ArticleNeuropathology : official journal of the Japanese Society of Neuropathology2010
Widespread distribution of reticulon-3 in various neurodegenerative diseases.
Article in Neuropathology : official journal of the Japanese Society of Neuropathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Shared diagnostic biomarkers and diagnostic models of age-related macular degeneration and systemic lupus erythematosus.International ophthalmology · 2026Article
- α-synuclein in Parkinson's disease: a central point of convergence with depression.NPJ Parkinson's disease · 2025Review
- 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
- The Overexpression of RTN4 Significantly Associated With an Unfavourable Prognosis in Patients With Lower-Grade Gliomas.Journal of cellular and molecular medicine · 2025Article
- Identification of four novel T cell autoantigens and personal autoreactive profiles in multiple sclerosis.Science advances · 2022Article
- The Clinical Significance of Cerebrospinal Fluid Reticulon 4 (RTN4) Levels in the Differential Diagnosis of Neurodegenerative Diseases.Journal of clinical medicine · 2021Article
- Untangling the origin and function of granulovacuolar degeneration bodies in neurodegenerative proteinopathies.Acta neuropathologica communications · 2020Review
- ER-phagy and human diseases.Cell death and differentiation · 2020Review
- Plasma protein profiling reveals candidate biomarkers for multiple sclerosis treatment.PloS one · 2019Article
- Lack of human-like extracellular sortilin neuropathology in transgenic Alzheimer's disease model mice and macaques.Alzheimer's research & therapy · 2018Article
- RTN1-C mediates cerebral ischemia/reperfusion injury via ER stress and mitochondria-associated apoptosis pathways.Cell death & disease · 2017Article
- Inhibition of Reticulon-1A-Mediated Endoplasmic Reticulum Stress in Early AKI Attenuates Renal Fibrosis Development.Journal of the American Society of Nephrology : JASN · 2017Article
- Dysfunctional tubular endoplasmic reticulum constitutes a pathological feature of Alzheimer's disease.Molecular psychiatry · 2016Article
- RTN1 mediates progression of kidney disease by inducing ER stress.Nature communications · 2015Article
- Impact of RTN3 deficiency on expression of BACE1 and amyloid deposition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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9 authors at 4 institutions in 1 country.
Funding
Abstract
Reticulons are a group of membrane-bound proteins involved in diverse cellular functions, and are suggested to act as inhibitors of β-secretase enzyme 1 (BACE1) activity that cleaves amyloid precursor protein. Reticulons are known to accumulate in the dystrophic neurites of Alzheimer's disease (AD), and studies have suggested that alterations in reticulons, such as increased aggregation, impair BACE1 binding, increasing amyloid-β production, and facilitating reticulon deposition in dystrophic neurites. To further characterize the cellular distribution of reticulon, we examined reticulon-3 expression in cases of AD, Parkinson's disease, and diffuse Lewy body disease. A more widespread cellular distribution of reticulon-3 was noted than in previous reports, including deposits in dystrophic neurites, neuropil threads, granulovacuolar degeneration, glial cells, morphologically normal neurons in both hippocampal pyramidal cell layer and cerebral neocortex, and specifically neurofibrillary tangles and Lewy bodies. These results are compatible with reticulon alterations as nonspecific downstream stress responses, consistent with its expression during periods of endoplasmic reticulum stress. This emphasizes the increasing recognition that much of the AD pathological spectrum represents a response to the disease rather than cause, and emphasizes the importance of examining upstream processes, such as oxidative stress, that have functional effects prior to the onset of structural alterations.
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Registered trials
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