ArticleNeurobiology of aging2023
Biologic that disrupts PDE11A4 homodimerization in hippocampus CA1 reverses age-related cognitive decline of social memories in mice.
Article in Neurobiology of aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Ononin, a Natural Isoflavone Glycoside, Alleviates Postoperative Cognitive Dysfunction in Aged Mice by Regulating Neuroinflammation and Oxidative Stress.Brain and behavior · 2025Article
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- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- First Demonstration ofJournal of medicinal chemistry · 2024Article
- Article
- The sleep quality- and myopia-linked PDE11A-Y727C variant impacts neural physiology by reducing catalytic activity and altering subcellular compartmentalization of the enzyme.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Age-related abnormalities in phosphodiesterase 11A (PDE11A), which degrades 3',5'-cAMP/cGMP and is enriched in the ventral hippocampus (VHIPP), drive age-related cognitive decline (ARCD) of social memories. Age-related PDE11A4 ectopically accumulates within the membrane compartment and in filamentous structures termed ghost axons. Previous studies show that expressing an isolated PDE11A4-GAF-B binding domain disrupts homodimerization and reverses aging-like PDE11A4 accumulations in vitro. Here, we show that in vivo lentiviral expression of the isolated PDE11A4-GAFB domain in hippocampal CA1 of aged mice reverses age-related PDE11A4 accumulations and ARCD of social transmission of food preference memory (STFP). It also improves 7-day remote long-term memory for social odor recognition without affecting non-social odor recognition. In vitro studies show that disrupting homodimerization does not alter the catalytic activity of PDE11A4 but may reverse age-related decreases in cGMP by relocating PDE11A4 from a cGMP-rich to a cAMP-rich pool independently of other intramolecular relocation signals (PDE11A4-pS162). Altogether, these data suggest that a biologic designed to disrupt PDE11A4 homodimerization may hold therapeutic potential for age-related PDE11A4 proteinopathies.
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