ReviewBMC neuroscience2023
Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders.
Review in BMC neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Allostatic and Circadian Drives in Patients with Bipolar Disorder in Depressive Episodes or with Post-Traumatic Stress Disorder Versus Healthy Controls: Neuroendocrine Comparison Through Cortisol and 6-Sulfatoxymelatonin Overnight Urine Excretion.International journal of molecular sciences · 2026Article
- Stress and resilience: cortisol hypo-response to acute stress in non-resilient individuals.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- The interplay between ruminative thinking, stress and emotional eating.BMC psychology · 2026Article
- Identification of distinct clinical phenotypes and their neurobiological signatures in stress-exposed individuals: A multimodal machine learning approach.European psychiatry : the journal of the Association of European Psychiatrists · 2026Article
- The Genetic Mosaic of Depression: Linking Polymorphisms to Neuroplasticity and Stress Regulation.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Type 2 diabetes and depression via microvascular dysfunction, neurodegeneration, inflammation, advanced glycation end products (AGEs), and arterial stiffness.Diabetes, obesity & metabolism · 2025Article
- Interaction between emotion lability, emotion regulation and structural brain abnormalities in patients with anorexia nervosa and borderline personality disorder.Frontiers in neuroscience · 2025Article
- Editorial: Molecular mechanisms in psychiatry 2023: anxiety and stress.Frontiers in psychiatry · 2025Article
- Near-infrared light induces neurogenesis and modulates anxiety-like behavior.Stem cell research & therapy · 2024Article
- Stress, coping profiles, and depression among nurses: a latent profile and mediation analysis.BMC nursing · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
In this narrative review, we examine biological processes linking psychological stress and cognition, with a focus on how psychological stress can activate multiple neurobiological mechanisms that drive cognitive decline and behavioral change. First, we describe the general neurobiology of the stress response to define neurocognitive stress reactivity. Second, we review aspects of epigenetic regulation, synaptic transmission, sex hormones, photoperiodic plasticity, and psychoneuroimmunological processes that can contribute to cognitive decline and neuropsychiatric conditions. Third, we explain mechanistic processes linking the stress response and neuropathology. Fourth, we discuss molecular nuances such as an interplay between kinases and proteins, as well as differential role of sex hormones, that can increase vulnerability to cognitive and emotional dysregulation following stress. Finally, we explicate several testable hypotheses for stress, neurocognitive, and neuropsychiatric research. Together, this work highlights how stress processes alter neurophysiology on multiple levels to increase individuals' risk for neurocognitive and psychiatric disorders, and points toward novel therapeutic targets for mitigating these effects. The resulting models can thus advance dementia and mental health research, and translational neuroscience, with an eye toward clinical application in cognitive and behavioral neurology, and psychiatry.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.