Articles de revues : « Neuroscore »

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Engelhorn, Tobias, Sophia Goerike, Arnd Doerfler, Christine Okorn, Michael Forsting, Gerd Heusch et Rainer Schulz. « The Angiotensin II Type 1—Receptor Blocker Candesartan Increases Cerebral Blood Flow, Reduces Infarct Size, and Improves Neurologic Outcome after Transient Cerebral Ischemia in Rats ». Journal of Cerebral Blood Flow & ; Metabolism 24, n^o 4 (avril 2004) : 467–74. http://dx.doi.org/10.1097/00004647-200404000-00012.

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The goal of the present study was to test the impact of administration time of the angiotensin II type 1–receptor blocker candesartan on cerebral blood flow (CBF), infarct size, and neuroscore in transient cerebral ischemia. Therefore, 1-hour middle cerebral artery occlusion (MCAO) was followed by reperfusion. Rats received 0.5-mg/kg candesartan intravenously 2 hours before MCAO (pretreatment), 24 hours after MCAO, every 24 hours after MCAO, or 2 hours before and every 24 hours after MCAO. Infarct size (mm3) and a neuroscore at day 7 were compared with controls. CBF was quantified by radiolabeled microspheres and laser-Doppler flowmetry. Compared with controls (95 ± 8), infarct size in candesartan-treated groups was smaller (59 ± 5, 68 ± 10, 28 ± 3, and 15 ± 3, respectively; P < 0.05). Although there was no difference in neuroscore between pretreatment and controls (1.55 ± 0.18, 1.80 ± 0.13), other treatment regimens resulted in improved neuroscores (1.33 ± 0.16, 1.11 ± 0.11, 0.73 ± 0.15; P < 0.05). CBF in pretreated animals at 0.5 hours after MCAO was significantly higher than in controls (0.58 ± 0.09 mL · g−1 ·· min−1 and 44% ± 7% of baseline compared with 0.49 ± 0.06 mL · g−1 ·· min−1 and 37% ± 6%, microspheres and laser-Doppler flowmetry; P < 0.05). Thus, candesartan reduces infarct size even if administered only during reperfusion. Apart from pretreatment, other treatment regimens result in significantly improved neuroscores. In the acute phase of cerebral ischemia, candesartan increases CBF.

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McBride, Devin W., Derek Nowrangi, Harpreet Kaur, Guangyong Wu, Lei Huang, Tim Lekic, Jiping Tang et John H. Zhang. « A composite neurobehavioral test to evaluate acute functional deficits after cerebellar haemorrhage in rats ». Journal of Cerebral Blood Flow & ; Metabolism 38, n^o 3 (20 mars 2017) : 433–46. http://dx.doi.org/10.1177/0271678x17696509.

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Cerebellar haemorrhage accounts for 5–10% of all intracerebral haemorrhages and leads to severe, long-lasting functional deficits. Currently, there is limited research on this stroke subtype, which may be due to the lack of a suitable composite neuroscoring system specific for cerebellar injury in rodents. The purpose of this study is to develop a comprehensive composite neuroscore test for cerebellar injury using a rat model of cerebellar haemorrhage. Sixty male Sprague-Dawley rats were subjected to either sham surgery or cerebellar haemorrhage. Twenty-four hours post-injury, neurological behaviour was evaluated using 17 cost-effective and easy-to-perform tests, and a composite neuroscore was developed. The composite neuroscore was then used to assess functional recovery over seven days after cerebellar haemorrhage. Differences in the composite neuroscore deficits for the mild and moderate cerebellar haemorrhage models were observed for up to five days post-ictus. Until now, a composite neuroscore for cerebellar injury was not available for rodent studies. Herein, using mild and moderate cerebellar haemorrhage rat models a composite neuroscore for cerebellar injury was developed and used to assess functional deficits after cerebellar haemorrhage. This composite neuroscore may also be useful for other cerebellar injury models.

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Wang, Zhengwei, Qi She, Alan F. Smeaton, Tomás E. Ward et Graham Healy. « Synthetic-Neuroscore : Using a neuro-AI interface for evaluating generative adversarial networks ». Neurocomputing 405 (septembre 2020) : 26–36. http://dx.doi.org/10.1016/j.neucom.2020.04.069.

