Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

被引:192
作者
Farkas, E
De Jong, GI
de Vos, RAI
Steur, ENHJ
Luiten, PGM
机构
[1] Univ Groningen, Grad Sch Behav & Cognit Neurosci, Dept Anim Physiol, NL-9750 Haren, Netherlands
[2] Reg Lab Pathol & Microbiol, Dept Pathol, Enschede, Netherlands
[3] Med Spectrum Twente, Dept Neurol, Enschede, Netherlands
关键词
Alzheimer's disease; capillary ultrastructure; cerebral hypoperfusion; Parkinson's disease;
D O I
10.1007/s004010000195
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cerebral capillaries represent a major interface between the general circulation and the central nervous system and are responsible for sufficient and selective nutrient transport to the brain. Structural damage or dysfunctioning carrier systems of such an active barrier leads to compromised nutrient trafficking. Subsequently, a decreased nutrient availability in the neural tissue may contribute to hampered neuronal metabolism, hence to behavioral and cognitive functional deficiencies. Here we focus on the ultrastrucutral abnormalities of cerebral microvessels in Alzheimer's disease (AD; n = 5) and Parkinson's diseasse (PD; n = 10). The capillary microanatomy in samples from the cingulate cortex was investigated by electron microscopy and severe damage to the vessel walls was observed. Characteristic pathological changes including capillary basement membrane thickening and collagen accumulation in the basement membrane were enhanced in both AD and PD. The incidence of capillaries with basement membrane deposits was two times higher in AD and PD than in age-matched controls. Degenerative pericytes in all groups appeared at a similar frequency. The data indicate that basement membrane deposists, as opposed to pericytic degeneration, represent an important pathological feature of AD and PD and suggest that capillary dysfunction may play a causal role in the development of these two major neurodegenerative diseases.
引用
收藏
页码:395 / 402
页数:8
相关论文
共 44 条
[1]  
Bennett SAL, 1998, NEUROREPORT, V9, P161
[2]   Cerebral metabolic changes in Alzheimer's disease: Neurobehavioral patterns [J].
Blesa, R ;
Mohr, E ;
Miletich, RS ;
Hildebrand, K ;
Sampson, M ;
Chase, TN .
DEMENTIA, 1996, 7 (05) :239-245
[3]   Pattern of brain destruction in Parkinson's and Alzheimer's diseases [J].
Braak, H ;
Braak, E ;
Yilmazer, D ;
deVos, RAI ;
Jansen, ENH ;
Bohl, J .
JOURNAL OF NEURAL TRANSMISSION, 1996, 103 (04) :455-490
[4]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[5]   Brain microvascular changes in Alzheimer's disease and other dementias [J].
Buee, L ;
Hof, PR ;
Delacourte, A .
CEREBROVASCULAR PATHOLOGY IN ALZHEIMER'S DISEASE, 1997, 826 :7-24
[6]  
Claudio L, 1996, ACTA NEUROPATHOL, V91, P6
[7]   Cerebral hypoperfusion yields capillary damage in the hippocampal Ca1 area that correlates with spatial memory impairment [J].
De Jong, GI ;
Farkas, E ;
Stienstra, CM ;
Plass, JRM ;
Keijser, JN ;
De la Torre, JC ;
Luiten, PGM .
NEUROSCIENCE, 1999, 91 (01) :203-210
[8]   Critical threshold cerebral hypoperfusion causes Alzheimer's disease? [J].
de la Torre, JC .
ACTA NEUROPATHOLOGICA, 1999, 98 (01) :1-8
[9]  
DeJong GI, 1997, ANN NY ACAD SCI, V826, P56
[10]   MICROVASCULAR CHANGES IN AGED RAT FOREBRAIN - EFFECTS OF CHRONIC NIMODIPINE TREATMENT [J].
DEJONG, GI ;
DEWEERD, H ;
SCHUURMAN, T ;
TRABER, J ;
LUITEN, PGM .
NEUROBIOLOGY OF AGING, 1990, 11 (04) :381-389