Correction to: Integrative approach to sporadic Alzheimer’s disease: deficiency of TYROBP in cerebral Aβ amyloidosis mouse normalizes clinical phenotype and complement subnetwork molecular pathology without reducing Aβ burden (Molecular Psychiatry, (2018), 10.1038/s41380-018-0255-6)

Jean Vianney Haure-Mirande, Minghui Wang, Mickael Audrain, Tomas Fanutza, Soong Ho Kim, Szilvia Heja, Benjamin Readhead, Joel T. Dudley, Robert D. Blitzer, Eric E. Schadt, Bin Zhang, Sam Gandy, Michelle E. Ehrlich

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

This article was originally published under standard licence, but has now been made available under a CC BY 4.0 license. The PDF and HTML versions of the paper have been modified accordingly.

Original languageEnglish (US)
JournalMolecular Psychiatry
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Molecular Pathology
Licensure
Psychiatry
Alzheimer Disease
Phenotype
Amyloid angiopathy

ASJC Scopus subject areas

  • Molecular Biology
  • Psychiatry and Mental health
  • Cellular and Molecular Neuroscience

Cite this

Correction to : Integrative approach to sporadic Alzheimer’s disease: deficiency of TYROBP in cerebral Aβ amyloidosis mouse normalizes clinical phenotype and complement subnetwork molecular pathology without reducing Aβ burden (Molecular Psychiatry, (2018), 10.1038/s41380-018-0255-6). / Haure-Mirande, Jean Vianney; Wang, Minghui; Audrain, Mickael; Fanutza, Tomas; Kim, Soong Ho; Heja, Szilvia; Readhead, Benjamin; Dudley, Joel T.; Blitzer, Robert D.; Schadt, Eric E.; Zhang, Bin; Gandy, Sam; Ehrlich, Michelle E.

In: Molecular Psychiatry, 01.01.2018.

Research output: Contribution to journalArticle

Haure-Mirande, Jean Vianney ; Wang, Minghui ; Audrain, Mickael ; Fanutza, Tomas ; Kim, Soong Ho ; Heja, Szilvia ; Readhead, Benjamin ; Dudley, Joel T. ; Blitzer, Robert D. ; Schadt, Eric E. ; Zhang, Bin ; Gandy, Sam ; Ehrlich, Michelle E. / Correction to : Integrative approach to sporadic Alzheimer’s disease: deficiency of TYROBP in cerebral Aβ amyloidosis mouse normalizes clinical phenotype and complement subnetwork molecular pathology without reducing Aβ burden (Molecular Psychiatry, (2018), 10.1038/s41380-018-0255-6). In: Molecular Psychiatry. 2018.
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