ArticleActa physiologica (Oxford, England)2018
Presenilin PS1∆E9 disrupts mobility of secretory organelles in rat astrocytes.
Article in Acta physiologica (Oxford, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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3 citing papers in PubMed, 4 citations in OpenAlex.
- Regulated exocytosis from astrocytes: a matter of vesicles?Frontiers in neuroscience · 2024Article
- Article
- Astroglia in Alzheimer's Disease.Advances in experimental medicine and biology · 2019Review
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6 authors at 3 institutions in 2 countries.
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Abstract
aimAlzheimer's disease (AD) is largely considered a neuron-derived insult, but also involves failure of astroglia. A recent study indicated that mutated presenilin 1 (PS1M146V), a putative endoplasmic reticulum (ER) Ca
methodsHere, we cotransfected rat astrocytes with plasmids encoding mutant PS1ΔE9 and atrial natriuretic peptide or vesicular glutamate transporter 1 tagged with fluorescent proteins (pANP.emd or pVGLUT1-EGFP respectively), to microscopically examine whether alterations in vesicle mobility and Ca
resultsIn PS1ΔE9 astrocytes, spontaneous mobility of both vesicle types was reduced (P < .001) when compared to controls. Post-stimulatory recovery of fast vesicle mobility was hampered in PS1ΔE9 astrocytes. The ATP-evoked peptide release was less efficient in PS1ΔE9 astrocytes than in the controls (P < .05), as was the pre-stimulatory mobility of these vesicles.
conclusionAlthough the PS1 mutants PS1M146V and PS1ΔE9 differently affect ER Ca
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