Topographical distribution of cerebral amyloid angiopathy and its effect on cognitive decline are influenced by Alzheimer disease pathology

被引:90
作者
Attems, Johannes
Quass, Magdalena
Jellinger, Kurt A.
Lintner, Felix
机构
[1] Otto Wagner Hosp, Inst Pathol, A-1145 Vienna, Austria
[2] Inst Clin Neurobiol, A-1070 Vienna, Austria
关键词
cerebral amyloid angiopathy; Alzheimer disease; dementia; topographical distribution;
D O I
10.1016/j.jns.2007.01.013
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cerebral amyloid angiopathy (CAA) is defined by -amyloid peptide (A) depositions in cerebral vessels and is associated with Alzheimer disease (AD). It has been suggested that severe CAA is an independent risk factor for cognitive decline. 171 autopsy brains underwent standardized neuropathological assessment, the patients age ranged from 54 to 104 years (mean age: 83.9 years, +/-9.2, 59.6% female, 56. 1 % clinically demented). Using inummohistochemistry, the severity of A depositions in vessels was assessed semiquantitatively in the frontal, frontobasal, hippocampal, and occipital region, respectively. CAA was present in 117 cases (68.4%), with the occipital region being affected significantly stronger than other regions. The overall incidence of CAA was significantly higher in cases with high grade neuritic AD pathology (ADP) compared to those with low grade or no ADP. The severity of CAA significantly increased with increasing ADP, with CAA in the occipital region increasing significantly stronger than that in other regions. The association of CAA and clinical dementia failed to remain statistically significant when adjusting for concomitant ADP. However, in cases devoid of any ADP CAA was significantly associated with the presence of clinical dementia. These results indicate a strong association of AD with CAA, but do not unequivocally support reports suggesting CAA to be an independent risk factor for cognitive decline, except for a subgroup of demented patients lacking any ADP. (c) 2007 Elsevier B.V.All rights reserved.
引用
收藏
页码:49 / 55
页数:7
相关论文
共 61 条
[1]   Progression of cerebral amyloid angiopathy:: Accumulation of amyloid-β40 in affected vessels [J].
Alonzo, NC ;
Hyman, BT ;
Rebeck, GW ;
Greenberg, SM .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1998, 57 (04) :353-359
[2]   Sporadic cerebral amyloid angiopathy: pathology, clinical implications, and possible pathomechanisms [J].
Attems, J .
ACTA NEUROPATHOLOGICA, 2005, 110 (04) :345-359
[3]   Amyloid β peptide 1-42 highly correlates with capillary cerebral amyloid angiopathy and Alzheimer disease pathology [J].
Attems, J ;
Lintner, F ;
Jellinger, KA .
ACTA NEUROPATHOLOGICA, 2004, 107 (04) :283-291
[4]   Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology - a pilot study [J].
Attems, J ;
Jellinger, KA .
ACTA NEUROPATHOLOGICA, 2004, 107 (02) :83-90
[5]  
BERGERON C, 1987, CAN J NEUROL SCI, V14, P564
[6]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[7]   Cerebral beta amyloid angiopathy is a risk factor for cerebral ischemic infarction. A case control study in human brain biopsies [J].
Cadavid, D ;
Mena, E ;
Koeller, K ;
Frommelt, RA .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2000, 59 (09) :768-773
[8]   Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid [J].
Calhoun, ME ;
Burgermeister, P ;
Phinney, AL ;
Stalder, M ;
Tolnay, M ;
Wiederhold, KH ;
Abramowski, D ;
Sturchler-Pierrat, C ;
Sommer, B ;
Staufenbiel, M ;
Jucker, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (24) :14088-14093
[9]   Alzheimer neuropathologic alterations in aged cognitively normal subjects [J].
Davis, DG ;
Schmitt, FA ;
Wekstein, DR ;
Markesbery, WR .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1999, 58 (04) :376-388
[10]   Cerebral amyloid angiopathy is a pathogenic lesion in Alzheimer's disease due to a novel presenilin 1 mutation [J].
Dermaut, B ;
Kumar-Singh, S ;
De Jonghe, C ;
Cruts, M ;
Löfgren, A ;
Lübke, U ;
Cras, P ;
Dom, R ;
De Deyn, PP ;
Martin, JJ ;
Van Broeckhoven, C .
BRAIN, 2001, 124 :2383-2392