ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
PKC ε activation prevents synaptic loss, Aβ elevation, and cognitive deficits in Alzheimer's disease transgenic mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.
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Who cites it
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 222 citations in OpenAlex.
- The Role of Astrocytes in Synapse Loss in Alzheimer's Disease: A Systematic Review.Frontiers in cellular neuroscience · 2022Pooled it
- A Randomized, Double-Blind, Placebo-Controlled, Phase II Study Assessing Safety, Tolerability, and Efficacy of Bryostatin in the Treatment of Moderately Severe to Severe Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Trial
- Bryostatin Effects on Cognitive Function and PKCɛ in Alzheimer's Disease Phase IIa and Expanded Access Trials.Journal of Alzheimer's disease : JAD · 2017Trial
- Rewiring mTOR signaling in Alzheimer's disease: emerging mTOR modulators beyond oncology.Bioscience reports · 2026Review
- Effects of UMP, Choline, and Fish Oil on Synaptic Integrity and Motor Coordination in an Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2026Article
- New Approach for Targeting Small-Molecule Candidates for Intrinsically Disordered Proteins.Methods and protocols · 2025Article
- Neuronal activity-induced GLUT3 plasma translocation supports energy demands for memory acquisition.Communications biology · 2025Article
- Protein Kinase C Family: Structures, Biological Functions, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- Bryostatins 1 and 3 inhibit TRPM8 and modify TRPM8- and TRPV1-mediated lung epithelial cell responses to a proinflammatory stimulus via protein kinase C.Molecular pharmacology · 2025Article
- The E3 Ubiquitin Ligase PRAJA1: A Key Regulator of Synaptic Dynamics and Memory Processes with Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Activating PKC-ε induces HIV expression with improved tolerability.PLoS pathogens · 2025Article
- Optogenetic control of Protein Kinase C-epsilon activity reveals its intrinsic signaling properties with spatiotemporal resolution.bioRxiv : the preprint server for biology · 2025Article
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- An insight into the concept of neuroinflammation and neurodegeneration in Alzheimer's disease: targeting molecular approach Nrf2, NF-κB, and CREB.Inflammopharmacology · 2024Review
- Higher-order interactions between hippocampal CA1 neurons are disrupted in amnestic mice.Nature neuroscience · 2024Article
- Behaviour Hallmarks in Alzheimer's Disease 5xFAD Mouse Model.International journal of molecular sciences · 2024Review
- Alzheimer's therapeutic development: shifting neurodegeneration to neuroregeneration.Trends in pharmacological sciences · 2024Review
- The effects of carvacrol and p-cymene on AβCNS neuroscience & therapeutics · 2024Article
- TPPB modulates PKC activity to attenuate neuroinflammation and ameliorate experimental multiple sclerosis.bioRxiv : the preprint server for biology · 2024Article
- TPPB modulates PKC activity to attenuate neuroinflammation and ameliorate experimental multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the pathologic hallmarks of Alzheimer's disease (AD) neurodegeneration, only synaptic loss in the brains of AD patients closely correlates with the degree of dementia in vivo. Here, we describe a molecular basis for this AD loss of synapses: pathological reduction of synaptogenic PKC isozymes and their downstream synaptogenic substrates, such as brain-derived neurotrophic factor. This reduction, particularly of PKC α and ε, occurs in association with elevation of soluble β amyloid protein (Aβ), but before the appearance of the amyloid plaques or neuronal loss in the Tg2576 AD transgenic mouse strain. Conversely, treatment of the Tg2576 mouse brain with the PKC activator, bryostatin-1, restores normal or supranormal levels of PKC α and ε, reduces the level of soluble Aβ, prevents and/or reverses the loss of hippocampal synapses, and prevents the memory impairment observed at 5 months postpartum. Similarly, the PKC ε-specific activator, DCP-LA, effectively prevents synaptic loss, amyloid plaques, and cognitive deficits (also prevented by bryostatin-1) in the much more rapidly progressing 5XFAD transgenic strain. These results suggest that synaptic loss and the resulting cognitive deficits depend on the balance between the lowering effects of Aβ on PKC α and ε versus the lowering effects of PKC on Aβ in AD transgenic mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.