Could a blood test for PTSD and depression be on the horizon?

Aspesi, Dario; Pinna, Graziano

doi:10.1080/14789450.2018.1544894

Cited by 21 publications

(21 citation statements)

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“…Consistently, in a cohort of Ugandan war survivors affected by PTSD, the hair levels of PEA, oleoylethanolamide (OEA), and stearoylethanolamide (SEA) were found to be decreased when compared with levels of war survivors without current or lifetime PTSD [100], thus suggesting a decreased PPAR-α signal pathway in PTSD. While it is important that these findings will be confirmed also in blood and post-mortem brain of PTSD patients [101], this observation provides support to the involvement of the PPAR-allopregnanolone axis dysfunction in PTSD. Together with the findings that allopregnanolone has been found decreased in cerebrospinal fluid (CSF) and plasma of both male and female PTSD and MDD patients [95,[97][98][99]102], these clinical data provide a translational example with PTSD animal models [103].…”

Section: Mood Disorderssupporting

confidence: 52%

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Tufano

Pinna

2020

Molecules

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Recently, peroxisome proliferator-activated receptor (PPAR)-α and γ isoforms have been gaining consistent interest in neuropathology and treatment of neuropsychiatric disorders. Several studies have provided evidence that either the receptor expression or the levels of their endogenously-produced modulators are downregulated in several neurological and psychiatric disorders and in their respective animal models. Remarkably, administration of these endogenous or synthetic ligands improves mood and cognition, suggesting that PPARs may offer a significant pharmacological target to improve several neuropathologies. Furthermore, various neurological and psychiatric disorders reflect sustained levels of systemic inflammation. Hence, the strategy of targeting PPARs for their anti-inflammatory role to improve these disorders is attracting attention. Traditionally, classical antidepressants fail to be effective, specifically in patients with inflammation. Non-steroidal anti-inflammatory drugs exert potent antidepressant effects by acting along with PPARs, thereby strongly substantiating the involvement of these receptors in the mechanisms that lead to development of several neuropathologies. We reviewed running findings in support of a role for PPARs in the treatment of neurological diseases, including Alzheimer’s disease or psychiatric disorders, such as major depression. We discuss the opportunity of targeting PPARs as a future pharmacological approach to decrease neuropsychiatric symptoms at the same time that PPAR ligands resolve neuroinflammatory processes.

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Section: Mood Disorderssupporting

confidence: 52%

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Tufano

Pinna

2020

Molecules

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“…[66][67][68] The literature surrounding trophic factors and PTSD remains particularly unclear, with findings often opposing one and other. [69][70][71] The intertwined relationship between trophic factors and sleep is particularly interesting in this case. BDNF and its molecular coplayers may have a central role in sleep homeostasis, particularly slow-wave sleep.…”

Section: Ptsd and Trophic Factorsmentioning

confidence: 98%

<p>Sleep, a Governor of Morbidity in PTSD: A Systematic Review of Biological Markers in PTSD-Related Sleep Disturbances</p>

Maguire¹,

Ruddock

Milanak

et al. 2020

NSS

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Background: Sleep disturbances (SD) are the most impactful and commonly reported symptoms in post-traumatic stress disorder (PTSD). Yet, they are often resistant to primary PTSD therapies. Research has identified two distinct SDs highly prevalent in PTSD; insomnia and nightmares. Those who report SDs prior to a traumatic event are at greater risk for developing PTSD; highlighting that sleep potentially plays a role in PTSD's pathology. To further understand the pathobiological mechanisms that lead to the development of PTSD, it is first imperative to understand the interplay which exists between sleep and PTSD on a biological level. The aim of this systematic review is to determine if biological or physiological markers are related to SD in PTSD. Methods: A systematic literature search was conducted on the electronic databases; Medline, Embase, AMED and PsycINFO, using Medical Subject Headings and associated keywords. Results: Sixteen studies were included in the final analyses. Physiological makers of autonomic function, and biochemical markers of HPA-axis activity; inflammatory processes; and trophic factor regulation were related to the severity of SDs in PTSD. Conclusion: These findings add to the growing literature base supporting a central focus on sleep in research aiming to define the pathophysiological processes which result in PTSD, as well as emphasising the importance of specifically targeting sleep as part of a successful PTSD intervention strategy. Resolving SDs will not only reduce PTSD symptom severity and improve quality of life but will also reduce all-cause mortality, hospital admissions and lifetime healthcare costs for those with PTSD. Limitations of the current literature are discussed, and key recommendations future research must adhere to are made within.

