ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2015
Atlas stumbled: kinesin light chain-1 variant E triggers a vicious cycle of axonal transport disruption and amyloid-β generation in Alzheimer's disease.
Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope.Oxidative medicine and cellular longevity · 2022Review
- Exogenous brain-derived neurotrophic factor attenuates cognitive impairment induced by okadaic acid in a rat model of Alzheimer's disease.Neural regeneration research · 2018Article
- Integrated analysis of human genetic association study and mouse transcriptome suggests LBH and SHF genes as novel susceptible genes for amyloid-β accumulation in Alzheimer's disease.Human genetics · 2018Article
- Microtubules in health and degenerative disease of the nervous system.Brain research bulletin · 2016Review
- New Insights into Epigenetic and Pharmacological Regulation of Amyloid-Degrading Enzymes.Neurochemical research · 2016Article
- Amyloid-β precursor protein: Multiple fragments, numerous transport routes and mechanisms.Experimental cell research · 2015Review
- Vaccinia virus protein complex F12/E2 interacts with kinesin light chain isoform 2 to engage the kinesin-1 motor complex.PLoS pathogens · 2015Article
- Kinesin light chain-1 variant E disrupts axonal transport and Aβ generation in Alzheimer's disease (comment on DOI 10.1002/bies.201400131).BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substantial evidence implicates fast axonal transport (FAT) defects in neurodegeneration. In Alzheimer's disease (AD), it is controversial whether transport defects cause or arise from amyloid-β (Aβ)-induced toxicity. Using a novel, unbiased genetic screen, Morihara et al. identified kinesin light chain-1 splice variant E (KLC1vE) as a modifier of Aβ accumulation. Here, we propose three mechanisms to explain this causal role. First, KLC1vE reduces APP transport, leading to Aβ accumulation. Second, reduced transport of APP by KLC1vE triggers an ER stress response that activates the amyloidogenic pathway. Third, KLC1vE impairs transport of other KLC1 cargos that regulate amyloidogenesis, promoting Aβ retention within the secretory pathway. Collectively, KLC1vE perpetuates a vicious cycle of Aβ generation, kinase dysregulation, and global FAT impairment that inevitably leads to cellular toxicity. These concepts implicate alternative splicing of KLC1 in AD and suggest that the reciprocal influence of transport mechanisms on disease states contributes to neurodegeneration.
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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.