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Updated: Jun 13, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

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Published on: July 14, 2010

Oligemic hypoperfusion differentially affects tau and amyloid-{beta}.

Maya A Koike¹, Kim N Green, Mathew Blurton-Jones

¹Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 3212 Biological Sciences III, Irvine, CA 92697-4545, USA.

The American Journal of Pathology

|May 18, 2010

Summary

A single mild brain hypoperfusion event significantly alters Alzheimer's disease pathology. This transient injury increases amyloid-beta and alters tau levels, impacting key proteins long-term.

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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

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Last Updated: Jun 13, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

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Published on: July 14, 2010

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Area of Science:

Neuroscience
Neuropathology
Molecular Biology

Background:

Decreased brain blood flow (hypoperfusion) is linked to Alzheimer's disease (AD) pathology.
Mechanisms connecting hypoperfusion to AD neuropathology are not fully understood.

Purpose of the Study:

To investigate the molecular and cellular effects of transient cerebral hypoperfusion on AD-related proteins in a mouse model.
To elucidate the pathways through which hypoperfusion influences tau and amyloid-beta.

Main Methods:

Developed an oligemic model of cerebral hypoperfusion in 3xTg-AD mice.
Transiently occluded the common carotid arteries.
Examined molecular and cellular changes in tau and amyloid-beta.

Main Results:

A single mild hypoperfusion insult acutely increased amyloid-beta levels by enhancing beta-secretase expression.
Hypoperfusion decreased total tau levels, activating macroautophagy and ubiquitin-proteosome pathways.
Oligemia increased tau phosphorylated at serine(212) and threonine(214), persisting for weeks.

Conclusions:

Mild, transient cerebral hypoperfusion has profound, long-lasting effects on both tau and amyloid-beta.
Hypoperfusion differentially impacts total tau and amyloid-beta, suggesting implications for AD pathogenesis.