ArticleJournal of Alzheimer's disease reports2018
The Bri2 and Bri3 BRICHOS Domains Interact Differently with Aβ
Article in Journal of Alzheimer's disease reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis 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, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- The Emerging Roles of E3 Ligases and DUBs in Neurodegenerative Diseases.Molecular neurobiology · 2023Pooled it
- HuR modulates disease-relevant alternative splicing of MAPT and other Alzheimer's disease-related genes.Molecular genetics and genomics : MGG · 2026Article
- The emerging roles of ITM2A: At the molecular crossroads of development and pathogenesis.iScience · 2026Review
- Circulating extracellular vesicles in plasma carry accessible molecular signatures of aging in mice.bioRxiv : the preprint server for biology · 2026Article
- BRI3 Orchestrates Lipid Metabolism and Autophagy in Glioblastoma: Implications for Tumor Cell Resilience.Biochemical genetics · 2026Article
- TNMD BRICHOS domain attenuates tau pathology and memory deficits in a mouse model of tauopathy.Cell death & disease · 2026Article
- Functional Specificity of Astrocyte Subtypes in Alzheimer's Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data.Molecular neurobiology · 2025Article
- Determinants for Substoichiometric Inhibition of IAPP and Aβ Amyloid Aggregations by Bri2 BRICHOS.ACS chemical neuroscience · 2025Article
- Comparison of the amyloid plaque proteome in Down syndrome, early-onset Alzheimer's disease, and late-onset Alzheimer's disease.Acta neuropathologica · 2025Article
- Role of OAF and smoking initiation in COPD risk: Insights from Mendelian randomization.Tobacco induced diseases · 2025Article
- The inhibitory action of the chaperone BRICHOS against the α-Synuclein secondary nucleation pathway.Nature communications · 2024Article
- Intravenous chaperone treatment of late-stage Alzheimer´s disease (AD) mouse model affects amyloid plaque load, reactive gliosis and AD-related genes.Translational psychiatry · 2024Article
- Comparison of the Amyloid Plaque Proteome in Down Syndrome, Early-Onset Alzheimer's Disease and Late-Onset Alzheimer's Disease.Research square · 2024Article
- Updates on Aβ Processing by Hsp90, BRICHOS, and Newly Reported Distinctive Chaperones.Biomolecules · 2023Review
- Human Alzheimer's disease reactive astrocytes exhibit a loss of homeostastic gene expression.Acta neuropathologica communications · 2023Article
- A new kid in the folding funnel: Molecular chaperone activities of the BRICHOS domain.Protein science : a publication of the Protein Society · 2023Review
- Short hydrophobic loop motifs in BRICHOS domains determine chaperone activity against amorphous protein aggregation but not against amyloid formation.Communications biology · 2023Article
- Extracellular chaperone networks and the export of J-domain proteins.The Journal of biological chemistry · 2023Review
- Abilities of the BRICHOS domain to prevent neurotoxicity and fibril formation are dependent on a highly conserved Asp residue.RSC chemical biology · 2022Article
- Endogenous Human Proteins Interfering with Amyloid Formation.Biomolecules · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of dementia and there is no successful treatment available. Evidence suggests that fibril formation of the amyloid β-peptide (Aβ) is a major underlying cause of AD, and treatment strategies that reduce the toxic effects of Aβ amyloid are sought for. The BRICHOS domain is found in several proteins, including Bri2 (also called integral membrane protein 2B (ITM2B)), mutants of which are associated with amyloid and neurodegeneration, and Bri3 (ITM2C). We have used mouse hippocampal neurons and brain tissues from mice and humans and show Bri3 deposits dispersed on AD plaques. In contrast to what has been shown for Bri2, Bri3 immunoreactivity is decreased in AD brain homogenates compared to controls. Both Bri2 and Bri3 BRICHOS domains interact with Aβ
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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.