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IC–102–05: Differential effects of white matter lesions on medial temporal lobe atrophy in early versus late onset Alzheimer's disease
Author(s) -
De Leeuw Frank-Erik,
Flier Wiesje,
Korf Esther,
Barkhof Frederik,
Scheltens Philip
Publication year - 2006
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.2006.05.2194
Subject(s) - atrophy , hyperintensity , white matter , early onset alzheimer's disease , medicine , cardiology , alzheimer's disease , disease , magnetic resonance imaging , radiology
Background: Alzheimer’s disease (AD) is usually diagnosed as a single disease entity. However, there is much variation in clinical and radiological characteristics between early ( 65 years; EOAD) and late ( 65 years; LOAD) onset AD. It has been postulated that EOAD is a primary neurodegenerative disorder, while vascular factors leading to white matter lesions (WML), are related with LOAD. Medial temporal lobe atrophy (MTA) is a key feature in both EOAD and LOAD, but this may have a different etiology in the EOAD than in LOAD since in LOAD a relation between WML and MTA has been described. Since WML are related with aging and LOAD we hypothesized that WML would be related with MTA only in the LOAD and not in the EOAD. Objective: To investigate the relation between WML and MTA in EOAD and LOAD. Methods: We investigated 179 ‘probable’ AD patients according to NINCDS-ADRDA criteria. All patients underwent 1T coronal T1and transverse PD or FLAIR scanning. WML and MTA were rated semi-quantitatively with the age-related white matter changes rating scale (ARWMC) and the Scheltens’ scale, respectively. The relation between MTA and WML was assessed by age and sex adjusted linear regression analysis for EOAD and LOAD separately. Adjustments were made for MMSE. Results: Mean age of the EOAD was 58.2 years of age (SD 4.0) and 73.6 (SD 5.1) in LOAD. There was no difference for MMSE between the groups (18.9 (SD5.0) vs. 20.9 (SD5.0), p 0.2). Mean ARWMC grade in the EOAD was 0.6 (SD2.2) and 1.5 (SD2.9) in the LOAD, p 0.2. There was a linear relation between the ARWMC grade and MTA ( 0.09; 95%CI 0.03-0.15), p 0.006 in the LOAD, and not in the EOAD. In the LOAD patients with WML had significantly more MTA than those without (2.1 (SD0.9) vs 1.7 (SD 1.0), p 0.04). This was not found among EOAD. Conclusion: Our data show differential effects of WML on MTA in EOAD vs LOAD. This may indicate that in the EOAD another, possibly neurodegenerative process leads to MTA while in LOAD WML are related to MTA. This suggests heterogeneity in the etiology of AD.