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Brain Res Bull. 2014 Apr;103:29-38. doi: 10.1016/j.brainresbull.2013.12.006. Epub 2013 Dec 12.

Abnormal kalirin signaling in neuropsychiatric disorders.

Author information

1
Department of Physiology, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
2
Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; VISN 4 Mental Illness Research, Education and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA, USA.
3
Department of Physiology, 303 E. Chicago Avenue, Chicago, IL 60611, USA; Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, 303 E. Chicago Avenue, Chicago, IL 60611, USA. Electronic address: p-penzes@northwestern.edu.

Abstract

Changes in dendritic spines structure and function play a critical role in a number of physiological processes, including synaptic transmission and plasticity, and are intimately linked to cognitive function. Alterations in dendritic spine morphogenesis occur in a number of neuropsychiatric disorders and likely underlie the cognitive and behavioral changes associated with these disorders. The neuronal guanine nucleotide exchange factor (GEF) kalirin is emerging as a key regulator of structural and functional plasticity at dendritic spines. Moreover, a series of recent studies have genetically and functionally linked kalirin signaling to several disorders, including schizophrenia and Alzheimer's disease. Kalirin signaling may thus represent a disease mechanism and provide a novel therapeutic target.

KEYWORDS:

Alzheimer's disease; Genetic; Glutamatergic; Mental disorder; Postmortem; Schizophrenia

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