Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

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 stres...

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Bibliographic Details
Published in:BMC neuroscience Vol. 24; no. 1; pp. 65 - 31
Main Authors: Palamarchuk, Iryna S., Slavich, George M., Vaillancourt, Tracy, Rajji, Tarek K.
Format: Journal Article
Language:English
Published: London BioMed Central 12.12.2023
BioMed Central Ltd
Springer Nature B.V
BMC
Subjects:
Animal Models
Anxiety
Behavior
Biomedical and Life Sciences
Biomedicine
Cognition
Cognitive ability
Cognitive Dysfunction - etiology
Dementia disorders
Depression
Development and progression
Epigenesis, Genetic
Epigenetics
Gonadal Steroid Hormones
Health aspects
Hormones
Humans
Hypotheses
Memory
Mental Disorders
Mental health
Mental illness
Nervous system
Nervous system diseases
Neurobiology
Neurodegeneration
Neurosciences
Occupational stress
Physiology
Post traumatic stress disorder
Psychoneuroimmunology
Review
Risk Factors
Sex hormones
Stress (Psychology)
Stress response
Suicides & suicide attempts
Synaptic plasticity
Synaptic transmission
Therapeutic targets
Canada
Psychological stress
Neurodegeneration
Kinase
Memory
Epigenetics
Depression
Anxiety
Cognition
Synaptic activity
ISSN:1471-2202, 1471-2202
Online Access:Get full text
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Description
Summary: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.
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ISSN:1471-2202
1471-2202
DOI:10.1186/s12868-023-00831-2