ArticleJournal of Alzheimer's disease : JAD2018
Diaphanous 1 (DIAPH1) is Highly Expressed in the Aged Human Medial Temporal Cortex and Upregulated in Myeloid Cells During Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2018. 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.
- Proteome-Based Plasma Biomarkers for Cognitive Dysfunction in an Androgen Deprivation Model.Molecular neurobiology · 2025Article
- Fundamental Neurochemistry Review: Lipids across microglial states.Journal of neurochemistry · 2025Review
- A Novel Homozygote Pathogenic Variant in the DIAPH1 Gene Associated With Seizures, Cortical Blindness, and Microcephaly Syndrome (SCBMS): Report of a Family and Literature Review.Molecular genetics & genomic medicine · 2024Review
- Fatty acid metabolism changes in association with neurobehavioral deficits in animal models of fetal alcohol spectrum disorders.Communications biology · 2023Article
- The Janus-Faced Role of Lipid Droplets in Aging: Insights from the Cellular Perspective.Biomolecules · 2023Review
- Mechanistic insights into the role of herpes simplex virus 1 in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- A New Hypothesis for Alzheimer's Disease: The Lipid Invasion Model.Journal of Alzheimer's disease reports · 2022Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- Formins in Human Disease.Cells · 2021Review
- The Genome-Wide Binding Profile for Human RE1 Silencing Transcription Factor Unveils a Unique Genetic Circuitry in Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Lipid droplets in the nervous system.The Journal of cell biology · 2021Review
- Article
- Lipid Droplets in Neurodegenerative Disorders.Frontiers in neuroscience · 2020Review
- Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models.Frontiers in cardiovascular medicine · 2020Review
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe receptor for advanced glycation end products (RAGE) is linked to cellular stress and inflammation during Alzheimer's disease (AD). RAGE signals through Diaphanous-1 (DIAPH1); however, the expression of DIAPH1 in the healthy and AD human brain has yet to be methodically addressed.
objectiveTo delineate the cell- and disease-state specific expression of DIAPH1 in the human medial temporal cortex during healthy aging and AD.
methodsWe used semi-quantitative immunohistochemistry in the human medial temporal cortex paired with widefield and confocal microscopy and automated analyses to determine colocalization and relative expression of DIAPH1 with key cell markers and molecules in the brains of subjects with AD versus age-matched controls.
resultsWe report robust colocalization of DIAPH1 with myeloid cells and increased expression during AD, which strongly correlated to increased neutral lipids and morphology of inflamed myeloid cells. DIAPH1 moderately colocalized with markers of endothelial cells, astrocytes, neurons, and oligodendrocytes. DISCUSSION: Our findings localize DIAPH1 particularly to myeloid cells in the CNS, especially in AD in the locations of lipid droplet accumulation, thereby implicating RAGE-DIAPH1 signaling in dysregulated lipid metabolism and morphological changes of inflamed myeloid cells in this disorder.
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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.