ArticleFrontiers in genetics2012
Age-by-disease biological interactions: implications for late-life depression.
Article in Frontiers in genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Mitochondrial DNA Polymorphism in HV1 and HV2 Regions and 12S rDNA in Perimenopausal Hypertensive Women.Biomedicines · 2023Article
- Telomere shortening in late-life depression: A potential marker of depression severity.Brain and behavior · 2021Article
- Major depression and enhanced molecular senescence abnormalities in young and middle-aged adults.Translational psychiatry · 2019Article
- DNA methylation in the human frontal cortex reveals a putative mechanism for age-by-disease interactions.Translational psychiatry · 2019Article
- Role of gamma-amino-butyric acid in the dorsal anterior cingulate in age-associated changes in cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Associations among prenatal stress, maternal antioxidant intakes in pregnancy, and child temperament at age 30 months.Journal of developmental origins of health and disease · 2017Article
- Increased levels of ascorbic acid in the cerebrospinal fluid of cognitively intact elderly patients with major depression: a preliminary study.Scientific reports · 2017Article
- The Role of BDNF in Age-Dependent Changes of Excitatory and Inhibitory Synaptic Markers in the Human Prefrontal Cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Does physical activity moderate the relationship between depression symptomatology and low back pain? Cohort and co-twin control analyses nested in the longitudinal study of aging Danish twins (LSADT).European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2016Article
- Hypermethylation of BDNF and SST Genes in the Orbital Frontal Cortex of Older Individuals: A Putative Mechanism for Declining Gene Expression with Age.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- The effect of gender, age, and symptom severity in late-life depression on the risk of all-cause mortality: the Bambuí Cohort Study of Aging.Depression and anxiety · 2014Article
- The role of the nervous system in aging and longevity.Frontiers in genetics · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Onset of depressive symptoms after the age of 65, or late-life depression (LLD), is common and poses a significant burden on affected individuals, caretakers, and society. Evidence suggests a unique biological basis for LLD, but current hypotheses do not account for its pathophysiological complexity. Here we propose a novel etiological framework for LLD, the age-by-disease biological interaction hypothesis, based on the observations that the subset of genes that undergoes lifelong progressive changes in expression is restricted to a specific set of biological processes, and that a disproportionate number of these age-dependent genes have been previously and similarly implicated in neurodegenerative and neuropsychiatric disorders, including depression. The age-by-disease biological interaction hypothesis posits that age-dependent biological processes (i) are "pushed" in LLD-promoting directions by changes in gene expression naturally occurring during brain aging, which (ii) directly contribute to pathophysiological mechanisms of LLD, and (iii) that individual variability in rates of age-dependent changes determines risk or resiliency to develop age-related disorders, including LLD. We review observations supporting this hypothesis, including consistent and specific age-dependent changes in brain gene expression and their overlap with neuropsychiatric and neurodegenerative disease pathways. We then review preliminary reports supporting the genetic component of this hypothesis. Other potential biological mediators of age-dependent gene changes are proposed. We speculate that studies examining the relative contribution of these mechanisms to age-dependent changes and related disease mechanisms will not only provide critical information on the biology of normal aging of the human brain, but will inform our understanding of age-dependent diseases, in time fostering the development of new interventions for prevention and treatment of age-dependent diseases, including LLD.
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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.