Hypertension drives parenchymal β-amyloid accumulation in the brain parenchyma

被引:34
作者
Bueche, Celine Z. [1 ,2 ]
Hawkes, Cheryl [3 ]
Garz, Cornelia [1 ]
Vielhaber, Stefan [1 ,2 ]
Attems, Johannes [4 ]
Knight, Robert T. [5 ,6 ]
Reymann, Klaus [2 ]
Heinze, Hans-Jochen [1 ,2 ]
Carare, Roxana O. [3 ]
Schreiber, Stefanie [1 ,2 ]
机构
[1] Otto von Guericke Univ, Dept Neurol, Leipziger Str 44, D-39120 Magdeburg, Germany
[2] German Ctr Neurodegenerat Dis DZNE, Magdeburg, Germany
[3] Univ Southampton, Fac Med, Southampton, Hants, England
[4] Newcastle Univ, Inst Hlth & Aging, Newcastle, NSW, Australia
[5] Univ Calif Berkeley, Helen Wills Neuroscience Inst, Berkeley, CA 94720 USA
[6] Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall, Berkeley, CA 94720 USA
基金
英国医学研究理事会;
关键词
ALZHEIMERS-DISEASE; DEMENTIA; MECHANISMS; MODELS;
D O I
10.1002/acn3.27
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
There is substantial controversy regarding the causative role of amyloid beta (A beta) deposition in Alzheimer's disease (AD). The cerebrovasculature plays an important role in the elimination of A beta from the brain and hypertension is a well-known risk factor for AD. In spontaneously hypertensive stroke-prone rats (SHRSP), an animal model of chronic arterial hypertension, cerebral small vessel disease (CSVD) leads to age-dependent parenchymal A beta accumulation similar to that observed in AD. These data approve the neuropathological link between CSVD and AD, confirm the challenge that parenchymal A beta deposition is a specific marker for AD and disclose the meaning of SHRSP as valid experimental model to investigate the association between hypertension, CSVD, and A beta plaques.
引用
收藏
页码:124 / 129
页数:6
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