title: Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits.
abstract: Amyloid-β (Aβ) is a major pathological mediator of both familial and sporadic Alzheimer's disease (AD). In the brains of AD patients, progressive accumulation of Aβ oligomers and plaques is observed. Such Aβ abnormalities are believed to block long-term potentiation, impair synaptic function, and induce cognitive deficits. Clinical and experimental evidences have revealed that the acute increase of Aβ levels in the brain allows development of Alzheimer-like phenotypes. Hence, a detailed protocol describing how to acutely generate an AD mouse model via the intracerebroventricular (ICV) injection of Aβ is necessary in many cases. In this protocol, the steps of the experiment with an Aβ-injected mouse are included, from the preparation of peptides to the testing of behavioral abnormalities. The process of preparing the tools and animal subjects before the injection, of injecting the Aβ into the mouse brain via ICV injection, and of assessing the degree of cognitive impairment are easily explained throughout the protocol, with an emphasis on tips for effective ICV injection of Aβ. By mimicking certain aspects of AD with a designated injection of Aβ, researchers can bypass the aging process and focus on the downstream pathology of Aβ abnormalities.
authors.affiliation: Center for Neuro-Medicine, Korea Institute of Science and Technology; Research Institute, GoshenBiotech, Inc.
authors.forename: Hye Yun
authors.initials: HY
authors.lastname: Kim
authors.affiliation: Center for Neuro-Medicine, Korea Institute of Science and Technology.
authors.forename: Dongkeun K
authors.initials: DK
authors.lastname: Lee
authors.affiliation: Center for Neuro-Medicine, Korea Institute of Science and Technology; Department of Chemical and Biological Engineering, Princeton University.
authors.forename: Bo-Ryehn
authors.initials: BR
authors.lastname: Chung
authors.affiliation: Center for Neuro-Medicine, Korea Institute of Science and Technology; Biological Chemistry Program, Korea University of Science and Technology.
authors.forename: Hyunjin V
authors.initials: HV
authors.lastname: Kim
authors.affiliation: Center for Neuro-Medicine, Korea Institute of Science and Technology; Biological Chemistry Program, Korea University of Science and Technology; yskim@bio.kist.re.kr.
authors.forename: YoungSoo
authors.initials: Y
authors.lastname: Kim
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D003072:Cognition Disorders / Q000139:chemically induced* / Q000473:pathology; D004195:Disease Models, Animal; D007276:Injections, Intraventricular; D017774:Long-Term Potentiation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D010446:Peptide Fragments; D058225:Plaque, Amyloid / Q000473:pathology; D011597:Psychomotor Performance
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments