (Reprinted, with permission, from reference 219.)

 

Figure 5
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  		Figure 5: MTR histograms of whole brain after correction for parenchymal volume. Y-axis scale is arbitrary and reflects number of voxels with specific MTR divided by total number of parenchymal voxels. Voxels with MTR < 20 are not shown, because they represent CSF. Lower peak heights in MCI and AD suggest less homogeneity in terms of magnetization transfer characteristics and reflect amount of parenchyma affected by the disease. (Reproduced, with permission, from reference 187.)

 

Figure 6
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  		Figure 6: Scatterplot shows T2 relaxation time as function of clinical status and suggests that T2 is sensitive to molecular properties of AD-related pathologic changes. Impairment at different stages of diagnosable dementia are classified as follows: Global Deterioration Scale score of 3, early confusional (eg, decreased performance in demanding settings); score of 4, late confusional (eg, inability to perform complex tasks); score of 5, early dementia (eg, patient cannot survive without assistance); and score of 6A–6E, middle dementia (eg, difficulty dressing at 6A to fecal incontinence at 6E). (Reprinted, with permission, from reference 200.)