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• W2079463522 abstract "Recent work has added strong support to the long-standing hypothesis that the stabilization of both long-term potentiation and memory requires rapid reorganization of the spine actin cytoskeleton. This development has led to new insights into the origins of cognitive disorders, and raised the possibility that a diverse array of memory problems, including those associated with diabetes, reflect disturbances to various components of the same mechanism. In accord with this argument, impairments to long-term potentiation in mouse models of Huntington's disease and in middle-aged rats have both been linked to problems with modulatory factors that control actin polymerization in spine heads. Complementary to the common mechanism hypothesis is the idea of a single treatment for addressing seemingly unrelated memory diseases. First tests of the point were positive: Brain-Derived Neurotrophic Factor (BDNF), a potent activator of actin signaling cascades in adult spines, rescued potentiation in Huntington's disease mutant mice, middle-aged rats, and a mouse model of Fragile-X syndrome. A similar reversal of impairments to long-term potentiation was obtained in middle-aged rats by up-regulating BDNF production with brief exposures to ampakines, a class of drugs that positively modulate AMPA-type glutamate receptors. Work now in progress will test if chronic elevation of BDNF enhances memory in normal animals." @default.
• W2079463522 created "2016-06-24" @default.
• W2079463522 creator A5004377423 @default.
• W2079463522 creator A5073965015 @default.
• W2079463522 creator A5074348666 @default.
• W2079463522 creator A5074538624 @default.
• W2079463522 date "2008-05-01" @default.
• W2079463522 modified "2023-10-16" @default.
• W2079463522 title "The substrates of memory: Defects, treatments, and enhancement" @default.
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• W2079463522 doi "https://doi.org/10.1016/j.ejphar.2007.11.082" @default.
• W2079463522 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2427007" @default.
• W2079463522 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18374328" @default.
• W2079463522 hasPublicationYear "2008" @default.
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