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Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology--a pilot study.
Acta Neuropathol. 2004 Feb; 107(2):83-90.AN

Abstract

Data on the relationship between cerebral amyloid angiopathy (CAA) ("congophilic angiopathy") and Alzheimer's disease (AD) pathology are conflicting. In the present study, CAA and capillary CAA (CapCAA) ("dyshoric angiopathy") were examined in the frontal cortex of 100 human brains obtained at autopsy from both male and female, demented and non-demented patients (mean age +/- SD 84.3+/-9.3 years); 50 brains with high (mean 5.0) and 50 with low (mean 2.4) Braak stages. CAA was assessed according to the method of Olichney et al. [25]; CapCAA was grouped into four grades by counting the affected capillaries in 10 high power fields. General CAA was present in 61% (87.5% demented, 55.6% non-demented; 70% with high and 52% low Braak stages). CAA did not correlate with either clinical diagnosis of dementia or high-grade AD pathology; CapCAA showed a low correlation with dementia and a medium positive correlation with high Braak stages. The severity of both lesions did not correlate with clinical dementia; whereas that of CAA showed low correlation with CERAD, Braak, and NIA-Reagan-Institute criteria, the severity of CapCAA correlated significantly with all three AD criteria. The presence and severity of CAA and CapCAA showed only low correlation, suggesting a different pathogenesis of these types of lesion. Since CapCAA represents insoluble amyloid peptide (Abeta) deposits in and around capillaries, its correlation with neuritic AD pathology supports the concept of neuronal origin of Abeta via drainage from interstitial fluid from the central nervous system to capillary walls. Studies to answer the question whether CapCAA represents an epiphenomenon or an indicator of a pathogenic association between tau cytopathology and Abeta deposition in capillaries are in progress.

Authors+Show Affiliations

Institute of Pathology, Otto Wagner Hospital, Baumgartner Hoehe 1, 1140 Vienna, Austria.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14655019

Citation

Attems, Johannes, and Kurt A. Jellinger. "Only Cerebral Capillary Amyloid Angiopathy Correlates With Alzheimer Pathology--a Pilot Study." Acta Neuropathologica, vol. 107, no. 2, 2004, pp. 83-90.
Attems J, Jellinger KA. Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology--a pilot study. Acta Neuropathol. 2004;107(2):83-90.
Attems, J., & Jellinger, K. A. (2004). Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology--a pilot study. Acta Neuropathologica, 107(2), 83-90.
Attems J, Jellinger KA. Only Cerebral Capillary Amyloid Angiopathy Correlates With Alzheimer Pathology--a Pilot Study. Acta Neuropathol. 2004;107(2):83-90. PubMed PMID: 14655019.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Only cerebral capillary amyloid angiopathy correlates with Alzheimer pathology--a pilot study. AU - Attems,Johannes, AU - Jellinger,Kurt A, Y1 - 2003/12/04/ PY - 2003/10/03/received PY - 2003/11/03/accepted PY - 2003/12/5/pubmed PY - 2004/4/6/medline PY - 2003/12/5/entrez SP - 83 EP - 90 JF - Acta neuropathologica JO - Acta Neuropathol. VL - 107 IS - 2 N2 - Data on the relationship between cerebral amyloid angiopathy (CAA) ("congophilic angiopathy") and Alzheimer's disease (AD) pathology are conflicting. In the present study, CAA and capillary CAA (CapCAA) ("dyshoric angiopathy") were examined in the frontal cortex of 100 human brains obtained at autopsy from both male and female, demented and non-demented patients (mean age +/- SD 84.3+/-9.3 years); 50 brains with high (mean 5.0) and 50 with low (mean 2.4) Braak stages. CAA was assessed according to the method of Olichney et al. [25]; CapCAA was grouped into four grades by counting the affected capillaries in 10 high power fields. General CAA was present in 61% (87.5% demented, 55.6% non-demented; 70% with high and 52% low Braak stages). CAA did not correlate with either clinical diagnosis of dementia or high-grade AD pathology; CapCAA showed a low correlation with dementia and a medium positive correlation with high Braak stages. The severity of both lesions did not correlate with clinical dementia; whereas that of CAA showed low correlation with CERAD, Braak, and NIA-Reagan-Institute criteria, the severity of CapCAA correlated significantly with all three AD criteria. The presence and severity of CAA and CapCAA showed only low correlation, suggesting a different pathogenesis of these types of lesion. Since CapCAA represents insoluble amyloid peptide (Abeta) deposits in and around capillaries, its correlation with neuritic AD pathology supports the concept of neuronal origin of Abeta via drainage from interstitial fluid from the central nervous system to capillary walls. Studies to answer the question whether CapCAA represents an epiphenomenon or an indicator of a pathogenic association between tau cytopathology and Abeta deposition in capillaries are in progress. SN - 0001-6322 UR - https://www.unboundmedicine.com/medline/citation/14655019/Only_cerebral_capillary_amyloid_angiopathy_correlates_with_Alzheimer_pathology__a_pilot_study_ L2 - https://dx.doi.org/10.1007/s00401-003-0796-9 DB - PRIME DP - Unbound Medicine ER -