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“…The finding that the traditional gold-standard treatment option for PTSD, the selective serotonin reuptake inhibitors (SSRIs), is efficient in about half of the treated patients (reviewed in Golden et al, 2002; Rush et al, 2006; Kemp et al, 2008; Bernardy and Friedman, 2015), suggests that mood disorders emerge from complex neurobiological backgrounds and only one molecular deficit may not reflect a valid biomarker for the disorder under examination. Likewise, only one treatment cannot be the answer to improve symptoms in all patients, following the one-fit-all treatment expectation (Brewin, 2001; Aspesi and Pinna, 2018). Overall, discovering biomarkers that may lead to precision medicine for PTSD is in high demand.…”

Section: Allopregnanolone From Its Discovery In Adrenal Glands To a Rmentioning

confidence: 99%

“…Developing suitable animal models for PTSD and discovering reliable biomarkers that allow a more accurate diagnosis, based on objective measures, may improve quality of healthcare. Biomarker discovery will indeed permit developing targeted drugs and may generally offer more treatment options, which is highly desirable and needed (discussed in Aspesi and Pinna, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…However, PTSD remains a neuropathology with no specific pharmacological treatments, no established and reliable biomarkers, and PTSD animal models only reproduce PTSD neurobiology to a limited degree. While previous recent articles examined a number of animal models of PTSD and the validity of several biomarker candidates that have been proposed for PTSD (Aspesi and Pinna, 2018, 2019), this review will focus on the socially isolated mouse model of stress-induced fear extinction deficits. Other abnormal behavioral deficits will be discussed as well as commonalities with PTSD neurobiology in humans, such as reproducing endophenotipic features observed in PTSD patients.…”

Section: Introductionmentioning

confidence: 99%

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Animal Models of PTSD: The Socially Isolated Mouse and the Biomarker Role of Allopregnanolone

Pinna

2019

Front. Behav. Neurosci.

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Post-traumatic stress disorder (PTSD) is a debilitating undertreated condition that affects 8%–13% of the general population and 20%–30% of military personnel. Currently, there are no specific medications that reduce PTSD symptoms or biomarkers that facilitate diagnosis, inform treatment selection or allow monitoring drug efficacy. PTSD animal models rely on stress-induced behavioral deficits that only partially reproduce PTSD neurobiology. PTSD heterogeneity, including comorbidity and symptoms overlap with other mental disorders, makes this attempt even more complicated. Allopregnanolone, a neurosteroid that positively, potently and allosterically modulates GABA A receptors and, by this mechanism, regulates emotional behaviors, is mainly synthesized in brain corticolimbic glutamatergic neurons. In PTSD patients, allopregnanolone down-regulation correlates with increased PTSD re-experiencing and comorbid depressive symptoms, CAPS-IV scores and Simms dysphoria cluster scores. In PTSD rodent models, including the socially isolated mouse, decrease in corticolimbic allopregnanolone biosynthesis is associated with enhanced contextual fear memory and impaired fear extinction. Allopregnanolone, its analogs or agents that stimulate its synthesis offer treatment approaches for facilitating fear extinction and, in general, for neuropsychopathologies characterized by a neurosteroid biosynthesis downregulation. The socially isolated mouse model reproduces several other deficits previously observed in PTSD patients, including altered GABA A receptor subunit subtypes and lack of benzodiazepines pharmacological efficacy. Transdiagnostic behavioral features, including expression of anxiety-like behavior, increased aggression, a behavioral component to reproduce behavioral traits of suicidal behavior in humans, as well as alcohol consumption are heightened in socially isolated rodents. Potentials for assessing novel biomarkers to predict, diagnose, and treat PTSD more efficiently are discussed in view of developing a precision medicine for improved PTSD pharmacological treatments.

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Could a blood test for PTSD and depression be on the horizon?

Cited by 21 publications

References 272 publications

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

<p>Sleep, a Governor of Morbidity in PTSD: A Systematic Review of Biological Markers in PTSD-Related Sleep Disturbances</p>

Animal Models of PTSD: The Socially Isolated Mouse and the Biomarker Role of Allopregnanolone

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