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Hayakawa, Kazuhide, Takafumi Nakano, Keiichi Irie, Sei Higuchi, Masayuki Fujioka, Kensuke Orito, Katsunori Iwasaki et al. « Inhibition of Reactive Astrocytes with Fluorocitrate Retards Neurovascular Remodeling and Recovery after Focal Cerebral Ischemia in Mice ». Journal of Cerebral Blood Flow & ; Metabolism 30, n^o 4 (9 décembre 2009) : 871–82. http://dx.doi.org/10.1038/jcbfm.2009.257.

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Glial scarring is traditionally thought to be detrimental after stroke. But emerging studies now suggest that reactive astrocytes may also contribute to neurovascular remodeling. Here, we assessed the effects and mechanisms of metabolic inhibition of reactive astrocytes in a mouse model of stroke recovery. Five days after stroke onset, astrocytes were metabolically inhibited with fluorocitrate (FC, 1 nmol). Markers of reactive astrocytes (glial fibrillary acidic protein (GFAP), HMGB1), markers of neurovascular remodeling (CD31, synaptophysin, PSD95), and behavioral outcomes (neuroscore, rotarod latency) were quantified from 1 to 14 days. As expected, focal cerebral ischemia induced significant neurological deficits in mice. But over the course of 14 days after stroke onset, a steady improvement in neuroscore and rotarod latencies were observed as the mice spontaneously recovered. Reactive astrocytes coexpressing GFAP and HMGB1 increased in peri-infarct cortex from 1 to 14 days after cerebral ischemia in parallel with an increase in the neurovascular remodeling markers CD31, synaptophysin, and PSD95. Compared with stroke-only controls, FC-treated mice demonstrated a significant decrease in HMGB1-positive reactive astrocytes and neurovascular remodeling, as well as a corresponding worsening of behavioral recovery. Our results suggest that reactive astrocytes in peri-infarct cortex may promote neurovascular remodeling, and these glial responses may aid functional recovery after stroke.

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Immonen, Riikka, Taneli Heikkinen, Leena Tähtivaara, Antti Nurmi, Taina-Kaisa Stenius, Jukka Puoliväli, Tinka Tuinstra et al. « Cerebral Blood Volume Alterations in the Perilesional Areas in the Rat Brain after Traumatic Brain Injury—Comparison with Behavioral Outcome ». Journal of Cerebral Blood Flow & ; Metabolism 30, n^o 7 (10 février 2010) : 1318–28. http://dx.doi.org/10.1038/jcbfm.2010.15.

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In the traumatic brain injury (TBI) the initial impact causes both primary injury, and launches secondary injury cascades. One consequence, and a factor that may contribute to these secondary changes and functional outcome, is altered hemodynamics. The relative cerebral blood volume (CBV) changes in rat brain after severe controlled cortical impact injury were characterized to assess their interrelations with motor function impairment. Magnetic resonance imaging (MRI) was performed 1, 2, 4 h, and 1, 2, 3, 4, 7, and 14 days after TBI to quantify CBV and water diffusion. Neuroscore test was conducted before, and 2, 7, and 14 days after the TBI. We found distinct temporal profile of CBV in the perilesional area, hippocampus, and in the primary lesion. In all regions, the first response was drop of CBV. Perifocal CBV was reduced for over 4 days thereafter gradually recovering. After the initial drop, the hippocampal CBV was increased for 2 weeks. Neuroscore demonstrated severely impaired motor functions 2 days after injury (33% decrease), which then slowly recovered in 2 weeks. This recovery parallelled the recovery of perifocal CBV. CBV MRI can detect cerebrovascular pathophysiology after TBI in the vulnerable perilesional area, which seems to potentially associate with time course of sensory-motor deficit.

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Siddiqui, Fazeel M., Chirantan Banerjee, Susanna M. Zuurbier, Qing Hao, Chul Ahn, Glenn L. Pride, Muhammad Wasay et al. « Mechanical Thrombectomy versus Intrasinus Thrombolysis for Cerebral Venous Sinus Thrombosis : A Non-Randomized Comparison ». Interventional Neuroradiology 20, n^o 3 (1 janvier 2014) : 336–44. http://dx.doi.org/10.15274/inr-2014-10032.

