scholarly journals Neurobiological Pathways between Chronic Stress and Depression: Dysregulated Adaptive Mechanisms?

2009 ◽  
Vol 2 ◽  
pp. CMPsy.S3658
Author(s):  
Christopher F. Sharpley

Stress-related diseases have been predicted to become major contributors to the Global Disease Burden within the next 20 years. Of these, depression is one of the principal identifiable sources of concern for public mental health, and has been hypothesized to be an outcome of prolonged stress. Examination of the hyper-responsiveness of the Hypothalamic-Pituitary-Adrenal axis, consequent elevated serum cortisol, plus the effects of this upon brain structure and function, provides a model for understanding how chronic stress may be a causal vector in the development of depression. Evidence from studies of the effectiveness of antidepressants aimed at reducing cortisol within depressed patients supports this model and suggests avenues for future research and treatment of stress-induced depression.

2019 ◽  
Author(s):  
Madeline Farber ◽  
Dylan Gee ◽  
Ahmad R. Hariri

Studies of early adversity such as trauma, abuse, and neglect highlight the critical importance of quality caregiving in brain development and mental health. However, the impact of normative range variability in caregiving on such biobehavioral processes remains poorly understood. Thus, we lack an essential foundation for understanding broader, population-representative developmental mechanisms of risk and resilience. Here, we conduct a scoping review of the extant literature centered on the question, “Is variability in normative range parenting associated with variability in brain structure and function?” After removing duplicates and screening by title, abstract, and full-text, 23 records were included in a qualitative review. The most striking outcome of this review was not only how few studies have explored associations between brain development and normative range parenting, but also how little methodological consistency exists across published studies. In light of these limitations, we propose recommendations for future research on normative range parenting and brain development. In doing so, we hope to facilitate evidence-based research that will help inform policies and practices that yield optimal developmental trajectories and mental health.


Author(s):  
Reagan R. Wetherill ◽  
Susan F. Tapert

This chapter focuses on adolescent brain development and associated functional implications. We focus on changes in brain tissue composition, fiber architecture and circuitry, and neurochemistry and discuss how these maturational processes affect adolescent brain functioning, sleep, cognition, and behaviors. Given the substantial developments that occur during adolescence, the effects of puberty and sex hormones on brain structure and function are reviewed, and literature on the effects of substance use on the adolescent brain are covered. The chapter reports on recent neuroimaging studies suggesting that atypical and/or asynchronous maturation patterns may contribute to adolescents’ proclivity for risk taking, heightened emotionality, and the emergence of psychopathology. Finally, future research opportunities are discussed.


2015 ◽  
Vol 114 (3) ◽  
pp. 1713-1724 ◽  
Author(s):  
Mark D. Kvarta ◽  
Keighly E. Bradbrook ◽  
Hannah M. Dantrassy ◽  
Aileen M. Bailey ◽  
Scott M. Thompson

Chronic stress is thought to impart risk for depression via alterations in brain structure and function, but contributions of specific mediators in generating these changes remain unclear. We test the hypothesis that stress-induced increases in corticosterone (CORT), the primary rodent glucocorticoid, are the key mediator of stress-induced depressive-like behavioral changes and synaptic dysfunction in the rat hippocampus. In rats, we correlated changes in cognitive and affective behavioral tasks (spatial memory consolidation, anhedonia, and neohypophagia) with impaired excitatory strength at temporoammonic-CA1 (TA-CA1) synapses, an archetypical stress-sensitive excitatory synapse. We tested whether elevated CORT was sufficient and necessary to generate a depressive-like behavioral phenotype and decreased excitatory signaling observed at TA-CA1 after chronic unpredictable stress (CUS). Chronic CORT administration induced an anhedonia-like behavioral state and neohypophagic behavior. Like CUS, chronic, but not acute, CORT generated an impaired synaptic phenotype characterized by reduced α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring glutamate receptor-mediated excitation at TA-CA1 synapses, decreased AMPA-type glutamate receptor subunit 1 protein expression, and altered serotonin-1B receptor-mediated potentiation. Repeatedly blunting stress-induced increases of CORT during CUS with the CORT synthesis inhibitor metyrapone (MET) prevented these stress-induced neurobehavioral changes. MET also prevented the CUS-induced impairment of spatial memory consolidation. We conclude that corticosterone is sufficient and necessary to mediate glutamatergic dysfunction underlying stress-induced synaptic and behavioral phenotypes. Our results indicate that chronic excessive glucocorticoids cause specific synaptic deficits in the hippocampus, a major center for cognitive and emotional processing, that accompany stress-induced behavioral dysfunction. Maintaining excitatory strength at stress-sensitive synapses at key loci throughout corticomesolimbic reward circuitry appears critical for maintaining normal cognitive and emotional behavior.


2015 ◽  
Vol 45 (12) ◽  
pp. 2461-2480 ◽  
Author(s):  
R. Gurung ◽  
D. P. Prata

The powerful genome-wide association studies (GWAS) revealed common mutations that increase susceptibility for schizophrenia (SZ) and bipolar disorder (BD), but the vast majority were not known to be functional or associated with these illnesses. To help fill this gap, their impact on human brain structure and function has been examined. We systematically discuss this output to facilitate its timely integration in the psychosis research field; and encourage reflection for future research. Irrespective of imaging modality, studies addressing the effect of SZ/BD GWAS risk genes (ANK3, CACNA1C, MHC, TCF4, NRGN, DGKH, PBRM1, NCANandZNF804A) were included. Most GWAS risk variations were reported to affect neuroimaging phenotypes implicated in SZ/BD: white-matter integrity (ANK3andZNF804A), volume (CACNA1CandZNF804A) and density (ZNF804A); grey-matter (CACNA1C, NRGN, TCF4andZNF804A) and ventricular (TCF4) volume; cortical folding (NCAN) and thickness (ZNF804A); regional activation during executive tasks (ANK3, CACNA1C, DGKH, NRGNandZNF804A) and functional connectivity during executive tasks (CACNA1CandZNF804A), facial affect recognition (CACNA1CandZNF804A) and theory-of-mind (ZNF804A); but inconsistencies and non-replications also exist. Further efforts such as standardizing reporting and exploring complementary designs, are warranted to test the reproducibility of these early findings.


