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Yamazaki, D., Horiuchi, J., Ueno, K., Ueno, T., Saeki, S., Matsuno, M., Naganos, S., Miyashita, T., Hirano, Y., Nishikawa, H., Taoka, M., Yamauchi, Y., Isobe, T., Honda, Y., Kodama, T., Masuda, T., Saitoe, M. (2014). Glial dysfunction causes age-related memory impairment in Drosophila.  Neuron 84(4): 753--763.
FlyBase ID
FBrf0226947
Publication Type
Research paper
Abstract

Several aging phenotypes, including age-related memory impairment (AMI), are thought to be caused by cumulative oxidative damage. In Drosophila, age-related impairments in 1 hr memory can be suppressed by reducing activity of protein kinase A (PKA). However, the mechanism for this effect has been unclear. Here we show that decreasing PKA suppresses AMI by reducing activity of pyruvate carboxylase (PC), a glial metabolic enzyme whose amounts increase upon aging. Increased PC activity causes AMI through a mechanism independent of oxidative damage. Instead, increased PC activity is associated with decreases in D-serine, a glia-derived neuromodulator that regulates NMDA receptor activity. D-serine feeding suppresses both AMI and memory impairment caused by glial overexpression of dPC, indicating that an oxidative stress-independent dysregulation of glial modulation of neuronal activity contributes to AMI in Drosophila.

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PubMed Central ID
Related Publication(s)
Note

Learn to forget: regulation of age-related memory impairment by neuronal-glial crosstalk.
Jackson, 2014, Neuron 84(4): 658--659 [FBrf0227013]

Aging: a slow slide in memory.
Lewis, 2015, Nat. Rev. Neurosci. 16(1): 2--3 [FBrf0227545]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Neuron
    Title
    Neuron
    Publication Year
    1988-
    ISBN/ISSN
    0896-6273
    Data From Reference