ArticleInternational journal of Alzheimer's disease2012
Lysosomal fusion dysfunction as a unifying hypothesis for Alzheimer's disease pathology.
Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Extracellular vesicles in neurodegenerative diseases: A systematic review.Frontiers in molecular neuroscience · 2022Pooled it
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- High reelin expression may explain why a subgroup of entorhinal cortex neurons functions as an initial nucleation site of Alzheimer's disease.PLoS computational biology · 2026Article
- Loss of PIKfyve drives the spongiform degeneration in prion diseases.EMBO molecular medicine · 2021Article
- Systemic Actions of SGLT2 Inhibition on Chronic mTOR Activation as a Shared Pathogenic Mechanism between Alzheimer's Disease and Diabetes.Biomedicines · 2021Review
- The ubiquitin ligase UBE4B regulates amyloid precursor protein ubiquitination, endosomal trafficking, and amyloid β42 generation and secretion.Molecular and cellular neurosciences · 2020Article
- TRPML1 links lysosomal calcium to autophagosome biogenesis through the activation of the CaMKKβ/VPS34 pathway.Nature communications · 2019Article
- The Interplay Between Apolipoprotein E4 and the Autophagic-Endocytic-Lysosomal Axis.Molecular neurobiology · 2018Review
- Dysregulation of Rab5-mediated endocytic pathways in Alzheimer's disease.Traffic (Copenhagen, Denmark) · 2018Review
- Peptides as Potential Therapeutics for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2018Review
- Biology and biogenesis of shed microvesicles.Small GTPases · 2017Review
- Sorting nexin-4 regulates β-amyloid production by modulating β-site-activating cleavage enzyme-1.Alzheimer's research & therapy · 2017Article
- The Pathogenic Role of Ganglioside Metabolism in Alzheimer's Disease-Cholinergic Neuron-Specific Gangliosides and Neurogenesis.Molecular neurobiology · 2017Review
- BK channel agonist represents a potential therapeutic approach for lysosomal storage diseases.Scientific reports · 2016Article
- ADAM30 Downregulates APP-Linked Defects Through Cathepsin D Activation in Alzheimer's Disease.EBioMedicine · 2016Article
- Autophagy and Mitochondrial Dysfunction in Tenon Fibroblasts from Exfoliation Glaucoma Patients.PloS one · 2016Article
- Protein Kinase Activity Decreases with Higher Braak Stages of Alzheimer's Disease Pathology.Journal of Alzheimer's disease : JAD · 2016Article
- Unfolded Protein Response and Macroautophagy in Alzheimer's, Parkinson's and Prion Diseases.Molecules (Basel, Switzerland) · 2015Review
- Neuronal-Targeted TFEB Accelerates Lysosomal Degradation of APP, Reducing Aβ Generation and Amyloid Plaque Pathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- The Na+/H+ exchanger NHE6 modulates endosomal pH to control processing of amyloid precursor protein in a cell culture model of Alzheimer disease.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease is characterized pathologically by extracellular senile plaques, intracellular neurofibrillary tangles, and granulovacuolar degeneration. It has been debated whether these hallmark lesions are markers or mediators of disease progression, and numerous paradigms have been proposed to explain the appearance of each lesion individually. However, the unfaltering predictability of these lesions suggests a single pathological nidus central to disease onset and progression. One of the earliest pathologies observed in Alzheimer's disease is endocytic dysfunction. Here we review the recent literature of endocytic dysfunction with particular focus on disrupted lysosomal fusion and propose it as a unifying hypothesis for the three most-studied lesions of Alzheimer's disease.
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.