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Small retrospective studies have shown the benefit of endovascular treatment with intrasinus thrombolysis (IST) or mechanical thrombectomy (MT) with/without IST (MT+/−IST) in cases of multifocal cerebral venous thrombosis (CVT). Our study compares the mortality, functional outcome and periprocedural complications among patients treated with MT +/– IST versus IST alone. We reviewed clinical and angiographic findings of 63 patients with CVT who received endovascular treatment at three tertiary care centers. Primary outcome variables were discharge mortality and neurological dysfunction, and intermediate (three months) and long-term (>six months) morbidity. The modified Rankin scale (mRS) was used to assess morbidity. mRS ≤1 was considered a good recovery. Neurological dysfunction was rated as neuroscore: 0, normal; 1, mild (ambulatory, communicative); 2, moderate (non-ambulatory, communicative); and 3, severe (non-ambulatory, non-communicative/comatose). In patients who received IST alone, presenting neurological deficits were comparatively minor (p<0.001). When the two groups were adjusted for admission neuroscore, there was no statistical significance between discharge mortality [7(21%) versus 4(14%), p=0.228], neurological dysfunction (p=0.442), intermediate (p=0.336) and long-term morbidity (p=0.988). Patients who received MT +/- IST had a higher percentage of periprocedural complications without reaching statistical significance. Compared to IST, MT was performed in severe cases with extensive sinus involvement. When adjusted for admission neurological dysfunction, both groups had similar mortality and discharge neurological dysfunction and similar intermediate and long-term morbidity.

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Basalay, Maryna V., Sean M. Davidson et Derek M. Yellon. « Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide ». Cardiovascular Drugs and Therapy 33, n^o 6 (13 novembre 2019) : 661–67. http://dx.doi.org/10.1007/s10557-019-06915-8.

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Abstract Purpose A substantial number of ischaemic stroke patients who receive reperfusion therapy in the acute phase do not ever fully recover. This reveals the urgent need to develop new adjunctive neuroprotective treatment strategies alongside reperfusion therapy. Previous experimental studies demonstrated the potential of glucagon-like peptide-1 (GLP-1) to reduce acute ischaemic damage in the brain. Here, we examined the neuroprotective effects of two GLP-1 analogues, liraglutide and semaglutide. Methods A non-diabetic rat model of acute ischaemic stroke involved 90, 120 or 180 min of middle cerebral artery occlusion (MCAO). Liraglutide or semaglutide was administered either i.v. at the onset of reperfusion or s.c. 5 min before the onset of reperfusion. Infarct size and functional status were evaluated after 24 h or 72 h of reperfusion. Results Liraglutide, administered as a bolus at the onset of reperfusion, reduced infarct size by up to 90% and improved neuroscore at 24 h in a dose-dependent manner, following 90-min, but not 120-min or 180-min ischaemia. Semaglutide and liraglutide administered s.c. reduced infarct size by 63% and 48%, respectively, and improved neuroscore at 72 h following 90-min MCAO. Neuroprotection by semaglutide was abolished by GLP1-R antagonist exendin(9-39). Conclusion Infarct-limiting and functional neuroprotective effects of liraglutide are dose-dependent. Neuroprotection by semaglutide is at least as strong as by liraglutide and is mediated by GLP-1Rs.

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Nakamura, Michio, Kathryn E. Saatman, James E. Galvin, Uwe Scherbel, Ramesh Raghupathi, John Q. Trojanowski et Tracy K. McIntosh. « Increased Vulnerability of NFH-LacZ Transgenic Mouse to Traumatic Brain Injury-Induced Behavioral Deficits and Cortical Damage ». Journal of Cerebral Blood Flow & ; Metabolism 19, n^o 7 (juillet 1999) : 762–70. http://dx.doi.org/10.1097/00004647-199907000-00006.

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The authors evaluated the neurobehavioral and neuropathologic sequelae after traumatic brain injury (TBI) in transgenic (TG) mice expressing truncated high molecular weight neurofilament (NF) protein fused to beta-galactosidase (NFH-LacZ), which develop Lewy body-like NF-rich inclusions throughout the CNS. TG mice and their wild-type (WT) littermates were subjected to controlled cortical impact brain injury (TG, n=19; WT, n=17) or served as uninjured controls (TG, n =11; WT, n =11). During a 3-week period, mice were evaluated with an array of neuromotor function tests including neuroscore, beam balance, and both fast and slow acceleration rotarod. Brain-injured WT and TG mice showed significant motor dysfunction until 15 days and 21 days post-injury, respectively ( P < .025). Compared with brain-injured WT mice, brain-injured TG mice had significantly greater motor dysfunction as assessed by neuroscore ( P < .01) up to and including 15 days post-injury. Similarly, brain-injured TG mice performed significantly worse than brain-injured WT mice on slow acceleration rotarod at 2, 8, and 15 days post-injury ( P < .05), and beam balance over 2 weeks post-injury ( P < .01). Histopathologic analysis showed significantly greater tissue loss in the injured hemisphere in TG mice at 4 weeks post-injury ( P < .01). Together these data show that NFH-LacZ TG mice are more behaviorally and histologically vulnerable to TBI than WT mice, suggesting that the presence of NF-rich inclusions may exacerbate neuromotor dysfunction and cell death after TBI.

