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A possible explanation could be that NMDA receptor antagonists increase 5-HT levels in the brain [ ], while also having a modulatory effect on pathways involved in neuroplasticity and cellular resilience [ ]. Glutamate-mediated effects on the cGMP-NO system leading to monoamine release that in turn can be targeted by pharmacological means, eg.

However this pathway can also lead to oxidative stress if excessive glutamate-mediated NO synthesis combines with O 2 - from aerobic metabolism. Also depicted is the effect of inflammatory mediators that promote iNOS-mediated NO synthesis thereby promoting the formation of cell-damaging reactive oxygen and nitrogen species. How this happens still needs illumination, although animal studies have begun to delve into the possible mechanisms involved [ ].

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The mTOR pathway plays a pivotal role in protein synthesis by stimulating mRNA translation via interaction with its downstream targets [ ], and leads to prolonged elevation of synapse-associated proteins in the prefrontal cortex [ ]. An overview of key neuroprotective and neurotoxic molecules involved in drug antidepressant, lithium etc.

Adapted from [ ]. Decreased glutamate release has been observed in the frontal cortices of Homer1 mutant mice, a putative animal model of schizophrenia [ ], while chronic phencyclidine PCP administration in rats is associated with a decreased expression of glutamate receptors in the prefrontal cortex [ ] and a reduced number of cortical and hippocampal PV-immunoreactive neurones [ 64 ].

Confirming this, partial deletion of the NMDA receptor in mice is associated with behavioural alterations akin to that observed in PCP treated mice [ ], while increased NMDA receptor binding has been described in the frontal cortex of SIR animals [ ]. Growth factors are intricately involved in the survival, growth and differentiation of specific groups of neurons.

Their relevance is gaining in importance in the light of increasing evidence that mood and psychotic disorders are associated with structural brain changes and that alterations in growth factors may precipitate or exacerbate depressive, BPD and psychotic episodes [ 13 , , ]. Antidepressant treatment up-regulates CREB in the cortex and hippocampus of humans [ ]. BDNF has been shown to originate from several sources including brain neurons, vascular endothelial cells and platelets.

BDNF regulates synaptic plasticity in neuronal networks and appears to be a particularly relevant factor for mood disorders with associated cognitive dysfunction [ - ]. Activation of CREB is associated with the regulation of synaptic plasticity as well as transcription of specific target genes involved in the production of proteins, BDNF being one example [ , ].

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Post-mortem studies have reported decreased hippocampal BDNF in MD patients who committed suicide, but elevated levels in patients who were being treated with antidepressant agents at the time of death [ , ]. Considering the growing evidence for an interaction between MD and metabolic and redox-related conditions [ - ], our group recently showed that altered serum BDNF may be linked to metabolic and redox factors, with BDNF levels indicating either a counter-regulatory action on the effects of glutathione oxidation or that BDNF may mediate the redox effects itself, leading to the development of a mood disorder [ ].

Various factors associated with an increased risk of developing MD, e. Thus decreased levels of BDNF have been found in smoking individuals when compared to non-smokers [ , ], while smoking cessation leads to improved BDNF levels [ , ]. Likewise, serum levels of BDNF have been shown to be significantly lower in subjects with Type II diabetes when compared to healthy controls [ , ], while cerebral output of BDNF is inhibited in the presence of high blood glucose levels [ ]. These findings reiterate the causal link between metabolic diseases, altered BDNF and the development of MD noted earlier.

On the other hand, for example, physical exercise has been shown to increase BDNF [ , ], to be neuroprotective, to improve mood and to have antidepressant effects [ , ]. Decreased peripheral BDNF levels have been observed in BPD patients, possibly associated with the pathophysiology and severity of manic symptoms [ ]. Exercise has also been shown to decrease depressive symptoms in BPD patients and to even increase the frequency of mania [ ]. The latter would indicate that elevated levels of BDNF may not always be beneficial, as has been proposed in a study in patients with MD [ ].

The authors suggest that, by adversely affecting resilience, BDNF facilitates activity-dependent plasticity that may translate to a variable effect on mood and other plasticity-dependent functions. In fact, BDNF has been noted to induce paradoxical depressogenic effects [ ]. As a mediator of synaptic plasticity, maladaptive secretion of BDNF eg.

Decreased peripheral BDNF levels have been observed in schizophrenia [ ].

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Importantly, a recent study indicated that clinically stable schizophrenia patients present with significantly increased serum levels of BDNF after exposure to cognitive training targeted at improving neuroplasticity [ ]. Furthermore, post-mortem studies reported a decreased concentration of BDNF-positive neurons [ ] and BDNF concentrations in brain tissue of schizophrenic patients, which include the cortical areas and the hippocampi [ ]. Antidepressant treatment up-regulates CREB in the cortex and hippocampus of rats [ ], while an overexpression of CREB in the dentate gyrus results in antidepressant effects in the FST and a learned helplessness paradigm — both animal models of MD [ ].

In the latter, decreased hippocampal BDNF levels were described. Although contrary to that in human subjects, some studies have also noted increased serum levels of BDNF [ , ]. In FSL rats, serum and whole blood BDNF levels have been found to be significantly increased compared to control but significantly decreased in the hippocampus, with no differences noted in the frontal cortex and CSF [ ], suggesting that BDNF is differentially regulated in hippocampus, serum, and whole blood in these animals.

