Affiliations: [a] Department of Biochemistry and Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea | [b] Institute on Aging, Seoul National University College of Medicine, Seoul, Korea
Correspondence:
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Correspondence to: Inhee Mook-Jung, PhD, Department of Biochemistry and Biomedical Sciences, Seoul National University College of Medicine, 28 Yungun-dong, Jongro-gu, Seoul, 110-799, Korea. Tel.: +82 2 740 8245; Fax: +82 2 3672 7352; E-mail: [email protected].
Note: [1] Authors contributed equally.
Abstract: Deposition of amyloid-β peptide (Aβ) and neurofibrillary tangles are pathological hallmarks of Alzheimer's disease (AD), a neurodegenerative disease characterized by cognitive deficits and neuronal loss. Recently, calcineurin (CaN) has been reported as a potential modulator of memory function, synaptic plasticity, and neural degeneration in brains of AD animal models. In the present study, we examined the relationship between Aβ accumulations and CaN activity in brains of the AβPP/PS1 double transgenic mice. Treatment with FK506, a CaN inhibitor, significantly reduces Aβ burden and restores synaptic proteins (synaptophysin and postsynaptic density protein-95; PSD-95) while inducing matrix metallopeptidase-9 (MMP-9) expression in GFAP-positive astrocytes in the brain. These results suggest a role of FK506 and control of CaN activity in neuroprotection associated with Aβ deposition in AD.
