ArticleNeuroscience and biobehavioral reviews2010
RTN/Nogo in forming Alzheimer's neuritic plaques.
Article in Neuroscience and biobehavioral reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- 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
- Dynactin 6 deficiency enhances aging-associated dystrophic neurite formation in mouse brains.Neurobiology of aging · 2021Article
- Activity of Alzheimer's γ-secretase is linked to changes of interferon-induced transmembrane proteins (IFITM) in innate immunity.Molecular neurodegeneration · 2020Article
- Increased Reticulon 3 (RTN3) Leads to Obesity and Hypertriglyceridemia by Interacting With Heat Shock Protein Family A (Hsp70) Member 5 (HSPA5).Circulation · 2018Article
- Identification of rare RTN3 variants in Alzheimer's disease in Han Chinese.Human genetics · 2018Article
- RTN1 and RTN3 protein are differentially associated with senile plaques in Alzheimer's brains.Scientific reports · 2017Article
- Overcoming translational barriers impeding development of Alzheimer's disease modifying therapies.Journal of neurochemistry · 2016Review
- Dysfunctional tubular endoplasmic reticulum constitutes a pathological feature of Alzheimer's disease.Molecular psychiatry · 2016Article
- Defining the earliest pathological changes of Alzheimer's disease.Current Alzheimer research · 2016Review
- Function of Nogo-A/Nogo-A receptor in Alzheimer's disease.CNS neuroscience & therapeutics · 2015Review
- Increased expression of reticulon 3 in neurons leads to reduced axonal transport of β site amyloid precursor protein-cleaving enzyme 1.The Journal of biological chemistry · 2013Article
- The Alzheimer's β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques.Acta neuropathologica · 2013Article
- Diabetes-induced central neuritic dystrophy and cognitive deficits are associated with the formation of oligomeric reticulon-3 via oxidative stress.The Journal of biological chemistry · 2013Article
- Preventing formation of reticulon 3 immunoreactive dystrophic neurites improves cognitive function in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Protrudin serves as an adaptor molecule that connects KIF5 and its cargoes in vesicular transport during process formation.Molecular biology of the cell · 2011Article
- Interaction between amyloid precursor protein and Nogo receptors regulates amyloid deposition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
One of the pathological hallmarks in brains of patients with Alzheimer's disease (AD) is the presence of neuritic plaques, in which amyloid deposits are surrounded by reactive gliosis and dystrophic neurites. Within neuritic plaques, reticulon 3 (RTN3), a homolog of Nogo protein, appears to regulate the formation of both amyloid deposition via negative modulation of BACE1 activity and dystrophic neurites via the formation of RTN3 aggregates. Transgenic mice over-expressing RTN3, but not the other known markers of dystrophic neurites in AD brain, spontaneously develop RTN3-immunoreactive dystrophic neurites. The presence of dystrophic neurites impairs cognition. Blocking abnormal RTN3 aggregation will increase the available RTN3 monomer and is therefore a promising therapeutic strategy for enhancing cognitive function in AD patients.
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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.