期刊
ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY
卷 1, 期 2, 页码 124-129出版社
WILEY
DOI: 10.1002/acn3.27
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资金
- Alzheimers Research UK [ARUK-SRF2012-2, ARUK-NCG2013B-1] Funding Source: researchfish
- Medical Research Council [G1100540, G0900652, G0400074, G0502157] Funding Source: researchfish
- Medical Research Council [G1100540, G0900652, G0502157, G0400074] Funding Source: Medline
- MRC [G1100540, G0400074, G0502157, G0900652] Funding Source: UKRI
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.
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