Stress-induced neuroplasticity: (Mal)adaptation to adverse life events in patients with PTSD – A critical overview

Deppermann, Saskia; Storchak, Helena; Fallgatter, Andreas J.; Ehlis, Ann‐Christine

doi:10.1016/j.neuroscience.2014.08.037

Cited by 72 publications

(45 citation statements)

References 107 publications

(168 reference statements)

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“…Both of these BDNF roles trigger a cascade of intercellular mechanisms that are components of adaptive mechanisms that are critical to re-establish homeostasis in response to stress (Depperman et al 2014). Hence, BDNF is an attractive molecular mediator for the experience of symptoms such as pain and depression, because these symptoms are thought to be contributed by alterations in homeostasis (Coenen et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Lower brain-derived neurotrophic factor levels associated with worsening fatigue in prostate cancer patients during repeated stress from radiation therapy

Saligan

Lukkahatai

Holder

et al. 2015

The World Journal of Biological Psychiatry

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Objectives Fatigue during cancer treatment is associated with depression. Neurotrophic factors play a major role in depression and stress and might provide insight into mechanisms of fatigue. This study investigated the association between plasma concentrations of three neurotrophic factors (BDNF, brain-derived neurotrophic factor; GDNF, glial-derived neurotrophic factor; and SNAPIN, soluble N-ethylmaleimide sensitive fusion attachment receptor-associated protein) and initial fatigue intensification during external beam radiation therapy (EBRT) in euthymic non-metastatic prostate cancer men. Methods Fatigue, as measured by the 13-item Functional Assessment of Cancer Therapy-Fatigue (FACT-F), and plasma neurotrophic factors were collected at baseline (prior to EBRT) and mid-EBRT. Subjects were categorized into fatigue and no fatigue groups using a >3-point change in FACT-F scores between the two time points. Multiple linear regressions analysed the associations between fatigue and neurotrophic factors. Results FACT-F scores of 47 subjects decreased from baseline (43.95 ± 1.3) to mid-EBRT (38.36 ± 1.5, P < 0.001), indicating worsening fatigue. SNAPIN levels were associated with fatigue scores (rs = 0.43, P = 0.005) at baseline. A significant decrease of BDNF concentration (P = 0.008) was found in fatigued subjects during EBRT (n = 39). Conclusions Baseline SNAPIN and decreasing BDNF levels may influence worsening fatigue during EBRT. Further investigations are warranted to confirm their role in the pathophysiology and therapeutics of fatigue.

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Section: Discussionmentioning

confidence: 99%

Lower brain-derived neurotrophic factor levels associated with worsening fatigue in prostate cancer patients during repeated stress from radiation therapy

Saligan

Lukkahatai

Holder

et al. 2015

The World Journal of Biological Psychiatry

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“…Following from the empirical evidence described above, we predicted that both positive and negative maladaptive metacognitive beliefs would be associated with PTS symptoms, and the association between negative metacognitive beliefs and PTS symptoms would be the largest in magnitude (Roussis and Wells, 2006; Fergus and Bardeen, 2017a). Additionally, based on evidence showing that individuals with PTSD exhibit relative deficits in the cognitive abilities associated with executive control (Deppermann et al, 2014; Scott et al, 2015), we predicted that executive control deficits would be positively associated with PTS symptoms. Importantly, based on metacognitive theory (Wells, 2009), which suggests that CAS-based coping is exacerbated by deficits in executive control, we predicted that the magnitude of the positive association between maladaptive metacognitive beliefs (i.e., positive and negative) and PTS symptoms would become significantly stronger as deficits in executive control increased.…”

Section: Present Studymentioning

confidence: 99%

Executive Control Deficits Potentiate the Effect of Maladaptive Metacognitive Beliefs on Posttraumatic Stress Symptoms

Bardeen

Fergus

2018

Front. Psychol.

