instnjctions): The Synaptic Ap Microdialysis Core will serve projects within this PPG to assess dynamic changes in extracellular, or interstitial fluid (ISF), Ap levels in living mice. Microdialysis enables us to measure Ap levels in the context of a living brain with intact neural networks, a functioning blood-brain barrier, and a normal extracellular milieau. This means that studies are performed in a physiologic setting. Having a core facility organize and conduct these studies, particularly for an intricate technique such as microdialysis, ensures experiments and data across all projects can be combined and compared.

Public Health Relevance

Alzheimer's disease is characterized and likely caused by accumulation of the Ap peptide within the bran extracellular space. Understanding how extracellular Ap changes over time will be critical for determining what factors contribute to disease risk as well as for developing therapeutic interventions. Microdialysis enables us to measure how genes, proteins, or behaviors rapidly change the levels of extracellular Ap.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Program Projects (P01)
Project #
5P01NS074969-03
Application #
8642684
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
Project End
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
3
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Washington University
Department
Type
DUNS #
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Kang, S S; Ren, Y; Liu, C-C et al. (2018) Lipocalin-2 protects the brain during inflammatory conditions. Mol Psychiatry 23:344-350
Hettinger, Jane C; Lee, Hyo; Bu, Guojun et al. (2018) AMPA-ergic regulation of amyloid-? levels in an Alzheimer's disease mouse model. Mol Neurodegener 13:22
Yuede, Carla M; Timson, Benjamin F; Hettinger, Jane C et al. (2018) Interactions between stress and physical activity on Alzheimer's disease pathology. Neurobiol Stress 8:158-171
Zhao, Na; Liu, Chia-Chen; Qiao, Wenhui et al. (2018) Apolipoprotein E, Receptors, and Modulation of Alzheimer's Disease. Biol Psychiatry 83:347-357
Musiek, Erik S; Bhimasani, Meghana; Zangrilli, Margaret A et al. (2018) Circadian Rest-Activity Pattern Changes in Aging and Preclinical Alzheimer Disease. JAMA Neurol 75:582-590
Kress, Geraldine J; Liao, Fan; Dimitry, Julie et al. (2018) Regulation of amyloid-? dynamics and pathology by the circadian clock. J Exp Med 215:1059-1068
Ogaki, Kotaro; Martens, Yuka A; Heckman, Michael G et al. (2018) Multiple system atrophy and apolipoprotein E. Mov Disord 33:647-650
Liao, Fan; Li, Aimin; Xiong, Monica et al. (2018) Targeting of nonlipidated, aggregated apoE with antibodies inhibits amyloid accumulation. J Clin Invest 128:2144-2155
Ising, Christina; Gallardo, Gilbert; Leyns, Cheryl E G et al. (2017) Correction: AAV-mediated expression of anti-tau scFvs decreases tau accumulation in a mouse model of tauopathy. J Exp Med 214:2163
Zhao, Jing; Davis, Mary D; Martens, Yuka A et al. (2017) APOE ?4/?4 diminishes neurotrophic function of human iPSC-derived astrocytes. Hum Mol Genet 26:2690-2700

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