4.6 Article

Hypertension drives parenchymal β-amyloid accumulation in the brain parenchyma

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WILEY
DOI: 10.1002/acn3.27

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  1. Alzheimers Research UK [ARUK-SRF2012-2, ARUK-NCG2013B-1] Funding Source: researchfish
  2. Medical Research Council [G1100540, G0900652, G0400074, G0502157] Funding Source: researchfish
  3. Medical Research Council [G1100540, G0900652, G0502157, G0400074] Funding Source: Medline
  4. MRC [G1100540, G0400074, G0502157, G0900652] Funding Source: UKRI

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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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