Traumatic brain injury, diabetic neuropathy and altered-psychiatric health: The fateful triangle

Dia, Batoul; Choucair, Khalil; Eid, Stéphanie; Najdi, Farah; Baki, Lama; Talih, Farid; Eid, Assaad A.; Kobeissy, Firas

doi:10.1016/j.mehy.2017.08.008

Cited by 18 publications

(14 citation statements)

References 171 publications

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“…Brain injury consists of two phases: primary and secondary injury (Table I, Figure 4). The original primary mechanical damage occurs at the time of the traumatic incident and is permanent and solely amenable to preventative actions (Abou-El-Hassan, Dia et al 2017). The secondary phase, which occurs subsequent to the primary insult, is a multifactorial process started at the time of impact and evolving over the successive subacute phases to the chronic stages of recovery (Vink and Nimmo 2009).…”

Section: The Kinin System In Neurological Disorders: a Novel Contrmentioning

confidence: 99%

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

Nokkari

Abou-El-Hassan

Mechref

et al. 2018

Progress in Neurobiology

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Neurological disorders represent major health concerns in terms of comorbidity and mortality worldwide. Despite a tremendous increase in our understanding of the pathophysiological processes involved in disease progression and prevention, the accumulated knowledge so far resulted in relatively moderate translational benefits in terms of therapeutic interventions and enhanced clinical outcomes. Aiming at specific neural molecular pathways, different strategies have been geared to target the development and progression of such disorders. The kallikrein-kinin system (KKS) is among the most delineated candidate systems due to its ubiquitous roles mediating several of the pathophysiological features of these neurological disorders as well as being implicated in regulating various brain functions. Several experimental KKS models revealed that the inhibition or stimulation of the two receptors of the KKS system (B1R and B2R) can exhibit neuroprotective and/or adverse pathological outcomes. This updated review provides background details of the KKS components and their functions in different neurological disorders including temporal lobe epilepsy, traumatic brain injury, stroke, spinal cord injury, Alzheimer's disease, multiple sclerosis and glioma. Finally, this work will highlight the putative roles of the KKS components as potential neurotherapeutic targets and provide future perspectives on the possibility of translating these findings into potential clinical biomarkers in neurological disease.

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Section: The Kinin System In Neurological Disorders: a Novel Contrmentioning

confidence: 99%

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

Nokkari

Abou-El-Hassan

Mechref

et al. 2018

Progress in Neurobiology

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“…Holinoreceptors are a superfamily of pentameric ligand-controlled channels, including receptor 5-hydroxytryptamin, able to inhibit anion-selective γ-aminobutyric acid type A (GABA-AR), glutamate [23]. At the same time, the activity of cholinoceptors is allosterically modulated by membrane lipids, fatty acids, steroids, instead of those in the brain tissue in TBI, it grows rapidly [8,9,25,26].…”

Section: No 5 (70) 2020 Sciencerise Issn 2313-8416mentioning

confidence: 99%

“…The sequence of events that occur after brain injury consists of necrosis, axonal damage, gliosis/microgliosis, apoptosis, demyelination and neuroregeneration [7]. The first acute period is of the greatest importance for the formation of an adequate response [8].…”

Section: Introductionmentioning

confidence: 99%

“…The latter serves as a trigger mechanism for events that ultimately lead to degeneration and death of neurons. The immediate cause of the primary phase is mechanical damage, which is irreversible, including cell destruction and vascular damage; manifested by brain contusion, intracranial hemorrhage, diffuse axonal damage [7]. A key role at this stage belongs to calpain (a family of cytosolic neutral Ca 2+ -activated cysteine proteases), which triggers neurodegeneration and apoptosis [11].…”

Section: Introductionmentioning

confidence: 99%

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Analysis of the Role of Central Cholinoreactivity in Experimental Traumatic Brain Injury

