SynthesisJournal of Alzheimer's disease : JAD2015
Comprehensive gene- and pathway-based analysis of depressive symptoms in older adults.
Synthesis in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Bi-ancestral depression GWAS in the Million Veteran Program and meta-analysis in >1.2 million individuals highlight new therapeutic directions.Nature neuroscience · 2021Pooled it
- Age-stratified genomic analyses reveal population-specific genetic determinants of exceptional longevity in Taiwan.GeroScience · 2026Article
- Overexpression of mGluMolecular neurobiology · 2025Article
- Profiling the Impact of mGluACS chemical neuroscience · 2025Article
- Unraveling the Complex Interplay Between Neuroinflammation and Depression: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Molecular pathogenesis of Alzheimer's disease onset in a mouse model: effects of cannabidiol treatment.Frontiers in neuroscience · 2025Article
- Two polygenic mouse models of major depressive disorders identify TMEM161B as a potential biomarker of disease in humans.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- LRFN5 and OLFM4 as novel potential biomarkers for major depressive disorder: a pilot study.Translational psychiatry · 2023Article
- Correlation between variants of the CREB1 and GRM7 genes and risk of depression.BMC psychiatry · 2023Article
- Article
- Therapeutic Targets and Mechanism of Xingpi Jieyu Decoction in Depression: A Network Pharmacology Study.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Blood biomarkers for memory: toward early detection of risk for Alzheimer disease, pharmacogenomics, and repurposed drugs.Molecular psychiatry · 2020Article
- A telescope GWAS analysis strategy, based on SNPs-genes-pathways ensamble and on multivariate algorithms, to characterize late onset Alzheimer's disease.Scientific reports · 2020Article
- Morphological changes in subregions of hippocampus and amygdala in major depressive disorder patients.Brain imaging and behavior · 2020Article
- Analysis of pleiotropic genetic effects on cognitive impairment, systemic inflammation, and plasma lipids in the Health and Retirement Study.Neurobiology of aging · 2019Article
- GRIK4 and GRM7 gene may be potential indicator of venlafaxine treatment reponses in Chinese of Han ethnicity.Medicine · 2019Article
- Stress, Depression, Resilience and Ageing: A Role for the LPA-LPA1 Pathway.Current neuropharmacology · 2018Review
- SALM/Lrfn Family Synaptic Adhesion Molecules.Frontiers in molecular neuroscience · 2018Review
- Genome-wide association study of language performance in Alzheimer's disease.Brain and language · 2017Article
- Genome-wide Regional Heritability Mapping Identifies a Locus Within the TOX2 Gene Associated With Major Depressive Disorder.Biological psychiatry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Depressive symptoms are common in older adults and are particularly prevalent in those with or at elevated risk for dementia. Although the heritability of depression is estimated to be substantial, single nucleotide polymorphism-based genome-wide association studies of depressive symptoms have had limited success. In this study, we performed genome-wide gene- and pathway-based analyses of depressive symptom burden. Study participants included non-Hispanic Caucasian subjects (n = 6,884) from three independent cohorts, the Alzheimer's Disease Neuroimaging Initiative (ADNI), the Health and Retirement Study (HRS), and the Indiana Memory and Aging Study (IMAS). Gene-based meta-analysis identified genome-wide significant associations (ANGPT4 and FAM110A, q-value = 0.026; GRM7-AS3 and LRFN5, q-value = 0.042). Pathway analysis revealed enrichment of association in 105 pathways, including multiple pathways related to ERK/MAPK signaling, GSK3 signaling in bipolar disorder, cell development, and immune activation and inflammation. GRM7, ANGPT4, and LRFN5 have been previously implicated in psychiatric disorders, including the GRM7 region displaying association with major depressive disorder. The ERK/MAPK signaling pathway is a known target of antidepressant drugs and has important roles in neuronal plasticity, and GSK3 signaling has been previously implicated in Alzheimer's disease and as a promising therapeutic target for depression. Our results warrant further investigation in independent and larger cohorts and add to the growing understanding of the genetics and pathobiology of depressive symptoms in aging and neurodegenerative disorders. In particular, the genes and pathways demonstrating association with depressive symptoms may be potential therapeutic targets for these symptoms in older adults.
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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.