Tags

Type your tag names separated by a space and hit enter

The lipophilic metal chelator DP-109 reduces amyloid pathology in brains of human beta-amyloid precursor protein transgenic mice.
Neurobiol Aging. 2004 Nov-Dec; 25(10):1315-21.NA

Abstract

Metals such as zinc, copper and iron contribute to aggregation of amyloid-beta (Abeta) protein and deposition of amyloid plaques in Alzheimer's disease (AD). We examined whether the lipophilic metal chelator DP-109 inhibited these events in aged female hAbetaPP-transgenic Tg2576 mice. Daily gavage administration of DP-109 for 3 months markedly reduced the burden of amyloid plaques and the degree of cerebral amyloid angiopathy in brains, compared to animals receiving vehicle treatment. Moreover, DP-109 treatment appeared to facilitate the transition of Abeta from insoluble to soluble forms in the cerebrum. These results further support the hypothesis that endogenous metals are involved in the deposition of aggregated Abeta in brains of AD patients, and that metal chelators may be useful therapeutic agents in the treatment of AD.

Authors+Show Affiliations

Department of Neurology, National Creative Research Initiative Center for the Study of CNS Zinc, College of Medicine, University of Ulsan, Seoul 138-736, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15465629

Citation

Lee, Joo-Yong, et al. "The Lipophilic Metal Chelator DP-109 Reduces Amyloid Pathology in Brains of Human Beta-amyloid Precursor Protein Transgenic Mice." Neurobiology of Aging, vol. 25, no. 10, 2004, pp. 1315-21.
Lee JY, Friedman JE, Angel I, et al. The lipophilic metal chelator DP-109 reduces amyloid pathology in brains of human beta-amyloid precursor protein transgenic mice. Neurobiol Aging. 2004;25(10):1315-21.
Lee, J. Y., Friedman, J. E., Angel, I., Kozak, A., & Koh, J. Y. (2004). The lipophilic metal chelator DP-109 reduces amyloid pathology in brains of human beta-amyloid precursor protein transgenic mice. Neurobiology of Aging, 25(10), 1315-21.
Lee JY, et al. The Lipophilic Metal Chelator DP-109 Reduces Amyloid Pathology in Brains of Human Beta-amyloid Precursor Protein Transgenic Mice. Neurobiol Aging. 2004 Nov-Dec;25(10):1315-21. PubMed PMID: 15465629.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The lipophilic metal chelator DP-109 reduces amyloid pathology in brains of human beta-amyloid precursor protein transgenic mice. AU - Lee,Joo-Yong, AU - Friedman,Jonathan E, AU - Angel,Itzchak, AU - Kozak,Alex, AU - Koh,Jae-Young, PY - 2003/10/06/received PY - 2003/12/18/revised PY - 2004/01/07/accepted PY - 2004/10/7/pubmed PY - 2004/12/16/medline PY - 2004/10/7/entrez SP - 1315 EP - 21 JF - Neurobiology of aging JO - Neurobiol. Aging VL - 25 IS - 10 N2 - Metals such as zinc, copper and iron contribute to aggregation of amyloid-beta (Abeta) protein and deposition of amyloid plaques in Alzheimer's disease (AD). We examined whether the lipophilic metal chelator DP-109 inhibited these events in aged female hAbetaPP-transgenic Tg2576 mice. Daily gavage administration of DP-109 for 3 months markedly reduced the burden of amyloid plaques and the degree of cerebral amyloid angiopathy in brains, compared to animals receiving vehicle treatment. Moreover, DP-109 treatment appeared to facilitate the transition of Abeta from insoluble to soluble forms in the cerebrum. These results further support the hypothesis that endogenous metals are involved in the deposition of aggregated Abeta in brains of AD patients, and that metal chelators may be useful therapeutic agents in the treatment of AD. SN - 0197-4580 UR - https://www.unboundmedicine.com/medline/citation/15465629/The_lipophilic_metal_chelator_DP_109_reduces_amyloid_pathology_in_brains_of_human_beta_amyloid_precursor_protein_transgenic_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197458004000430 DB - PRIME DP - Unbound Medicine ER -