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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