%0 Journal Article %J J Alzheimers Dis %D 2018 %T The Impact of APOE ɛ4 in Alzheimer's Disease Differs According to Age. %A Kim, Jaeho %A Park, Seongbeom %A Yoo, Heejin %A Jang, Hyemin %A Kim, Yeshin %A Kim, Ko Woon %A Jang, Young Kyoung %A Lee, Jin San %A Kim, Sung Tae %A Kim, Seonwoo %A Lee, Jong Min %A Ki, Chang-Seok %A Na, Duk L %A Seo, Sang Won %A Kim, Hee Jin %K Age Factors %K Aged %K Alzheimer Disease %K Apolipoprotein E4 %K Atrophy %K Brain %K Case-Control Studies %K Cognition %K Female %K Heterozygote %K Humans %K Magnetic Resonance Imaging %K Male %K Memory %K Middle Aged %K Republic of Korea %X

We evaluated how the impact of apolipoprotein E4 (APOE4) differs according to age in Alzheimer's disease (AD) patients. We recruited 846 AD patients and 815 cognitively normal controls and categorized into three groups with respect to their age (<65, 65-74, and ≥75 years). We evaluated the risk of AD in APOE4 carriers and compared cortical thickness and cognitive function according to APOE4 status in each age group. At the point of this study, in young (<65 years) AD, APOE4 noncarriers had the most severe frontal and perisylvian atrophy, while in old (≥75 years) AD, APOE4 carriers had the most severe medial temporal atrophy. In AD under 75 years, APOE4 noncarriers and heterozygotes showed worse performance in language, visuospatial, and frontal function compared to homozygotes, while, in old (≥75 years) AD, APOE4 homozygotes showed worse performance in memory compared to noncarriers. As the detrimental effects of APOE4 seen in older AD patients were not found in younger AD patients, we suggest that some unrevealed factors are associated with cortical atrophy and non-amnestic cognitive dysfunction in young AD with APOE4 noncarriers.

%B J Alzheimers Dis %V 61 %P 1377-1385 %8 2018 %G eng %N 4 %1 http://www.ncbi.nlm.nih.gov/pubmed/29376853?dopt=Abstract %R 10.3233/JAD-170556 %0 Journal Article %J J Alzheimers Dis %D 2017 %T 18F-AV-1451 PET Imaging in Three Patients with Probable Cerebral Amyloid Angiopathy. %A Kim, Hee Jin %A Cho, Hanna %A Werring, David J %A Jang, Young Kyoung %A Kim, Yeo Jin %A Lee, Jin San %A Lee, Juyoun %A Jun, Soomin %A Park, Seongbeom %A Ryu, Young Hoon %A Choi, Jae Yong %A Cho, Young Seok %A Moon, Seung Hwan %A Na, Duk L %A Lyoo, Chul Hyoung %A Seo, Sang Won %K Aged %K Aged, 80 and over %K Aniline Compounds %K Brain %K Carbolines %K Cerebral Amyloid Angiopathy %K Female %K Humans %K Image Processing, Computer-Assisted %K Male %K Positron-Emission Tomography %K Thiazoles %X

Cerebrovascular deposition of amyloid-β, known as cerebral amyloid angiopathy (CAA), is associated with MRI findings of lobar hemorrhage, cerebral microbleeds, and cortical superficial siderosis. Although pathological studies suggest that tau may co-localize with vascular amyloid, this has not yet been investigated in CAA in vivo. Three patients with probable CAA underwent 11C-Pittsburgh Compound B (PiB) PET or 18F-florbetaben PET to evaluate amyloid burden, and 18F-AV-1451 PET to evaluate paired helical filament tau burden. Regions that had cerebral microbleeds or cortical superficial siderosis largely overlapped with those showing increased 18F-AV-1451. Our preliminary study raised the possibility that lobar cerebral microbleeds, and cortical superficial siderosis, which are characteristic markers of vascular amyloid, may be associated with local production of paired helical filament tau.

%B J Alzheimers Dis %V 57 %P 711-716 %8 2017 %G eng %N 3 %1 http://www.ncbi.nlm.nih.gov/pubmed/28282808?dopt=Abstract %R 10.3233/JAD-161139