ArticleNeurobiology of aging2014
Alzheimer amyloid beta inhibition of Eg5/kinesin 5 reduces neurotrophin and/or transmitter receptor function.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Lysosome trafficking across intracellular and intercellular networks in the brain.Frontiers in molecular neuroscience · 2026Article
- Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025Review
- The multifaceted role of KIF15 in cancer progression and therapy.Investigational new drugs · 2025Review
- Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025Review
- An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation.Actas espanolas de psiquiatria · 2024Review
- Eg5 and Diseases: From the Well-Known Role in Cancer to the Less-Known Activity in Noncancerous Pathological Conditions.Biochemistry research international · 2024Review
- Disrupted Maturation of Prefrontal Layer 5 Neuronal Circuits in an Alzheimer's Mouse Model of Amyloid Deposition.Neuroscience bulletin · 2023Article
- Repurposing ibudilast to mitigate Alzheimer's disease by targeting inflammation.Brain : a journal of neurology · 2023Article
- Mitochondrial Dysfunction Links to Impaired Hippocampal Serotonin Release in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- IncreasediScience · 2022Article
- Upregulation of KIF18B facilitates malignant phenotype of esophageal squamous cell carcinoma by activating CDCA8/mTORC1 pathway.Journal of clinical laboratory analysis · 2022Article
- Early impairment of cortical circuit plasticity and connectivity in the 5XFAD Alzheimer's disease mouse model.Translational psychiatry · 2022Article
- Decreased anterograde transport coupled with sustained retrograde transport contributes to reduced axonal mitochondrial density in tauopathy neurons.Frontiers in molecular neuroscience · 2022Article
- TheInternational journal of molecular sciences · 2021Article
- GSG2 (Haspin) promotes development and progression of bladder cancer through targeting KIF15 (Kinase-12).Aging · 2020Article
- Identification of KIF15 as a potential therapeutic target and prognostic factor for glioma.Oncology reports · 2020Article
- Truncated Tau Induces Mitochondrial Transport Failure Through the Impairment of TRAK2 Protein and Bioenergetics Decline in Neuronal Cells.Frontiers in cellular neuroscience · 2020Article
- Research progress on KIF3B and related diseases.Annals of translational medicine · 2019Review
- High kinesin family member 11 expression predicts poor prognosis in patients with clear cell renal cell carcinoma.Journal of clinical pathology · 2019Article
- Neurotrophin Signaling and Stem Cells-Implications for Neurodegenerative Diseases and Stem Cell Therapy.Molecular neurobiology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
The mechanism by which amyloid beta (Aβ) causes neuronal dysfunction and/or death in Alzheimer's disease (AD) is unclear. Previously, we showed that Aβ inhibits several microtubule-dependent kinesin motors essential for mitosis and also present in mature neurons. Here, we show that inhibition of kinesin 5 (Eg5) by Aβ blocks neuronal function by reducing transport of neurotrophin and neurotransmitter receptors to the cell surface. Specifically, cell-surface NGF/NTR(p75) and NMDA receptors decline in cells treated with Aβ or the kinesin 5 inhibitor monastrol, or expressing APP. Aβ and monastrol also inhibit NGF-dependent neurite outgrowth from PC12 cells and glutamate-dependent Ca++ entry into primary neurons. Like Aβ, monastrol inhibits long-term potentiation, a cellular model of NMDA-dependent learning and memory, and kinesin 5 activity is absent from APP/PS transgenic mice brain or neurons treated with Aβ. These data imply that cognitive deficits in AD may derive in part from inhibition of neuronal Eg5 by Aβ, resulting in impaired neuronal function and/or survival through receptor mislocalization. Preventing inhibition of Eg5 or other motors by Aβ may represent a novel approach to AD therapy.
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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.