Tags

Type your tag names separated by a space and hit enter

Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model.
Ann Neurol 2000; 47(6):739-47AN

Abstract

The epsilon4 allele of apolipoprotein E (ApoE) is an important genetic risk factor for Alzheimer's disease (AD). Increasing evidence suggests that this association may be linked to the ability of ApoE to interact with the amyloid-beta (Abeta) peptide and influence its concentration and structure. To determine the effect of ApoE on Abeta and other AD pathology in vivo, we used APPsw transgenic mice and ApoE knockout (-/-) mice to generate APPsw animals that carried two (ApoE +/+), one (ApoE +/-), or no copies (ApoE -/-) of the normal mouse ApoE gene. At 12 months of age, Abeta deposition was present in the cortex and hippocampus and was also prominent within leptomeningeal and cortical blood vessels of all APPsw ApoE +/+ mice. Importantly, although Abeta deposition still occurred in APPsw ApoE -/- mice, no fibrillar Abeta deposits were detected in the brain parenchyma or cerebrovasculature. There was also no neuritic degeneration associated with Abeta deposition in the absence of ApoE. These data demonstrate that ApoE facilitates the formation of both neuritic and cerebrovascular plaques, which are pathological hallmarks of AD and cerebral amyloid angiopathy.

Authors+Show Affiliations

Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10852539

Citation

Holtzman, D M., et al. "Apolipoprotein E Facilitates Neuritic and Cerebrovascular Plaque Formation in an Alzheimer's Disease Model." Annals of Neurology, vol. 47, no. 6, 2000, pp. 739-47.
Holtzman DM, Fagan AM, Mackey B, et al. Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model. Ann Neurol. 2000;47(6):739-47.
Holtzman, D. M., Fagan, A. M., Mackey, B., Tenkova, T., Sartorius, L., Paul, S. M., ... Hyman, B. T. (2000). Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model. Annals of Neurology, 47(6), pp. 739-47.
Holtzman DM, et al. Apolipoprotein E Facilitates Neuritic and Cerebrovascular Plaque Formation in an Alzheimer's Disease Model. Ann Neurol. 2000;47(6):739-47. PubMed PMID: 10852539.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model. AU - Holtzman,D M, AU - Fagan,A M, AU - Mackey,B, AU - Tenkova,T, AU - Sartorius,L, AU - Paul,S M, AU - Bales,K, AU - Ashe,K H, AU - Irizarry,M C, AU - Hyman,B T, PY - 2000/6/14/pubmed PY - 2000/7/6/medline PY - 2000/6/14/entrez SP - 739 EP - 47 JF - Annals of neurology JO - Ann. Neurol. VL - 47 IS - 6 N2 - The epsilon4 allele of apolipoprotein E (ApoE) is an important genetic risk factor for Alzheimer's disease (AD). Increasing evidence suggests that this association may be linked to the ability of ApoE to interact with the amyloid-beta (Abeta) peptide and influence its concentration and structure. To determine the effect of ApoE on Abeta and other AD pathology in vivo, we used APPsw transgenic mice and ApoE knockout (-/-) mice to generate APPsw animals that carried two (ApoE +/+), one (ApoE +/-), or no copies (ApoE -/-) of the normal mouse ApoE gene. At 12 months of age, Abeta deposition was present in the cortex and hippocampus and was also prominent within leptomeningeal and cortical blood vessels of all APPsw ApoE +/+ mice. Importantly, although Abeta deposition still occurred in APPsw ApoE -/- mice, no fibrillar Abeta deposits were detected in the brain parenchyma or cerebrovasculature. There was also no neuritic degeneration associated with Abeta deposition in the absence of ApoE. These data demonstrate that ApoE facilitates the formation of both neuritic and cerebrovascular plaques, which are pathological hallmarks of AD and cerebral amyloid angiopathy. SN - 0364-5134 UR - https://www.unboundmedicine.com/medline/citation/10852539/Apolipoprotein_E_facilitates_neuritic_and_cerebrovascular_plaque_formation_in_an_Alzheimer's_disease_model_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0364-5134&date=2000&volume=47&issue=6&spage=739 DB - PRIME DP - Unbound Medicine ER -