Relationships in Alzheimer's disease between the extent of Aβ deposition in cerebral blood vessel walls, as cerebral amyloid angiopathy, and the amount of cerebrovascular smooth muscle cells and collagen

被引:54
作者
Tian, J
Shi, J
Smallman, R
Iwatsubo, T
Mann, DMA [1 ]
机构
[1] Univ Manchester, Hope Hosp, Clin Neurosci Res Grp, Fac Med & Human Sci, Salford M6 8HD, Lancs, England
[2] Beijing Univ Chinese Med, Dongzhimen Hosp, Dept Care Elderly, Beijing, Peoples R China
[3] Univ Tokyo, Dept Neuropathol, Tokyo, Japan
关键词
Alzheimer's disease; amyloid beta protein; cerebral amyloid angiopathy; smooth muscle cells; collagen IV; vascular disease;
D O I
10.1111/j.1365-2990.2006.00732.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The relationship between degree of cerebral amyloid angiopathy (CAA) and the amount of smooth muscle cells (SMCs) and deposition of collagen IV fibres (COL IV) was investigated in the frontal and occipital cortex of 70 patients with autopsy confirmed Alzheimer's disease (AD). The extent of CAA was significantly greater in occipital than in frontal cortex, although SMC loss was greater in frontal than in occipital cortex. COL IV staining was significantly higher in occipital than in frontal cortex. The degree of SMC loss correlated with CAA, as A beta(40) but not as A beta(42) or total A beta, in frontal cortex, but not in occipital cortex. Leptomeningeal arteries within occipital cortex showed significantly greater external diameter, greater wall thickness and greater luminal area than those in frontal cortex. The degree of CAA correlated with thickness of blood vessel wall and external diameter in frontal cortex, whereas extent of SMC loss correlated with thickness of blood vessel wall in occipital cortex. There were significant negative correlations between duration of disease and thickness of vessel wall, external diameter and luminal area. In patients with disease durations exceeding 10 years, external vessel diameter and thickness of the vessel wall were both halved compared with patients with durations less than 5 years; luminal area was reduced by about 75%. Blood vessels in AD undergo degenerative changes involving deposition of A beta and COL IV with loss of SMC. SMC loss may relate to increasing A beta deposition in early stages of disease, but this relationship may be lost with disease progression.
引用
收藏
页码:332 / 340
页数:9
相关论文
共 36 条
[11]   Increased collagen content of cerebral microvessels in Alzheimer's disease [J].
Kalaria, RN ;
Pax, AB .
BRAIN RESEARCH, 1995, 705 (1-2) :349-352
[12]   Production and increased detection of amyloid beta protein and amyloidogenic fragments in brain microvessels, meningeal vessels and choroid plexus in Alzheimer's disease [J].
Kalaria, RN ;
Premkumar, DRD ;
Pax, AB ;
Cohen, DL ;
Lieberburg, I .
MOLECULAR BRAIN RESEARCH, 1996, 35 (1-2) :58-68
[13]   DEGENERATION OF VASCULAR MUSCLE-CELLS IN CEREBRAL AMYLOID ANGIOPATHY OF ALZHEIMER-DISEASE [J].
KAWAI, M ;
KALARIA, RN ;
CRAS, P ;
SIEDLAK, SL ;
VELASCO, ME ;
SHELTON, ER ;
CHAN, HW ;
GREENBERG, BD ;
PERRY, G .
BRAIN RESEARCH, 1993, 623 (01) :142-146
[14]   The apolipoprotein E ε2 allele and the pathological features in cerebral amyloid angiopathy-related hemorrhage [J].
McCarron, MO ;
Nicoll, JAR ;
Stewart, J ;
Ironside, JW ;
Mann, DMA ;
Love, S ;
Graham, DI ;
Dewar, D .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1999, 58 (07) :711-718
[15]   THE CONSORTIUM TO ESTABLISH A REGISTRY FOR ALZHEIMERS-DISEASE (CERAD) .2. STANDARDIZATION OF THE NEUROPATHOLOGIC ASSESSMENT OF ALZHEIMERS-DISEASE [J].
MIRRA, SS ;
HEYMAN, A ;
MCKEEL, D ;
SUMI, SM ;
CRAIN, BJ ;
BROWNLEE, LM ;
VOGEL, FS ;
HUGHES, JP ;
VANBELLE, G ;
BERG, L .
NEUROLOGY, 1991, 41 (04) :479-486
[16]   Amyloid β precursor protein-mRNA is expressed throughout cerebral vessel walls [J].
Natté, R ;
de Boer, WI ;
Maat-Schieman, MLC ;
Baelde, HJ ;
Vinters, HV ;
Roos, RAC ;
van Duinen, SG .
BRAIN RESEARCH, 1999, 828 (1-2) :179-183
[17]   CEREBRAL INFARCTION IN ALZHEIMERS-DISEASE IS ASSOCIATED WITH SEVERE AMYLOID ANGIOPATHY AND HYPERTENSION [J].
OLICHNEY, JM ;
HANSEN, LA ;
HOFSTETTER, CR ;
GRUNDMAN, M ;
KATZMAN, R ;
THAL, LJ .
ARCHIVES OF NEUROLOGY, 1995, 52 (07) :702-708
[18]   Cerebrovascular muscle atrophy is a feature of Alzheimer's disease [J].
Perry, G ;
Smith, MA ;
McCann, CE ;
Siedlak, SL ;
Jones, PK ;
Friedland, RP .
BRAIN RESEARCH, 1998, 791 (1-2) :63-66
[19]   Capillary and arterial cerebral amyloid angiopathy in Alzheimer's disease:: defining the perivascular route for the elimination of amyloid β from the human brain [J].
Preston, SD ;
Steart, PV ;
Wilkinson, A ;
Nicoll, JAR ;
Weller, RO .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2003, 29 (02) :106-117
[20]   BETA-AMYLOID-(1-42) IS A MAJOR COMPONENT OF CEREBROVASCULAR AMYLOID DEPOSITS - IMPLICATIONS FOR THE PATHOLOGY OF ALZHEIMER-DISEASE [J].
ROHER, AE ;
LOWENSON, JD ;
CLARKE, S ;
WOODS, AS ;
COTTER, RJ ;
GOWING, E ;
BALL, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (22) :10836-10840