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George Mason University

An Investigation into the Role of Dietary Copper and Zinc on Copper/Zinc Cellular Bioavailability, Inflammation, and Species Typical Behaviors in a Late Onset Mouse Model of Alzheimer’s Disease

Abstract

Research in the field of Alzheimer’s disease (AD) often focuses on the early onset form (EOAD); however, the majority of AD cases are late onset (LOAD). The reason for this is the genetic nature of EOAD, and thus relative ease of developing animal models for EOAD through genetic manipulation. The present study was an attempt to model LOAD in mice by crossing the J20 mouse, which overexpresses human mutated amyloid precursor protein (hAPP), with the ApoE4 mouse, which expresses the E4 allele of the apolipoprotein, resulting in J20/E4 offspring. The E4 allele is the only known genetic risk factor for the development of LOAD.

Author and committee

dc:creator, dc:contributor.*
Author
  • Boggs, Katelyn Nicole

Subjects

dc:subject × 6

Identifiers

dc:identifier.*
Identifier
hdl:1920/11153
OAI identifier oai:identifier
oai:MARS:1920/11153

Chain of custody

source
Harvested from
George Mason University
Base URL
mars.gmu.edu/server/oai/request
Last updated
2026-07-27
Source record
OAI-PMH GetRecord
citation

Boggs, Katelyn Nicole. An Investigation into the Role of Dietary Copper and Zinc on Copper/Zinc Cellular Bioavailability, Inflammation, and Species Typical Behaviors in a Late Onset Mouse Model of Alzheimer’s Disease. 2017.