2016 ◽  
Vol 113 (26) ◽  
pp. E3755-E3763 ◽  
Author(s):  
Sofia Lopes ◽  
João Vaz-Silva ◽  
Vitor Pinto ◽  
Christina Dalla ◽  
Nikolaos Kokras ◽  
...  

Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer’s-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory deficits. Here, we demonstrate that stress-driven hippocampal deficits in wild-type mice are accompanied by synaptic missorting of Tau and enhanced Fyn/GluN2B-driven synaptic signaling. In contrast, mice lacking Tau [Tau knockout (Tau-KO) mice] do not exhibit stress-induced pathological behaviors and atrophy of hippocampal dendrites or deficits of hippocampal connectivity. These findings implicate Tau as an essential mediator of the adverse effects of stress on brain structure and function.


1999 ◽  
Vol 12 (2) ◽  
pp. 231-253 ◽  
Author(s):  
M. J. Dauncey ◽  
R. J. Bicknell

AbstractNutrition plays a central role in linking the fields of developmental neurobiology and cognitive neuroscience. It has a profound impact on the development of brain structure and function and malnutrition can result in developmental dysfunction and disease in later life. A number of diseases, including schizophrenia, may be related to neurodevelopmental insults such as malnutrition, hypoxia, viruses or in utero drug exposure. Some of the most significant findings on nutrition and neurodevelopment during the last three decades, and especially during the last few years, are discussed in this review. Attention is focused on the underlying cellular and molecular mechanisms by which diet exerts its effects. Randomized intervention studies have revealed important effects of early nutrition on later cognitive development, and recent epidemiological findings show that both genetics and environment are risk factors for schizophrenia. Particularly important is the effect of early nutrition on development of the hippocampus, a brain structure important in establishing learning and memory, and hence for cognitive performance. A major aim of future research should be to elucidate the molecular mechanisms underlying nutritionally-induced impairment of neurodevelopment and specifically to determine the mechanisms by which early nutritional experience affects later cognitive performance. Key research objectives should include: (1) increased understanding of mechanisms underlying the normal processes of ageing and neurodegenerative disorders; (2) assessment of the role of susceptibility genes in modulating the effects of early nutrition on neurodevelopment; and (3) development of nutritional and pharmaceutical strategies for preventing and/or ameliorating the adverse effects of early malnutrition on long-term programming.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoyan Zhan ◽  
Rongjun Yu

Functional magnetic resonance imaging (fMRI) plays a key role in modern psychiatric research. It provides a means to assay differences in brain systems that underlie psychiatric illness, treatment response, and properties of brain structure and function that convey risk factor for mental diseases. Here we review recent advances in fMRI methods in general use and progress made in understanding the neural basis of mental illness. Drawing on concepts and findings from psychiatric fMRI, we propose that mental illness may not be associated with abnormalities in specific local regions but rather corresponds to variation in the overall organization of functional communication throughout the brain network. Future research may need to integrate neuroimaging information drawn from different analysis methods and delineate spatial and temporal patterns of brain responses that are specific to certain types of psychiatric disorders.


2021 ◽  
Vol 13 ◽  
Author(s):  
Caitlin Ware ◽  
Sophie Dautricourt ◽  
Julie Gonneaud ◽  
Gael Chételat

As the population ages, understanding how to maintain older adults' cognitive abilities is essential. Bilingualism has been linked to higher cognitive reserve, better performance in executive control, changes in brain structure and function relative to monolinguals, and delay in dementia onset. Learning a second language thus seems a promising avenue for cognitive enhancement in older adults. Our review aims to determine whether learning a foreign language in later life improves cognition and promotes neuroplasticity. We screened articles from the Pubmed, Scopus, and Science Direct databases to identify interventional studies using second language training in senior participants, including either cognition or neuroimaging as outcome measures. A total of nine articles were found, with only one neuroimaging study. Results from these studies are inconsistent, but tend to suggest that second language learning is associated with improvement in attentional switching, inhibition, working memory, and increased functional connectivity. We discuss the implications of these results, and suggest new directions and methodological recommendations for future research.


Author(s):  
Nirupama R. Akella

This chapter is a meta-analysis of teen brain research and social media technology such as Facebook that could result in spiraling rates of teenage pregnancy. The author discusses contemporary theories of brain circuitry including teen brain structure and function as one of the plausible reasons for rising teenage pregnancy rates. The author argues that the challenge is to control the quality and influence of Facebook on teen behaviors, actions, and decisions to minimize the growing influence of social networking sites. In the conclusive section of the chapter, the author focuses on the expansion and extension of instructional and non-instructional physical activities, exergames, and active video games strategies to control the quality and influence of Facebook content by presenting research that advocates use of such activities and games within the Facebook interface. The author ends the chapter by mapping a future research direction of cross-cultural empirical investigation. The author wraps the chapter with a summative conclusion.


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