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KMID : 1225120100020010026
Vascular Neurology
2010 Volume.2 No. 1 p.26 ~ p.30
Cerebral Amyloid Angiopathy Presenting as Alzheimer¡¯s Disease: Four Case Reports
Yang Young-Soon

Seo Hee-Jeong
Noh Yong-Woo
Kwak Yong-Tae
Han Il-Woo
Lee Choong-Soon
Abstract
Cerebral amyloid angiopathy (CAA) is well known to present with lobar intracerebral hemorrhage, dementia or transient neurological events. CAA is a microangiopathy that frequently cooccurs with Alzheimer¡¯s disease (AD) and appears to increase with age. In AD, CAA is due to the deposition of amyloid alpha protein (Abeta) within the adventitia and media of leptomeningeal and brain parenchymal arteries. We present 4 cases with rapidly progressive dementia in whom magnetic resonance imaging brain showed multiple microbleed in the whole cerebral lobe, mainly parieto-occipital lobe. Brain positron emission tomography revealed symmetrical hypometabolism in temporal and parietal cortex as features of AD. Apolipoprotein E (ApoE) genotype revealed Apo e3/e3. The presence of one or two ApoE E4 alleles is considered to be a risk factor for AD. Evidence suggests that the ApoE4 isoform promotes fibril formation of the amyloid b protein (Ab). ApoE2, on the other hand, may play an opposite role, protecting against Ab deposition and the development of AD. The role of ApoE in the genetics and pathogenesis of AD has been well established. As with AD, the 4 allele of ApoE is a risk factor for developing CAA, whereas the 2 allele is a risk factor for developing hemorrhage associated with CAA. We found ApoE3 in 4 patients, and we can¡¯t prospect AD accompanied with CAA in ApoE genotype.
KEYWORD
Cerebral amyloid angiopathy, Alzheimer¡¯s disease, ApoE genotype
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