Khudoley¹

2020

ScienceRise

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The aim of the research. To study effects of activation and inhibition of the central cholinergic systems (CCS) in traumatic brain injury (TBI). Studied problem. To investigate the influence of the reactivity of the central cholinergic systems on the course of the acute period of traumatic brain injury, in an acute experiment on laboratory animals in vivo. The main scientific results. It was found that in the acute period of TBI (the first three days), both activation and blockade of CCS led to a decrease in mortality, which was statistically confirmed only for their activation. The control group was characterized by the progression of neurological deficit, which was realized due to motor disorders and reflex sphere. Upon activation of the CCS, the degree of neurological deficit was significantly less than in other groups, but, nevertheless, it increased from 48 hours after the injury, as regards behavioral and consciousness disorders. Inhibition of cholinergic systems led to a sharp increase in neurological deficit in all areas immediately after injury, to a greater extent due to reflex disorders. This, together with a high mortality rate, indicated a negative effect of the pharmacological shutdown of CCS in TBI. The area of practical use of the research results. The obtained results will allow a deeper study of the influence of the central cholinergic systems on the course and descent of TBI. To develop effective methods of pharmacological correction in the treatment of patients in the acute period of TBI. Innovative technological product: pathogenetically substantiated medical treatment of the acute period of traumatic brain injury, development of new methods of pharmacological neuroprotection for persons with a priori high risk of injury, development of effective options for reducing mortality and disability from TBI. Scope of the innovative technological product. The important role of CCS in the realization of the response of the central nervous system to TBI was established, and the possibility of using pharmacological stimulation of the central nervous system with cholinomimetics of the central type of action was justified.

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“…Послідовність подій, що відбуваються після травми мозку, складається з некрозу, аксонального пошкодження, гліозу/мікрогліозу, апоптозу, демієлінізації та нейрорегенерації [5]. Найбільше значення для формування адекватної відповіді має перший гострий період [6].…”

Section: вступunclassified

State of Neuroendocrine Systems During Activation and Inhibition of Central Cholinergic Systems in Brain Injury

Зябліцев¹,

Khudoley²

2020

Fiziol Zh

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The aim of the study was to determine the state of the neuroendocrine systems during the activation and inhibition of the central cholinergic systems (CChS) in traumatic brain injury (TBI) and their effect on mortality and neurological deficit. TBI was applied by the standard method with the free fall of metal weight on the fixed animal head. 161 white male Wistar rats were divided into three groups: in the 1st group, 0.5 ml of Ringer’s solution was injected intraperitoneally before injury (control), in the 2nd – solution of choline alfoscerate at a dose 6 mg/kg (CChS activation), in the 3rd – solution of biperidene hydrochloride at a dose 0.6 mg/kg (CChS blockade). Neurological deficits were assessed using the 100-point Todd scale. In the blood was determined the content of Adrenocorticotropic (ACTH) and Thyroid-Stimulating Hormones, Corticosterone (Cs), free Thyroxine and Triiodothyronine (fT3) by the enzyme immunoassay. It was established that in the acute period of TBI, post-traumatic stress central hypercortisolism is formed with an increase in blood levels of ACTH and Cs, and central hypothyroidism with a predominant decrease in blood fT3. The CChS activation significantly reduced mortality and neurological deficit, which was accompanied by moderate activation of ACTH and Cs and no effect on the thyroid system. The CChS blockade led to the suppression of the post-traumatic reaction of ACTH and Cs activation and the development of deep central hypothyroidism against the significant neurological deficit. Thus, the important role of CChS in the implementation of the post-traumatic stress reaction of the neuroendocrine system has been established, and the possibility of using pharmacological stimulation of the CNS with central cholinomimetics has been substantiated.

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Traumatic brain injury, diabetic neuropathy and altered-psychiatric health: The fateful triangle

Cited by 18 publications

References 171 publications

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms

Analysis of the Role of Central Cholinoreactivity in Experimental Traumatic Brain Injury

State of Neuroendocrine Systems During Activation and Inhibition of Central Cholinergic Systems in Brain Injury

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