ArticleThe Journal of clinical investigation2024
KIBRA repairs synaptic plasticity and promotes resilience to tauopathy-related memory loss.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Generating models for isoform-specific PKM-KIBRA interactions with BIFC, stabilization and AlphaFold 3.Molecular brain · 2026Article
- Oligomer logic of memory molecules.Molecular brain · 2026Review
- Tau oligomers modulate synapse fate by eliciting progressive bipartite synapse dysregulation and synapse loss.Molecular neurodegeneration · 2026Article
- CD38 Inhibition Ameliorates Age-Related CognitiveDecline via a Choroid Plexus-Cerebrospinal Fluid-Hippocampus Axis.Research square · 2026Article
- Microglia-Neuron Interactions in Alzheimer's Disease.Current neuropharmacology · 2026Review
- WWC proteins as emerging biomarkers and therapeutic targets in cancer pathogenesis.Frontiers in cell and developmental biology · 2026Review
- The Hippo signaling pathway as a therapeutic target in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Maintenance of memory by negative-feedback of synaptic protein elimination: Modeling KIBRA-bioRxiv : the preprint server for biology · 2025Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Structures and functions of the MICOS: Pathogenesis and therapeutic implications in Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Review
- PICK1 links KIBRA and AMPA receptor subunit GluA2 in coiled-coil-driven supramolecular complexes.The Journal of biological chemistry · 2025Article
- Synaptic sabotage: How Tau and α-Synuclein undermine synaptic health.The Journal of cell biology · 2025Review
- Synapse vulnerability and resilience underlying Alzheimer's disease.EBioMedicine · 2025Review
- KIBRA anchoring the action of PKMζ maintains the persistence of memory.Science advances · 2024Article
- Extreme value statistics of nerve transmission delay.PloS one · 2024Article
- Maintenance of memory by negative feedback of synaptic protein elimination: modeling KIBRA-PKMζ dynamics in LTP.Learning & memory (Cold Spring Harbor, N.Y.)Article
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Authors and funding
20 authors at 5 institutions in 1 country.
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Abstract
Synaptic plasticity is obstructed by pathogenic tau in the brain, representing a key mechanism that underlies memory loss in Alzheimer's disease (AD) and related tauopathies. Here, we found that reduced levels of the memory-associated protein KIdney/BRAin (KIBRA) in the brain and increased KIBRA protein levels in cerebrospinal fluid are associated with cognitive impairment and pathological tau levels in disease. We next defined a mechanism for plasticity repair in vulnerable neurons using the C-terminus of the KIBRA protein (CT-KIBRA). We showed that CT-KIBRA restored plasticity and memory in transgenic mice expressing pathogenic human tau; however, CT-KIBRA did not alter tau levels or prevent tau-induced synapse loss. Instead, we found that CT-KIBRA stabilized the protein kinase Mζ (PKMζ) to maintain synaptic plasticity and memory despite tau-mediated pathogenesis. Thus, our results distinguished KIBRA both as a biomarker of synapse dysfunction and as the foundation for a synapse repair mechanism to reverse cognitive impairment in tauopathy.
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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.