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Enhanced capillary amyloid angiopathy-associated pathology in Tg-SwDI mice with deleted nitric oxide synthase 2.
Stroke. 2010 Oct; 41(10 Suppl):S135-8.S

Abstract

BACKGROUND AND PURPOSE

Cerebral amyloid angiopathy Type 1 is characterized by amyloid β protein deposition along cerebral capillaries and is accompanied by perivascular neuroinflammation and accumulation of phospho-tau protein. Tg-SwDI mice recapitulate capillary amyloid deposition and associated neuroinflammation but lack accumulation of perivascular phospho-tau protein.

METHODS

Tg-SwDI mice were bred onto a nitric oxide synthase 2 gene knockout background and aged for 1 year. Brains were harvested and analyzed using immunohistochemical and quantitative stereological methods to determine the extent of capillary amyloid deposition, perivascular activated microglia, and cell-specific accumulation of phospho-tau protein. Similar methods were also used to compare Tg-SwDI/NOS2(-/-) and human cerebral amyloid angiopathy Type 1 brain tissues.

RESULTS

The absence of nitric oxide synthase 2 gene had no effect on the regional pattern or frequency of capillary cerebral amyloid angiopathy or the numbers of perivascular activated microglia in Tg-SwDI mice. On the other hand, Tg-SwDI/NOS2(-/-) mice accumulated phospho-tau protein in perivascular neurons and activated microglia. Tg-SwDI/NOS2(-/-) mice exhibited a very similar distribution of capillary amyloid, activated microglia, and perivascular phospho-tau protein as seen in human cerebral amyloid angiopathy Type 1.

CONCLUSIONS

These findings indicate that Tg-SwDI/NOS2(-/-) mice more fully recapitulate the pathological changes observed with capillary amyloid in human cerebral amyloid angiopathy Type 1.

Authors+Show Affiliations

Department of Neurosurgery, HSC T-12/086, Stony Brook University, Stony Brook, NY 11794-8122, USA. William.VanNostrand@stonybrook.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20876489

Citation

Van Nostrand, William E., et al. "Enhanced Capillary Amyloid Angiopathy-associated Pathology in Tg-SwDI Mice With Deleted Nitric Oxide Synthase 2." Stroke, vol. 41, no. 10 Suppl, 2010, pp. S135-8.
Van Nostrand WE, Xu F, Rozemuller AJ, et al. Enhanced capillary amyloid angiopathy-associated pathology in Tg-SwDI mice with deleted nitric oxide synthase 2. Stroke. 2010;41(10 Suppl):S135-8.
Van Nostrand, W. E., Xu, F., Rozemuller, A. J., & Colton, C. A. (2010). Enhanced capillary amyloid angiopathy-associated pathology in Tg-SwDI mice with deleted nitric oxide synthase 2. Stroke, 41(10 Suppl), S135-8. https://doi.org/10.1161/STROKEAHA.110.595272
Van Nostrand WE, et al. Enhanced Capillary Amyloid Angiopathy-associated Pathology in Tg-SwDI Mice With Deleted Nitric Oxide Synthase 2. Stroke. 2010;41(10 Suppl):S135-8. PubMed PMID: 20876489.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced capillary amyloid angiopathy-associated pathology in Tg-SwDI mice with deleted nitric oxide synthase 2. AU - Van Nostrand,William E, AU - Xu,Feng, AU - Rozemuller,Annemieke J M, AU - Colton,Carol A, PY - 2010/9/30/entrez PY - 2010/10/12/pubmed PY - 2010/11/3/medline SP - S135 EP - 8 JF - Stroke JO - Stroke VL - 41 IS - 10 Suppl N2 - BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy Type 1 is characterized by amyloid β protein deposition along cerebral capillaries and is accompanied by perivascular neuroinflammation and accumulation of phospho-tau protein. Tg-SwDI mice recapitulate capillary amyloid deposition and associated neuroinflammation but lack accumulation of perivascular phospho-tau protein. METHODS: Tg-SwDI mice were bred onto a nitric oxide synthase 2 gene knockout background and aged for 1 year. Brains were harvested and analyzed using immunohistochemical and quantitative stereological methods to determine the extent of capillary amyloid deposition, perivascular activated microglia, and cell-specific accumulation of phospho-tau protein. Similar methods were also used to compare Tg-SwDI/NOS2(-/-) and human cerebral amyloid angiopathy Type 1 brain tissues. RESULTS: The absence of nitric oxide synthase 2 gene had no effect on the regional pattern or frequency of capillary cerebral amyloid angiopathy or the numbers of perivascular activated microglia in Tg-SwDI mice. On the other hand, Tg-SwDI/NOS2(-/-) mice accumulated phospho-tau protein in perivascular neurons and activated microglia. Tg-SwDI/NOS2(-/-) mice exhibited a very similar distribution of capillary amyloid, activated microglia, and perivascular phospho-tau protein as seen in human cerebral amyloid angiopathy Type 1. CONCLUSIONS: These findings indicate that Tg-SwDI/NOS2(-/-) mice more fully recapitulate the pathological changes observed with capillary amyloid in human cerebral amyloid angiopathy Type 1. SN - 1524-4628 UR - https://www.unboundmedicine.com/medline/citation/20876489/Enhanced_capillary_amyloid_angiopathy_associated_pathology_in_Tg_SwDI_mice_with_deleted_nitric_oxide_synthase_2_ L2 - http://www.ahajournals.org/doi/full/10.1161/STROKEAHA.110.595272?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -