Physiologic Reelin does not play a strong role in protection against acute stroke

Courtney Lane-Donovan, Charisma Desai, Theresa Pohlkamp, Erik J. Plautz, Joachim Herz, Ann M. Stowe

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Stroke and Alzheimer's disease, two diseases that disproportionately affect the aging population, share a subset of pathological findings and risk factors. The primary genetic risk factor after age for late-onset Alzheimer's disease, ApoE4, has also been shown to increase stroke risk and the incidence of post-stroke dementia. One mechanism by which ApoE4 contributes to disease is by inducing in neurons a resistance to Reelin, a neuromodulator that enhances synaptic function. Previous studies in Reelin knockout mice suggest a role for Reelin in protection against stroke; however, these studies were limited by the developmental requirement for Reelin in neuronal migration. To address the question of the effect of Reelin loss on stroke susceptibility in an architecturally normal brain, we utilized a novel mouse with induced genetic reduction of Reelin. We found that after transient middle cerebral artery occlusion, mice with complete adult loss of Reelin exhibited a similar level of functional deficit and extent of infarct as control mice. Together, these results suggest that physiological Reelin does not play a strong role in protection against stroke pathology.

Original languageEnglish (US)
Pages (from-to)1295-1303
Number of pages9
JournalJournal of Cerebral Blood Flow and Metabolism
Volume36
Issue number7
DOIs
StatePublished - Jul 1 2016

Keywords

  • ApoE4
  • Reelin
  • Reelin conditional knockout
  • stroke
  • transient middle cerebral artery occlusion

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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