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Abstract #4724

Resting state functional connectivity in a triple-transgenic mouse model of Alzheimers Disease: preliminary results

Hanbing Lu 1 , Dong Liu 2 , Joshua Banks 1 , Elliot A. Stein 1 , Mark P Mattson 2 , and Yihong Yang 1

1 Neuroimaging Research Branch, National Insitute on Drug Abuse, NIH, Baltimore, Maryland, United States, 2 Laboratory of Neurosciences, National Institute on Aging, NIH, Baltimore, Maryland, United States

Human neuroimaging studies suggest that brain regions associated with A deposition and cortical atrophy in AD patients overlap remarkably well with the so-called default mode network (DMN), indicating that compromise in spontaneous activity within the DMN may serve as a biomarker for diagnosis and for monitoring the progression of AD. The triple-transgenic mouse model of AD (3~TgAD) shares amyloid and tau pathologies, and cognitive deficits similar to human AD patients, and has been valuable in studying the pathophysiology and progression of AD. In the present study, we aimed to identify the mouse DMN and to investigate its potential dysregulation in a 3~TgAD mouse model.

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