ArticleASN neuro2014
Accumulation of amyloid-like Aβ1-42 in AEL (autophagy-endosomal-lysosomal) vesicles: potential implications for plaque biogenesis.
Article in ASN neuro, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exploitation of Autophagy Inducers in the Management of Dementia: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Article
- Alzheimer's disease linked Aβ42 exerts product feedback inhibition on γ-secretase impairing downstream cell signaling.bioRxiv : the preprint server for biology · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Review
- Article
- The Emerging Role of the Interaction of Extracellular Vesicle and Autophagy-Novel Insights into Neurological Disorders.Journal of inflammation research · 2022Review
- Defects of Nutrient Signaling and Autophagy in Neurodegeneration.Frontiers in cell and developmental biology · 2022Review
- A multitude of signaling pathways associated with Alzheimer's disease and their roles in AD pathogenesis and therapy.Medicinal research reviews · 2021Review
- Targeting autophagy in neurodegenerative diseases: From molecular mechanisms to clinical therapeutics.Clinical and experimental pharmacology & physiology · 2021Review
- Structural aspects of the aging invertebrate brain.Cell and tissue research · 2021Review
- Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021Review
- VPS35 Downregulation Alters Degradation Pathways in Neuronal Cells.Journal of Alzheimer's disease : JAD · 2021Article
- Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease.FEBS open bio · 2020Article
- Exploring the bi-directional relationship between autophagy and Alzheimer's disease.CNS neuroscience & therapeutics · 2020Review
- A Human Embryonic Stem Cell Model of Aβ-Dependent Chronic Progressive Neurodegeneration.Frontiers in neuroscience · 2019Article
- UsingBioMed research international · 2018Review
- Amyloid precursor protein and endosomal-lysosomal dysfunction in Alzheimer's disease: inseparable partners in a multifactorial disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Review
- Lysosomal dysfunction in the brain of a mouse model with intraneuronal accumulation of carboxyl terminal fragments of the amyloid precursor protein.Molecular psychiatry · 2017Article
- Autophagy and Alzheimer's Disease.Cellular and molecular neurobiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal accumulation of Aβ (amyloid β) within AEL (autophagy-endosomal-lysosomal) vesicles is a prominent neuropathological feature of AD (Alzheimer's disease), but the mechanism of accumulation within vesicles is not clear. We express secretory forms of human Aβ1-40 or Aβ1-42 in Drosophila neurons and observe preferential localization of Aβ1-42 within AEL vesicles. In young animals, Aβ1-42 appears to associate with plasma membrane, whereas Aβ1-40 does not, suggesting that recycling endocytosis may underlie its routing to AEL vesicles. Aβ1-40, in contrast, appears to partially localize in extracellular spaces in whole brain and is preferentially secreted by cultured neurons. As animals become older, AEL vesicles become dysfunctional, enlarge and their turnover appears delayed. Genetic inhibition of AEL function results in decreased Aβ1-42 accumulation. In samples from older animals, Aβ1-42 is broadly distributed within neurons, but only the Aβ1-42 within dysfunctional AEL vesicles appears to be in an amyloid-like state. Moreover, the Aβ1-42-containing AEL vesicles share properties with AD-like extracellular plaques. They appear to be able to relocate to extracellular spaces either as a consequence of age-dependent neurodegeneration or a non-neurodegenerative separation from host neurons by plasma membrane infolding. We propose that dysfunctional AEL vesicles may thus be the source of amyloid-like plaque accumulation in Aβ1-42-expressing Drosophila with potential relevance for AD.
Indexed as
Identifiers
What OpenQuestion holds
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.