Abstract

This project is a multi-disciplinary approach with the goal of identifying the neurobiological basis of behavior changes in the aged. Dr. J. McGaugh and his group are studying the relationship between stress, pain threshold and transmitter systems in the aged. Their recent studies have identified age related changes in opiate receptor activity in various brain areas which appear to correlate with observed behavioral changes. Dr. Marshall and co-workers have continued to investigate sensorimotor disturbances in the aging rodent; most recently examining the pharmacological characteristics of central dopamine systems. Dr. Lynch and co-workers are studying the neurochemical and physiological correlates of long term potentiation. Dr. Cotman and co-workers are continuing their studies on lesion induced synaptic growth in aged brain. It now seems established that new connections for slower and there are fewer following brain injury in aged. Dr. Moldave and co-workers have shown that beta endorphin and enkephalins can inhibit protein synthesis in vitro. Their studies continue to analyze the capacity of aged cells to synthesize proteins.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Program Projects (P01)
Project #
5P01AG000538-12
Application #
3090513
Study Section
Aging Review Committee (AGE)
Project Start
1985-09-30
Project End
1990-08-31
Budget Start
1988-09-01
Budget End
1989-08-31
Support Year
12
Fiscal Year
1988
Total Cost
Indirect Cost

  Institution

Name
University of California Irvine
Department
Type
Schools of Arts and Sciences
DUNS #
161202122
City
Irvine
State
CA
Country
United States
Zip Code
92697

  Publications

Sosna, Justyna; Philipp, Stephan; Albay 3rd, Ricardo et al. (2018) Early long-term administration of the CSF1R inhibitor PLX3397 ablates microglia and reduces accumulation of intraneuronal amyloid, neuritic plaque deposition and pre-fibrillar oligomers in 5XFAD mouse model of Alzheimer's disease. Mol Neurodegener 13:11
Tong, Liqi; Prieto, G Aleph; Cotman, Carl W (2018) IL-1? suppresses cLTP-induced surface expression of GluA1 and actin polymerization via ceramide-mediated Src activation. J Neuroinflammation 15:127
Hainsworth, A H; Lee, S; Foot, P et al. (2018) Super-resolution imaging of subcortical white matter using stochastic optical reconstruction microscopy (STORM) and super-resolution optical fluctuation imaging (SOFI). Neuropathol Appl Neurobiol 44:417-426
Krotee, Pascal; Griner, Sarah L; Sawaya, Michael R et al. (2018) Common fibrillar spines of amyloid-? and human islet amyloid polypeptide revealed by microelectron diffraction and structure-based inhibitors. J Biol Chem 293:2888-2902
Prieto, G Aleph; Tong, Liqi; Smith, Erica D et al. (2018) TNF? and IL-1? but not IL-18 Suppresses Hippocampal Long-Term Potentiation Directly at the Synapse. Neurochem Res :
Krotee, Pascal; Rodriguez, Jose A; Sawaya, Michael R et al. (2017) Atomic structures of fibrillar segments of hIAPP suggest tightly mated ?-sheets are important for cytotoxicity. Elife 6:
Hernandez, Michael X; Jiang, Shan; Cole, Tracy A et al. (2017) Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss. Mol Neurodegener 12:66
Thielens, Nicole M; Tedesco, Francesco; Bohlson, Suzanne S et al. (2017) C1q: A fresh look upon an old molecule. Mol Immunol 89:73-83
Prieto, G Aleph; Trieu, Brian H; Dang, Cindy T et al. (2017) Pharmacological Rescue of Long-Term Potentiation in Alzheimer Diseased Synapses. J Neurosci 37:1197-1212
Carlos, Anthony J; Tong, Liqi; Prieto, G Aleph et al. (2017) IL-1? impairs retrograde flow of BDNF signaling by attenuating endosome trafficking. J Neuroinflammation 14:29

Showing the most recent 10 out of 281 publications