MAPPING LOCAL STRUCTURAL HIPPOCAMPAL CHANGES IN ALZHEIMER?S DISEASE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. "Mapping local structural hippocampal changes in Alzheimer's disease and normal aging on MR imaging at 3T" Background: Some studies have shown significant hippocampal volume loss with increasing age. An accurate characterization of the typical age-related hippocampal changes in vivo is very important because Alzheimer's disease in the early stages is also associated with hippocampal volume loss. Objective: To study local hippocampal changes in aging and moderate to severe Alzheimer's patients disease with radial atrophy mapping (RAM) based on high resolution magnetic resonance (MR) images at 3 Tesla. Methods. 3D high resolution T1-weighted magnetic resonance (MR) were acquired on a 3.0 T scanner from 14 AD (age 75¿5 years, 3 males, Mini Mental State Examination 13¿4) and 14 controls (age 71¿5 years 9 males, Mini-Mental State Examination 29¿1). The hippocampal formation was isolated by manual tracing. RAM allows to assess group differences and correlations by averaging hippocampal shapes across subjects using 3-dimensional parametric surface mesh models. Percentage difference, Pearson's r, and significance 3-dimensional maps were produced. Results: Hippocampal volumes were inversely correlated with age in older healthy controls (r .53 and .56 to the right and left, p< 0,05, corresponding to 17% lower volume for every 10 years of older age from age 65). Aging-associated atrophy mapped to dorsal and lateral areas of the tail and body corresponding to the CA1 subfield and to ventral areas of the head corresponding to the subiculum. Significantly increased volume with older age mainly mapped to restricted dorsal areas of the head bilaterally corresponding to the CA1 subfield. Volumes were 37% and 30% smaller in AD patients to the right and left (p<.0005). AD-associated atrophy mapped to areas of the body and tail corresponding to those also associated with age, and dorsal areas of the head corresponding to the CA1 subfield unaffected by age. Regions corresponding to the CA2-3 fields were relatively spared in both aging and AD. Conclusions: Hippocampal atrophy in AD maps to areas in the body and in the tail partly overlapping to those affected by normal aging. Specific areas map to the anterior and dorsal CA1 subfield involved in AD were not involved in normal aging. Such differences might relate to the different systems involved in two conditions and to the clinical syndromes of AD. The anterior hippocampal areas spared in aging might be specific to Alzheimer's disease.