Correlations between peripheral blood mononuclear cell production of BDNF, TNF‐alpha, IL‐6, IL‐10 and cognitive performances in multiple sclerosis patients

Patanella, Agata Katia; Zinno, Massimiliano; Quaranta, Davide; Nociti, Viviana; Frisullo, Giovanni; Gainotti, Guido; Tonali, P.; Batocchi, Anna Paola; Marra, Camillo

doi:10.1002/jnr.22276

Cited by 112 publications

(74 citation statements)

References 44 publications

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“…Interestingly, upregulation of BDNF with a positive modulator of AMPA-type glutamate receptors rescues synaptic plasticity and memory in murine models of HD [236], while its downregulation resulted in earlier and more accentuated cognitive impairment [237]. A correlation between low BDNF production by peripheral blood mononuclear cells and poorer performances in cognitive tasks has also been reported in relapsing-remitting MS patients, suggesting a possible role of BDNF in cognitive impairment in MS [238].…”

Section: Modeling a Feasible No-orchestrated Mechanism For Synaptic Lmentioning

confidence: 95%

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

2010

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Synapse elimination is the main factor responsible for the cognitive decline accompanying many of the neuropathological conditions affecting humans. Synaptic stripping of motoneurons is also a common hallmark of several motor pathologies. Therefore, knowledge of the molecular basis underlying this plastic process is of central interest for the development of new therapeutic tools. Recent advances from our group highlight the role of nitric oxide (NO) as a key molecule triggering synapse loss in two models of motor pathologies. De novo expression of the neuronal isoform of NO synthase (nNOS) in motoneurons commonly occurs in response to the physical injury of a motor nerve and in the course of amyotrophic lateral sclerosis. In both conditions, this event precedes synaptic withdrawal from motoneurons. Strikingly, nNOS-synthesized NO is "necessary" and "sufficient" to induce synaptic detachment from motoneurons. The mechanism involves a paracrine/retrograde action of NO on pre-synaptic structures, initiating a downstream signaling cascade that includes sequential activation of (1) soluble guanylyl cyclase, (2) cyclic guanosine monophosphate-dependent protein kinase, and (3) RhoA/Rho kinase (ROCK) signaling. Finally, ROCK activation promotes phosphorylation of regulatory myosin light chain, which leads to myosin activation and actomyosin contraction. This latter event presumably contributes to the contractile force to produce ending axon retraction. Several findings support that this mechanism may operate in the most prevalent neurodegenerative diseases.

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Section: Modeling a Feasible No-orchestrated Mechanism For Synaptic Lmentioning

confidence: 95%

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

2010

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“…Memory, in particular, is disrupted in states that trigger brain inflammation, including traumatic brain injury, infections, neurodegenerative disorders like Alzheimer's disease (AD), and normal aging. Both chronic and acute inflammation have been associated with significant memory impairments in humans (e.g., Hilsabeck et al 2002;Schmidt et al 2006;Patanella et al 2010). Neuronal damage and death are an immediate source of cognitive deficits in the wake of brain injury, infection, and neurodegeneration.…”

mentioning

confidence: 99%

MHC class I immune proteins are critical for hippocampus-dependent memory and gate NMDAR-dependent hippocampal long-term depression

et al. 2013

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Memory impairment is a common feature of conditions that involve changes in inflammatory signaling in the brain, including traumatic brain injury, infection, neurodegenerative disorders, and normal aging. However, the causal importance of inflammatory mediators in cognitive impairments in these conditions remains unclear. Here we show that specific immune proteins, members of the major histocompatibility complex class I (MHC class I), are essential for normal hippocampus-dependent memory, and are specifically required for NMDAR-dependent forms of long-term depression (LTD) in the healthy adult hippocampus. In b2m 2/2 TAP 2/2 mice, which lack stable cell-surface expression of most MHC class I proteins, NMDAR-dependent LTD in area CA1 of adult hippocampus is abolished, while NMDAR-independent forms of potentiation, facilitation, and depression are unaffected. Altered NMDAR-dependent synaptic plasticity in the hippocampus of b2m 2/2 TAP 2/2 mice is accompanied by pervasive deficits in hippocampus-dependent memory, including contextual fear memory, object recognition memory, and social recognition memory. Thus normal MHC class I expression is essential for NMDAR-dependent hippocampal synaptic depression and hippocampus-dependent memory. These results suggest that changes in MHC class I expression could be an unexpected cause of disrupted synaptic plasticity and cognitive deficits in the aging, damaged, and diseased brain.

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“…(3) Decreased sBDNF concentrations have been correlated with increased severity of Alzheimer's disease [54] , and high BDNF concentrations are predictive of slow cognitive decline [55] . (4) Low sBDNF has been associated with poor executive and attentional performance in multiple sclerosis [56] . (5) Patients with major depression have had low sBDNF levels along with poor cognitive function in several cognitive domains [9] .…”

Section: Introductionmentioning

confidence: 99%

Improved Alertness Is Associated with Early Increase in Serum Brain-Derived Neurotrophic Factor and Antidepressant Treatment Outcome in Major Depression

Mikoteit¹,

Hemmeter²,

Brand³

et al. 2015

Neuropsychobiology

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Background/Aims: In major depression cognitive impairment is common and may persist despite improvement in psychopathology. So far it is unclear how closely related improvement in cognitive functioning is to the clinical course of depression. Further, it is unclear whether recovery from cognitive impairment is linked to changes in serum brain-derived neurotrophic factor (sBDNF). The objectives of this study were (1) to explore the predictive value of cognitive impairment for therapeutic outcome, and (2) to assess the association between cognitive performance and sBDNF levels over a 6-week course of antidepressant treatment. Methods: Twenty-five adult patients suffering from major depression underwent standardized treatment with duloxetine. Both severity of depression as assessed by the Hamilton Depression Rating Scale and sBDNF levels were measured at baseline, and after 1, 2 and 6 weeks of treatment. Cognitive performance, i.e. alertness, working memory, and divided attention, was assessed at baseline, after 1 week, and at the end of treatment after 6 weeks. Results: Higher performance in alertness and divided attention at baseline correlated with less severe depression at week 6. During the first week of treatment, a greater increase in sBDNF was associated with a greater improvement in alertness at week 6. Conclusion: Greater alertness at baseline was a predictor of favorable antidepressive treatment outcome. Moreover, the early increase in sBDNF correlated with improvement in attention functioning. Thus, recovery from cognitive impairment and an early increase in sBDNF seem to be associated.

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Correlations between peripheral blood mononuclear cell production of BDNF, TNF‐alpha, IL‐6, IL‐10 and cognitive performances in multiple sclerosis patients

Cited by 112 publications

References 44 publications

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

MHC class I immune proteins are critical for hippocampus-dependent memory and gate NMDAR-dependent hippocampal long-term depression

Improved Alertness Is Associated with Early Increase in Serum Brain-Derived Neurotrophic Factor and Antidepressant Treatment Outcome in Major Depression

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