ArticleNature communications2020
FAM222A encodes a protein which accumulates in plaques in Alzheimer's disease.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Early oligodendrocyte dysfunction signature in Alzheimer's disease: Insights from DNA methylomics and transcriptomics.Molecular psychiatry · 2026Article
- Genome-wide selection and association analyses implicate retinal and reproductive genes in laying-period variation of domestic geese.Poultry science · 2026Article
- Transcriptional and cellular maturation of the chick spinal cord in the context of distinct neuromuscular circuits.iScience · 2026Article
- Evolutionary analysis through structural modeling of FAM222 proteins reveals a novel disordered conserved domain in vertebrates that interacts with NLK.Scientific reports · 2025Article
- Protein co-aggregates of dense core amyloid plaques and CSF differ in rapidly progressive Alzheimer's disease and slower sporadic Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Aggregatin is a mitochondrial regulator of MAVS activation to drive innate immunity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Deciphering novel mitochondrial signatures: multi-omics analysis uncovers cross-disease markers and oligodendrocyte pathways in Alzheimer's disease and glioblastoma.Frontiers in aging neuroscience · 2025Article
- Estimation of a genetic Gaussian network using GWAS summary data.Biometrics · 2024Article
- Map conformational landscapes of intrinsically disordered proteins with polymer physics quantities.Biophysical journal · 2024Article
- Agomirs upregulating carboxypeptidase E expression rescue hippocampal neurogenesis and memory deficits in Alzheimer's disease.Translational neurodegeneration · 2024Article
- Deciphering the Role of Rapidly Evolving Conserved Elements in Primate Brain Development and Exploring Their Potential Involvement in Alzheimer's Disease.Molecular biology and evolution · 2024Article
- Immunoproteasome Subunit Low Molecular Mass Peptide 2 (LMP2) Deficiency Ameliorates LPS/AβMolecular neurobiology · 2024Article
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Gene Co-Expression Analysis of Multiple Brain Tissues Reveals Correlation of FAM222A Expression with Multiple Alzheimer's Disease-Related Genes.Journal of Alzheimer's disease : JAD · 2024Article
- Revealing the correlations between brain cortical characteristics and susceptibility genes for Alzheimer disease: a cross-sectional study.Quantitative imaging in medicine and surgery · 2023Article
- Using the Alzheimer's Disease Neuroimaging Initiative to improve early detection, diagnosis, and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Review
- An iterative approach to detect pleiotropy and perform Mendelian Randomization analysis using GWAS summary statistics.Bioinformatics (Oxford, England) · 2021Article
- Transgenerational Effects of Di(2-Ethylhexyl) Phthalate on Anogenital Distance, Sperm Functions and DNA Methylation in Rat Offspring.International journal of molecular sciences · 2021Article
- Reactive astrocytes express Aggregatin (Intractable & rare diseases research · 2020Article
- Role of Kalirin and mouse strain in retention of spatial memory training in an Alzheimer's disease model mouse line.Neurobiology of aging · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 20 institutions in 4 countries.
Funding
Abstract
Alzheimer's disease (AD) is characterized by amyloid plaques and progressive cerebral atrophy. Here, we report FAM222A as a putative brain atrophy susceptibility gene. Our cross-phenotype association analysis of imaging genetics indicates a potential link between FAM222A and AD-related regional brain atrophy. The protein encoded by FAM222A is predominantly expressed in the CNS and is increased in brains of patients with AD and in an AD mouse model. It accumulates within amyloid deposits, physically interacts with amyloid-β (Aβ) via its N-terminal Aβ binding domain, and facilitates Aβ aggregation. Intracerebroventricular infusion or forced expression of this protein exacerbates neuroinflammation and cognitive dysfunction in an AD mouse model whereas ablation of this protein suppresses the formation of amyloid deposits, neuroinflammation and cognitive deficits in the AD mouse model. Our data support the pathological relevance of protein encoded by FAM222A in AD.
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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.