The latter is not unlike similar paradoxical findings in humans, where BDNF has been suggested to play a counter-regulatory role [ ]. Preclinical studies have indicated that BDNF administration produces antidepressant-like behaviour [ ], while antidepressants and electroconvulsive therapy increase BDNF levels [ ]. After animals were subjected to repeated stress, they constantly presented with decreased BDNF levels as measured in the hippocampus and serum, while corticosterone levels returned to normal levels, suggesting that changes in brain plasticity occur following a second stressful event [ ].

The presence of decreased serum BDNF levels accompanied by normal serum cortisol levels may therefore represent a relevant biomarker for identifying individuals who are more likely to develop depressive symptoms in the subset of a population which may be predisposed to developing affective disorders. These alterations may even be expanded to other disorders provoked by stressful life events, for instance schizophrenia [ ]. With smoking having been found to affect BDNF levels in humans, decreased levels of BDNF have also been found in rats repeatedly exposed to nicotine [ ].

Similarly, physical exercise also increases BDNF in animals [ , ]. BDNF levels are decreased in both the amygdala and hippocampus of rats in the ouabain model of mania, and reversed by lithium [ ]. Moreover, in an amphetamine-induced model of mania, BDNF was also decreased in the hippocampus and increased by valproate and lithium [ ]. Neonatal PCP administration produced a sustained elevation of BDNF in the hippocampus and the entorhinal cortex of 8-week-old rats [ ]. Insulin-like growth factor-1 IGF-1 is involved in regulating peripheral cell growth and metabolism [ ]; and plays a crucial role in the growth and differentiation of nerves and also in the synthesis and release of neurotransmitters [ ].

Unfortunately, there have not been sufficient clinical studies to determine whether peripheral IGF-1 is altered in MD patients or following antidepressant administration. Antipsychotic-free schizophrenia patients have been found to present with a decrease in plasma IGF levels [ ]. Unfortunately, we are not aware of any extensive IGF-related data in established animal models of MD.

Moreover, after chronically treating rats with antidepressants, elevated IGF-1 expression was observed in the brains of these animals [ ]. Finally, IGF-1 has been found to regulate adult hippocampal neurogenesis in rats [ ]. To the best of our knowledge there is no pre-clinical data in established animal models of IGF-1 as a preclinical biomarker in BPD or schizophrenia.

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Vascular endothelial growth factor VEGF acts as a neurotrophic factor, is a cytokine implicated in angiogenesis [ ] and has been related to the vascular niche hypothesis of adult neurogenesis [ ]. This hypothesis attributes increases in the proliferation of neurons in the adult hippocampus to VEGF-induced angiogenesis. VEGF is purported to play a role in several features associated with neuronal growth, including neuronal regeneration and differentiation as well as axonal outgrowth [ ].

MD patients present with higher plasma VEGF levels which can be reversed with antidepressant treatment [ ], while earlier studies have confirmed said increase in MD [ ].

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Furthermore, remitted MD patients have significantly elevated VEGF levels, while MD patients with a family history of psychiatric disorders also have higher baseline levels of VEGF, compared to MD patients without a family history and healthy controls [ ]. VEGF data in schizophrenia patients are limited, although previous studies have not observed any differences in serum VEGF in schizophrenia vs.

The relationship between central and peripheral levels of VEGF still needs clarification. However, a pre-clinical study did observe that VEGF levels are increased in rat hippocampi following 14 days haloperidol or olanzapine treatment [ ].

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Interestingly, in the case of haloperidol treatment this increase was lost 45 days later, while olanzapine treatment bolstered the initial increase in VEGF [ ], reaffirming that first and second generation antipsychotics are not therapeutically equivalent. This underlines VEGF as a possible marker in schizophrenia treatment but not diagnosis per se.

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Several neurochemical markers have been associated with neuroprotective effects and positive antidepressant treatment response. With the increased evidence for a neurodegenerative profile for MD, BPD and schizophrenia and the progressive nature of these illnesses, identifying neuroresilience markers is gaining in relevance.

In this regard, resilience markers linked to the BDNF pathway are especially attractive. Stress and environmental adversity is a common thread throughout all three illnesses under review [ , , ]. Stress-induced increases in glucocorticoid levels have been shown to decrease the synthesis of neurotrophic factors, particularly BDNF, which is an effective neuroprotective factor and protagonist of neurogenesis [ ]. As noted earlier, BDNF expression is decreased during MD, BPD and schizophrenia, a response that is reversed by effective pharmacological treatment [ , - ].

Furthermore, increased structural atrophy observed in treatment resistant MD has been correlated with greater decreases in BDNF levels [ ] in patients failing to respond to SRI treatment compared to treatment responsive patients.

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The cAMP cascade is activated following increased serotonergic and adrenergic receptor activity which results in downstream activation of CREB [ ]. Activation of Akt following phosphorylation leads to enhanced activity of mTOR which is responsible for regulating the expression of several genes involved in cell growth, particularly a group of synapse-associated genes that have been directly linked to neuroplastic events [ ].

It also regulates various proteins and is involved in neuroplasticity and neurotransmission [ ].

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Therefore, agents involved in the modulation of GSK-3b and its downstream pathways may serve as valuable biomarkers in the diagnosis and treatment of BPD — e. GSK-3b also plays an important role in the regulation of the Wnt [ ] and PI-3K [ ] signalling pathways linked to cellular resilience [ , ] Fig.