Cited by 452Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

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Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

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Gong, Bing, Vitolo, Ottavio V., Trinchese, Fabrizio, Liu, Shumin, Shelanski, Michael, Arancio, Ottavio·2004·Journal of Clinical Investigation

DOI 10.1172/jci22831PMC PMC529285

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Abstract

Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42). Both synaptic and cognitive deficits are reproduced in mice double transgenic for amyloid precursor protein (AA substitution K670N,M671L) and presenilin-1 (AA substitution M146V). Here we demonstrate that brief treatment with the phosphodiesterase 4 inhibitor rolipram ameliorates deficits in both long-term potentiation (LTP) and contextual learning in the double-transgenic mice. Most importantly, this beneficial effect can be extended beyond the duration of the administration. One course of long-term systemic treatment with rolipram improves LTP and basal synaptic transmission as well as working, reference, and associative memory deficits for at least 2 months after the end of the treatment. This protective effect is possibly due to stabilization of synaptic circuitry via alterations in gene expression by activation of the cAMP-dependent protein kinase (PKA)/cAMP regulatory element-binding protein (CREB) signaling pathway that make the synapses more resistant to the insult inflicted by Abeta. Thus, agents that enhance the cAMP/PKA/CREB pathway have potential for the treatment of AD and other diseases associated with elevated Abeta42 levels.

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Background
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Method
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Background
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A Model of the Roles of Essential Kinases in the Induction and Expression of Late Long-Term Potentiation
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“In addition to pro-cognitive action, rolipram was shown to reverse plasticity impairments and cognitive decline in several transgenic AD mouse models (Barad et al., 1998; Costa et al., 2007; Gong et al., 2004; Rutten et al., 2006).”
A Novel Phosphodiesterase Type 4 Inhibitor, HT-0712, Enhances Rehabilitation-Dependent Motor Recovery and Cortical Reorganization After Focal Cortical Ischemia
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“In addition, cognitive improvements are also observed in a mouse model of Alzheimer’s disease after enhancement of cAMP/CREB signaling with rolipram.(32) Within the cerebral cortex, cAMP signaling is important for functional reorganization and plasticity of both visual(33-35) and somatosensory cortical areas.”
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Selective Phosphodiesterase (PDE)-4 Inhibitors
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Identification of a Novel 1,2,3,4-Tetrahydrobenzo[b][1,6]naphthyridine Analogue as a Potent Phosphodiesterase 5 Inhibitor with Improved Aqueous Solubility for the Treatment of Alzheimer’s Disease
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Beneficial effects of rolipram in a quinolinic acid model of striatal excitotoxicity
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Amelioration of recognition memory impairment associated with iron loading or aging by the type 4-specific phosphodiesterase inhibitor rolipram in rats
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“In a similar experimental design, rolipram treatments at this dose chronically for 3 weeks have been demonstrated to have effects several months after treatment cessation with regard to behavior, electrophysiology, and biochemistry where increased phosphorylation of CREB at s133 continued to be increased after treatme…”
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Identification of compounds that potentiate CREB signaling as possible enhancers of long-term memory
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“The activation of CREB downstream in TrkA signaling also inhibits the oligomerization and formation of Aβ and Aβ-induced toxicity (De Felice et al., 2007; Gong et al., 2004).”
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Novel behavioural characteristics of female APPSwe/PS1ΔE9 double transgenic mice
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Novel Phosphodiesterase 4 Inhibitor FCPR03 Alleviates Lipopolysaccharide-Induced Neuroinflammation by Regulation of the cAMP/PKA/CREB Signaling Pathway and NF-κB Inhibition
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“…for PDE4 inhibitors in a wide range of neurodegenerative diseases where neuroinflammation plays an important role, including Alzheimer disease (Gong et al., 2004), Parkinson disease (Blandini, 2013), major depressive disorder (Plattner et al., 2015), and multiple sclerosis (Gonzalez-Garcia et…”
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Age-dependent alterations in cAMP signaling contribute to synaptic plasticity deficits following traumatic brain injury
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Protection against β-amyloid induced abnormal synaptic function and cell death by Ginkgolide J
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“Rolipram, like resveratrol, has cardioprotective and anti-inflammatory properties and has been shown to be neuroprotective in animal models of Alzheimer’s disease and axonal degeneration (42,43).”
Analysis of functional polymorphisms in three synaptic plasticity-related genes (BDNF, COMT AND UCHL1) in Alzheimer's disease in Colombia
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Targeting Phosphodiesterases—Towards a Tailor-Made Approach in Multiple Sclerosis Treatment
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Background

Authors: Gong, B., Vitolo, O. V., Trinchese, F., Liu, S., Shelanski, M., & Arancio, O.
Affiliations: Nathan Kline Institute for Psychiatric Research (US)
Columbia University (US)
ORCID: Gong, Bing
Vitolo, Ottavio V.
Trinchese, Fabrizio
Liu, Shumin
Shelanski, Michael
Arancio, Ottavio
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2004-12-01
Volume: 114
Issue: 11
Pages: 1624-1634
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci22831
PMC: PMC529285
OpenAlex: W2034986487
Cited by: 442
References: 60
Citations by year: 2026: 12 · 2025: 14 · 2024: 16 · 2023: 15 · 2022: 11 · 2021: 13 · 2020: 21 · 2019: 20 · 2018: 17 · 2017: 33 · 2016: 17 · 2015: 20 · 2014: 28 · 2013: 23 · 2012: 23
FWCI: 12.13
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association
University of Minnesota
York University
National Institutes of Health
School of Medicine, New York University
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, rolipram, amyloid-beta 42, synaptic plasticity, long-term potentiation, contextual learning, memory impairment, phosphodiesterase-4 inhibitors, cAMP/PKA/CREB signaling, synaptic transmission, APP/PS1 double transgenic mice
MeSH terms: Alzheimer Disease, Animals, Cognition, Disease Models, Animal, Hippocampus, Humans, Learning, Male, Membrane Proteins, Mice, Transgenic, Synaptic Transmission, Phosphodiesterase Inhibitors, Amyloid beta-Protein Precursor, Cyclic AMP Response Element-Binding Protein, Long-Term Potentiation, Rolipram, Mice, Presenilin-1, In Vitro Techniques

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Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

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