Pathophysiological implications of neuroinflammation mediated HPA axis dysregulation in the prognosis of cancer and depression

Ahmad, Mir Hilal; Rizvi, Moshahid Alam; Fatima, Mahino; Mondal, Amal Chandra

doi:10.1016/j.mce.2020.111093

Cited by 52 publications

(32 citation statements)

References 90 publications

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“…Excessive stress causes negative feedback loops to become dysfunctional elevating cortisol levels. Pathophysiology related to depression and diseases such as cancer lead to neuroinflammation and HPA axis dysregulation (Ahmad et al., 2021). Both diabetes and depression are associated with HPA axis dysregulation (Champaneri et al., 2010).…”

Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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Diabetes increases the likelihood of developing depression and vice versa. Research on this bidirectional association has somewhat managed to delineate the interplay among implicated physiological processes. Still, further exploration is required in this context. This review addresses the comorbidity by investigating suspected common pathophysiological mechanisms. One such factor is psychological stress which disturbs the hypothalamic–pituitary–adrenal axis causing hormonal imbalance. This includes elevated cortisol levels, a common biomarker of both depression and diabetes. Disrupted insulin signaling drives the hampered neurotransmission of serotonin, dopamine, and norepinephrine. Also, adipokine hormones such as adiponectin, leptin, and resistin and the orexigenic hormone, ghrelin, are involved in both depression and T2DM. This disarray further interferes with physiological processes encompassing sleep, the gut–brain axis, metabolism, and mood stability. Behavioral coping mechanisms, such as unhealthy eating, mediate disturbed glucose homeostasis, and neuroinflammation. This is intricately linked to oxidative stress, redox imbalance, and mitochondrial dysfunction. However, interventions such as psychotherapy, physical exercise, fecal microbiota transplantation, and insulin‐sensitizing agents can help to manage the distressing condition. The possibility of glucagon‐like peptide 1 possessing a therapeutic role has also been discussed. Nonetheless, there stands an urgent need for unraveling new correlating targets and biological markers for efficient treatment.

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Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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“…Several studies [ 9 , 10 , 11 ] showed that cancer patients suffer from a high prevalence of depression, anxiety, and cognitive disorders. The fact that these disorders are common among other populations afflicted with chronic inflammatory disease stimulated discussion of potential shared biological mechanisms of neuroinflammation and depressed mood to precede major changes resulting, later, in diagnosis of cancer [ 12 ]. Potentially, two mechanisms may be involved—cytokine-related or glucocorticoid responses-related.…”

Section: Neuroinflammation In Cancermentioning

confidence: 99%

“…Cortisol is released by the hypothalamic-pituitary-adrenal (HPA) axis in response to psychosocial stress. Preliminary evidence indicates that tumors can affect endocrine function [ 12 ]. Studies by Pyter et al [ 13 , 35 ] showed that corticosterone (the primary glucocorticoid in most animals) levels are generally higher in tumor-bearing rodents than in tumor-free controls, and that the hormone’s responsivity to stress is reduced in these animals.…”

Section: Neuroinflammation In Cancermentioning

confidence: 99%

Neuroinflammation as a Common Denominator of Complex Diseases (Cancer, Diabetes Type 2, and Neuropsychiatric Disorders)

Asslih

Damri

Agam

2021

IJMS

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The term neuroinflammation refers to inflammation of the nervous tissue, in general, and in the central nervous system (CNS), in particular. It is a driver of neurotoxicity, it is detrimental, and implies that glial cell activation happens prior to neuronal degeneration and, possibly, even causes it. The inflammation-like glial responses may be initiated in response to a variety of cues such as infection, traumatic brain injury, toxic metabolites, or autoimmunity. The inflammatory response of activated microglia engages the immune system and initiates tissue repair. Through translational research the role played by neuroinflammation has been acknowledged in different disease entities. Intriguingly, these entities include both those directly related to the CNS (commonly designated neuropsychiatric disorders) and those not directly related to the CNS (e.g., cancer and diabetes type 2). Interestingly, all the above-mentioned entities belong to the same group of “complex disorders”. This review aims to summarize cumulated data supporting the hypothesis that neuroinflammation is a common denominator of a wide variety of complex diseases. We will concentrate on cancer, type 2 diabetes (T2DM), and neuropsychiatric disorders (focusing on mood disorders).

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“…Prolonged and cumulative exposure to these stimuli dysregulates and hyperactivates one of the body's major stress system, being the hypothalamus-pituitary-adrenal (HPA)-axis, causing a generalized stress response by the release of stress hormones such as cortisol (Starr et al, 2019). A dysregulated HPA-axis negatively impacts overall health and activates the body's immunoinflammatory system (Tapp et al, 2019;Ahmad et al, 2020). Rather than being considered as an individual pathophysiology that comprises a simple "cause or consequence" connection, we propose that stress-driven, age-related perturbation of a chronic low-grade pro-inflammatory status, coined as inflammaging, (Franceschi et al, 2007;Chadwick et al, 2012) underlies arterial stiffness.…”

Section: Causes Of Arterial Stiffnessmentioning

confidence: 99%

Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer’s Disease

Hendrickx

Martinet

Dam

et al. 2021

Front. Mol. Biosci.

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The average age of the world’s elderly population is steadily increasing. This unprecedented rise in the aged world population will increase the prevalence of age-related disorders such as cardiovascular disease (CVD) and neurodegeneration. In recent years, there has been an increased interest in the potential interplay between CVDs and neurodegenerative syndromes, as several vascular risk factors have been associated with Alzheimer’s disease (AD). Along these lines, arterial stiffness is an independent risk factor for both CVD and AD. In this review, we discuss several inflammaging-related disease mechanisms including acute tissue-specific inflammation, nitro-oxidative stress, impaired autophagy, and insulin resistance which may contribute to the proposed synergism between arterial stiffness and AD.

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Pathophysiological implications of neuroinflammation mediated HPA axis dysregulation in the prognosis of cancer and depression

Cited by 52 publications

References 90 publications

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Neuroinflammation as a Common Denominator of Complex Diseases (Cancer, Diabetes Type 2, and Neuropsychiatric Disorders)

Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer’s Disease

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