The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Angiotensin‐converting enzyme (ACE) levels and activity in Alzheimer's disease, and relationship of perivascular ACE‐1 to cerebral amyloid angiopathy
Abstract
Aims: Several observations point to the involvement of angiotensin‐converting enzyme‐1 (ACE‐1) in Alzheimer's disease (AD): ACE‐1 cleaves amyloid‐β peptide (Aβ) in vitro, the level and activity of ACE‐1 are reportedly increased in AD, and variations in the ACE‐1 gene are associated with AD. We analysed ACE‐1 activity and expression in AD and control brains, particularly in relation to Aβ load and cerebral amyloid angiopathy (CAA). Methods: ACE‐1 activity was measured in the frontal cortex from 58 control and 114 AD cases of known Aβ load and CAA severity. The distribution of ACE‐1 was examined immunohistochemically. In five AD cases with absent or mild CAA, five with moderate to severe CAA and five controls with absent or mild CAA, levels of vascular ACE‐1 were assessed by quantitative immunofluorescence. Results: ACE‐1 activity was increased in AD (P < 0.001) and correlated directly with parenchymal Aβ load (P = 0.05). Immunohistochemistry revealed ACE‐1 in neurones and cortical blood vessels – in the intima but most abundant perivascularly. Cases with moderate to severe CAA had significantly more vessel‐associated ACE‐1 than did those with little or no CAA. Perivascular ACE‐1 did not colocalize with Aβ, smooth muscle actin, glial fibrillary acidic protein, collagen IV, vimentin or laminin, but was similarly distributed to extracellular matrix (ECM) proteins fibronectin and decorin. Conclusions: Our findings indicate that ACE‐1 activity is increased in AD, in direct relationship to parenchymal Aβ load. Increased ACE‐1, probably of neuronal origin, accumulates perivascularly in severe CAA and colocalizes with vascular ECM. The possible relationship of ACE‐1 to the deposition of perivascular ECM remains to be determined.
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Variation in DCP1, encoding ACE, is associated with susceptibility to Alzheimer disease
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Ballard, C., Gauthier, S., Corbett, A., Brayne, C., Aarsland, D., & Jones, E. (2011) · The Lancet · doi:10.1016/s0140-6736(10)61349-9 · Cited by 2,336
Angiotensin II revisited: new roles in inflammation, immunology and aging
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Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses
Bertram, L., & Tanzi, R. E. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2494 · Cited by 747
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Metadata
- Authors
- Miners, J. S., Ashby, E., Van Helmond, Z., Chalmers, K. A., Palmer, L. E., Love, S., & Kehoe, P. G.
- Venue
- Neuropathology and Applied Neurobiology
- Publisher
- Wiley
- Published
- 2007-10-31
- Volume
- 34
- Issue
- 2
- Pages
- 181-193
- ISSN
- 0305-1846 (ISSN-L)
- 1365-2990
- OpenAlex
- W1969501720
- Cited by
- 166
- References
- 11
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- closed
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- Miners, J. S., Ashby, E., Van Helmond, Z., Chalmers, K. A., Palmer, L. E., Love, S., & Kehoe, P. G. (2008). Angiotensin‐converting enzyme (ACE) levels and activity in Alzheimer's disease, and relationship of perivascular ACE‐1 to cerebral amyloid angiopathy. Neuropathology and Applied Neurobiology. https://doi.org/10.1111/j.1365-2990.2007.00885.x
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