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Osteocalcin is a bone-derived hormone that regulates a growing number of physiological functions. In particular, although Osteocalcin is not expressed in any part of the brain before or after birth, Osteocalcin-/- mice have increased anxiety-like behavior and depression, decreased exploratory behavior, and impaired learning and memory when compared to wildtype littermates. In the brain, osteocalcin promotes the synthesis of monoamine neurotransmitters and inhibits synthesis of GABA by regulating the expression of key enzymes. Given that osteocalcin is produced only by osteoblasts, Khrimian et al. asked whether an impairment in osteoblast differentiation and function, as may occur in various skeletal dysplasias or with aging, could affect cognition or anxiety. They studied Runx2+/- mice, which phenocopy the haploinsufficiency that is observed in patients with cleidocranial dysplasia (CCD), a classical skeletal dysplasia in which cognitive functions are also affected. Their results suggest that a decrease in osteocalcin is indeed the cause for these cognitive impairments. Moreover, it is implied that bone anabolic treatments for degenerative diseases of the skeleton, such as osteoporosis, may also have a beneficial effect on cognitive function and anxiety-like behavior, whereas anti-resorptive agents may potentially be detrimental.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Luc Pellerin
Université de Lausanne, Switzerland
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