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The metacognitive model and recent preliminary research suggests that metacognitive beliefs (i.e., beliefs about thinking) may be particularly important for understanding the pathogenesis of posttraumatic stress (PTS). The metacognitive model also suggests that deficits in executive control (i.e., metacognitive control) may increase the impact of metacognitive beliefs on PTS symptoms. Trauma-exposed adult participants (N = 469), recruited through an online crowdsourcing website, completed a battery of measures assessing the constructs of interest. As predicted, deficits in executive control strengthened the positive association between metacognitive beliefs and PTS symptoms. This effect was found in relation to positive (e.g., “Worrying will keep me safe”), but not negative (e.g., “My thoughts are uncontrollable”), metacognitive beliefs. Supplemental analyses, indicated that the interaction between positive metacognitive beliefs and executive control significantly predicted all PTS cluster scores (i.e., Intrusion, Cognition, Arousal, Avoidance). Taken together, results support the proposal that executive control deficits potentiate the effect of metacognitive beliefs on PTS symptoms. Intervention strategies designed to strengthen executive control (e.g., the attention training technique) may be useful in treating individuals with PTS.

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“…In addition to memory formation, processes such as memory reconsolidation and extinction also play important roles in normal cognitive function, and deficits in these processes are thought to contribute to anxiety and posttraumatic stress disorder (PTSD) (48). Although it appears not to have a major role in hippocampal synaptic plasticity or memory formation, HDAC1 does promote the extinction of recently formed (1-day-old) fear memories (49).…”

Section: Which Hdacs Are Important In Cognition?mentioning

confidence: 99%

“…GR is a steroid receptor and transcriptional activator whose activity can be modulated by systemic or cellular stress (48). Activated GR (pGR) can bind to elements in the HDAC2 promoter and is thought to contribute to the increased abundance of HDAC2 seen in AD patients and mouse models (55).…”

Section: Molecular Mechanisms Of Hdac Signalingmentioning

confidence: 99%

“…Treating hippocampal neurons with cellular stressors such as hydrogen peroxide or Ab induces the activation of GR, binding of GR to the HDAC2 promoter, and HDAC2 expression. Intriguingly, GR activity can also be regulated by emotional stress (48), suggesting the possibility that GR-mediated up-regulation of HDAC2 could contribute to stress-induced cognitive dysfunction and depression.…”

Section: Molecular Mechanisms Of Hdac Signalingmentioning

confidence: 99%

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Histone deacetylases in memory and cognition

2014

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Over the past 30 years, lysine acetylation of histone and nonhistone proteins has become established as a key modulator of gene expression regulating numerous aspects of cell biology. Neuronal growth and plasticity are no exception; roles for lysine acetylation and deacetylation in brain function and dysfunction continue to be uncovered. Transcriptional programs coupling synaptic activity to changes in gene expression are critical to the plasticity mechanisms underlying higher brain functions. These transcriptional programs can be modulated by changes in histone acetylation, and in many cases, transcription factors and histone-modifying enzymes are recruited together to plasticity-associated genes. Lysine acetylation, catalyzed by lysine acetyltransferases (KATs), generally promotes cognitive performance, whereas the opposing process, catalyzed by histone lysine deacetylases (HDACs), appears to negatively regulate cognition in multiple brain regions. Consistently, mutation or deregulation of different KATs or HDACs contributes to neurological dysfunction and neurodegeneration. HDAC inhibitors have shown promise as a treatment to combat the cognitive decline associated with aging and neurodegenerative disease, as well as to ameliorate the symptoms of depression and posttraumatic stress disorder, among others. In this review, we discuss the evidence for the roles of HDACs in cognitive function as well as in neurological disorders and disease. In particular, we focus on HDAC2, which plays a central role in coupling lysine acetylation to synaptic plasticity and mediates many of the effects of HDAC inhibition in cognition and disease.

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Stress-induced neuroplasticity: (Mal)adaptation to adverse life events in patients with PTSD – A critical overview

Cited by 72 publications

References 107 publications

Lower brain-derived neurotrophic factor levels associated with worsening fatigue in prostate cancer patients during repeated stress from radiation therapy

Lower brain-derived neurotrophic factor levels associated with worsening fatigue in prostate cancer patients during repeated stress from radiation therapy

Executive Control Deficits Potentiate the Effect of Maladaptive Metacognitive Beliefs on Posttraumatic Stress Symptoms

Histone deacetylases in memory and cognition

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