ArticleMolecular psychiatry2016
Dysfunctional tubular endoplasmic reticulum constitutes a pathological feature of Alzheimer's disease.
Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer's disease.Nature neuroscience · 2026Article
- The diverse forms and roles of the neuronal endoplasmic reticulum.Nature reviews. Neuroscience · 2026Review
- Loss of mouse C19orf12 homolog disturbs tubular ER homeostasis and leads to neuroaxonal dystrophy.Acta neuropathologica communications · 2025Article
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- Organelle perturbation in Alzheimer's disease: do intracellular amyloid-ß and the fragmented Golgi mediate early intracellular neurotoxicity?Frontiers in cell and developmental biology · 2025Review
- Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025Article
- Highly prevalent geriatric medications and their effect on β-amyloid fibril formation.BMC neurology · 2024Article
- Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency.Molecular neurodegeneration · 2024Article
- Accumulation of neutral lipids in dystrophic neurites surrounding amyloid plaques in Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Luminal transport through intact endoplasmic reticulum limits the magnitude of localized CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Loss and recovery of myocardial mitochondria in mice under different tail suspension time: Apoptosis and mitochondrial fission, fusion and autophagy.Experimental physiology · 2023Article
- Reticulons 1 and 3 are essential for axonal growth and synaptic maintenance associated with intellectual development.Human molecular genetics · 2023Article
- Neurodegenerative Proteinopathies Induced by Environmental Pollutants: Heat Shock Proteins and Proteasome as Promising Therapeutic Tools.Pharmaceutics · 2023Review
- Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK-IDH2 pathway.MedComm · 2023Article
- Deficiency of Perry syndrome-associated p150NPJ Parkinson's disease · 2023Article
- The nanoscale organization of reticulon 4 shapes local endoplasmic reticulum structurebioRxiv : the preprint server for biology · 2023Article
- Identification of novel gene signatures and immune cell infiltration in intervertebral disc degeneration using bioinformatics analysis.Frontiers in molecular biosciences · 2023Article
- Recent advances in pre-clinical diagnosis of Alzheimer's disease.Metabolic brain disease · 2022Review
- Circ_0043947 contributes to interleukin 1β-induced injury in chondrocytes by sponging miR-671-5p to up-regulate RTN3 expression in osteoarthritis pathology.Journal of orthopaedic surgery and research · 2022Article
- Alzheimer's disease - the journey of a healthy brain into organ failure.Molecular neurodegeneration · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pathological features in Alzheimer's brains include mitochondrial dysfunction and dystrophic neurites (DNs) in areas surrounding amyloid plaques. Using a mouse model that overexpresses reticulon 3 (RTN3) and spontaneously develops age-dependent hippocampal DNs, here we report that DNs contain both RTN3 and REEPs, topologically similar proteins that can shape tubular endoplasmic reticulum (ER). Importantly, ultrastructural examinations of such DNs revealed gradual accumulation of tubular ER in axonal termini, and such abnormal tubular ER inclusion is found in areas surrounding amyloid plaques in biopsy samples from Alzheimer's disease (AD) brains. Functionally, abnormally clustered tubular ER induces enhanced mitochondrial fission in the early stages of DN formation and eventual mitochondrial degeneration at later stages. Furthermore, such DNs are abrogated when RTN3 is ablated in aging and AD mouse models. Hence, abnormally clustered tubular ER can be pathogenic in brain regions: disrupting mitochondrial integrity, inducing DNs formation and impairing cognitive function in AD and aging brains.
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