Cerebral protection

Riedel, Bernhard; Browne, Kimberley; Silbert, Brendan

doi:10.1097/aco.0000000000000032

Cited by 102 publications

(34 citation statements)

References 59 publications

(43 reference statements)

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“…Many mental disorders are associated with both a loss of PFC synapses and increased signs of neuroinflammation e.g. ( Pace and Heim, 2011 , Raison and Miller, 2013 , Yoshiyama et al., 2007 , Schizophrenia Working Gro, 2014 , Sharma et al., 2014 , Riedel et al., 2014 , Masi et al., 2014 ). Given that guanfacine can protect working memory ( Birnbaum et al., 2000 ) and PFC dendritic spines, as well as reducing inflammation, it may be helpful across a wide spectrum of mental disorders.…”

Section: Discussionmentioning

confidence: 99%

Chronic stimulation of alpha-2A-adrenoceptors with guanfacine protects rodent prefrontal cortex dendritic spines and cognition from the effects of chronic stress

Hains

Yabe

Arnsten

2015

Neurobiology of Stress

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The prefrontal cortex (PFC) provides top-down regulation of behavior, cognition, and emotion, including spatial working memory. However, these PFC abilities are greatly impaired by exposure to acute or chronic stress. Chronic stress exposure in rats induces atrophy of PFC dendrites and spines that correlates with working memory impairment. As similar PFC grey matter loss appears to occur in mental illness, the mechanisms underlying these changes need to be better understood. Acute stress exposure impairs PFC cognition by activating feedforward cAMP-calcium- K+ channel signaling, which weakens synaptic inputs and reduces PFC neuronal firing. Spine loss with chronic stress has been shown to involve calcium-protein kinase C signaling, but it is not known if inhibiting cAMP signaling would similarly prevent the atrophy induced by repeated stress. The current study examined whether inhibiting cAMP signaling through alpha-2A-adrenoceptor stimulation with chronic guanfacine treatment would protect PFC spines and working memory performance during chronic stress exposure. Guanfacine was selected due to 1) its established effects on cAMP signaling at post-synaptic alpha-2A receptors on spines in PFC, and 2) its increasing clinical use for the treatment of pediatric stress disorders. Daily guanfacine treatment compared to vehicle control was found to prevent dendritic spine loss in layer II/III pyramidal neurons of prelimbic PFC in rats exposed to chronic restraint stress. Guanfacine also protected working memory performance; cognitive performance correlated with dendritic spine density. These findings suggest that chronic guanfacine use may have clinical utility by protecting PFC gray matter from the detrimental effects of stress.

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Section: Discussionmentioning

confidence: 99%

Chronic stimulation of alpha-2A-adrenoceptors with guanfacine protects rodent prefrontal cortex dendritic spines and cognition from the effects of chronic stress

Hains

Yabe

Arnsten

2015

Neurobiology of Stress

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“…The underlying mechanisms of POCD are not yet fully understood. Clinical studies have consistently suggested that the main causes of this injury include an exaggerated systemic inflammation [ 6 ], endothelial dysfunction [ 7 ], cerebral hypoperfusion, and microembolism [ 8 ]. Others have specifically reported that POCD is indeed correlated with the serum protein levels of IL-6, TNF-α, S100β, neuron-specific enolase (NSE), and malonaldehyde (MDA) [ 9 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Intravenous Lidocaine on Early Postoperative Cognitive Dysfunction in Elderly Patients Following Spine Surgery

et al. 2015

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BackgroundThis study aimed to evaluate the effects of lidocaine treatment on cognitive impairment in aged patients undergoing spine surgery and to explore the underlying mechanism.Material/MethodsPatients were randomly divided into 2 treatment groups: (1) saline (control) and (2) lidocaine. After induction of anesthesia, the lidocaine group received lidocaine as a bolus of 1 mg/kg over 5 minutes, followed by a continuous infusion at 1.5 mg/kg/h until the end of the surgery. We examined the effects of lidocaine treatment on the improvement of cognitive function using the Mini-Mental State Examination (MMSE) at preoperation and 3 days postoperation. Serum samples were collected to assess the levels of IL-6, TNF-α, MDA, S100β, and NSE before inducing anesthesia, at the end of surgery, and 3 days after the end of surgery.ResultsWe found that the MMSE scores in the lidocaine group were markedly higher than those in the control group at 3 days after surgery. Moreover, lidocaine treatment markedly suppressed the release of IL-6, S100β, and NSE into the serum at the end of surgery and 3 days after the end of surgery. In the control group, serum MDA levels increased by 3 days after the end of surgery. The lidocaine group had lower serum MDA levels than those in the control group.ConclusionsLidocaine may be an effective neuroprotective agent in treating early postoperative cognitive dysfunction in elderly patients undergoing spine surgery.

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“…Хирургическое вмешательство рассматривается лишь как фактор, запускающий каскад воспалительных реакций, а анестезия, напротив, служит ключевой причиной ПОКД. При этом операция или любая инвазивная манипуляция только усугубляют когнитив-ные нарушения у пациентов, «склонных» к регрессу ментальных функций [28].…”

Section: Keywtrbunclassified

To the mechanisms of the protective effects of regional anesthesia in relation to the development of postoperative cognitive dysfunction

Strashnov

Иванович²,

Galstyan

et al. 2018

Rev Clin Pharm Drug Ther

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The review of data on epidemiology, etiology and pathogenesis, methods of prevention and treatment of postoperative cognitive dysfunction (POCD) is presented. A comparative analysis of the influence on the development of POCD of general anesthesia (OA) and regional anesthesia (RA) was carried out. The substantiation of advantages of RA and its combination with components of OA against OA is given. (For citation: Strashnov VI, Zabrodin ON. To the mechanisms of the protective effects of regional anesthesia in relation to the development of postoperative cognitive dysfunction. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(2):62-68. doi: 10.17816/RCF16262-68).

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Cerebral protection

Cited by 102 publications

References 59 publications

Chronic stimulation of alpha-2A-adrenoceptors with guanfacine protects rodent prefrontal cortex dendritic spines and cognition from the effects of chronic stress

Chronic stimulation of alpha-2A-adrenoceptors with guanfacine protects rodent prefrontal cortex dendritic spines and cognition from the effects of chronic stress

Neuroprotective Effects of Intravenous Lidocaine on Early Postoperative Cognitive Dysfunction in Elderly Patients Following Spine Surgery

To the mechanisms of the protective effects of regional anesthesia in relation to the development of postoperative cognitive dysfunction

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