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Laurer, Helmut L., Florence M. Bareyre, Virginia M. Y. C. Lee, John Q. Trojanowski, Luca Longhi, Rachel Hoover, Kathryn E. Saatman et al. « Mild head injury increasing the brain's vulnerability to a second concussive impact ». Journal of Neurosurgery 95, n^o 5 (novembre 2001) : 859–70. http://dx.doi.org/10.3171/jns.2001.95.5.0859.

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Object. Mild, traumatic repetitive head injury (RHI) leads to neurobehavioral impairment and is associated with the early onset of neurodegenerative disease. The authors developed an animal model to investigate the behavioral and pathological changes associated with RHI. Methods. Adult male C57BL/6 mice were subjected to a single injury (43 mice), repetitive injury (two injuries 24 hours apart; 49 mice), or no impact (36 mice). Cognitive function was assessed using the Morris water maze test, and neurological motor function was evaluated using a battery of neuroscore, rotarod, and rotating pole tests. The animals were also evaluated for cardiovascular changes, blood—brain barrier (BBB) breakdown, traumatic axonal injury, and neurodegenerative and histopathological changes between 1 day and 56 days after brain trauma. No cognitive dysfunction was detected in any group. The single-impact group showed mild impairment according to the neuroscore test at only 3 days postinjury, whereas RHI caused pronounced deficits at 3 days and 7 days following the second injury. Moreover, RHI led to functional impairment during the rotarod and rotating pole tests that was not observed in any animal after a single impact. Small areas of cortical BBB breakdown and axonal injury, observed after a single brain injury, were profoundly exacerbated after RHI. Immunohistochemical staining for microtubule-associated protein—2 revealed marked regional loss of immunoreactivity only in animals subjected to RHI. No deposits of β-amyloid or tau were observed in any brain-injured animal. Conclusions. On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma.

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Davis, Kyle, Moises Serrano, Megan Martin, Rena Vanzo, Megan Rimmasch, Yolanda Hom, Mohammed Uddin et Colleen Bilancia. « NeuroSCORE : A genome-wide OMICs based model to identify disease associated genes of the central nervous system ». Molecular Genetics and Metabolism 132 (avril 2021) : S263—S264. http://dx.doi.org/10.1016/s1096-7192(21)00488-1.

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Evangelisti, Maria A., Roberta Deiana, Valentino Melosu, Giovanni P. Burrai, Isabella Ballocco, Antonio Varcasia, Antonio Scala et Maria L. Manunta. « Relationships among neuroscore, magnetic resonance imaging features, and intracranial pressure in sheep affected by slow-growing brain lesions ». Veterinary Radiology & ; Ultrasound 59, n^o 3 (22 décembre 2017) : 305–11. http://dx.doi.org/10.1111/vru.12589.

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Jayaraman, Keshav, Meizi Liu, Gregory J. Zipfel et Umeshkumar Athiraman. « Sevoflurane and Desflurane Exposures Following Aneurysmal Subarachnoid Hemorrhage Confer Multifaceted Protection against Delayed Cerebral Ischemia ». Biomedicines 9, n^o 7 (14 juillet 2021) : 820. http://dx.doi.org/10.3390/biomedicines9070820.

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Numerous studies have demonstrated the ability of isoflurane conditioning to provide multifaceted protection against aneurysmal subarachnoid hemorrhage (SAH)-associated delayed cerebral ischemia (DCI); however, preclinical studies have not yet examined whether other commonly used inhalational anesthetics in neurological patients such as sevoflurane or desflurane are also protective against SAH-induced neurovascular deficits. We therefore sought to identify the potential for sevoflurane and desflurane conditioning to protect against DCI in an endovascular perforation mouse model of SAH. Neurological function was assessed daily via neuroscore. Large artery vasospasm and microvessel thrombosis were assessed three days after SAH or sham surgery. Four groups were examined: Sham, SAH + room air, SAH + 2% Sevoflurane, and SAH + 6% Desflurane. For the SAH groups, one hour after surgery, mice received 2% sevoflurane, 6% desflurane, or room air for one hour. We found that conditioning with sevoflurane or desflurane attenuated large artery vasospasm, reduced microvessel thrombosis, and improved neurologic function. Given their frequent clinical use and strong safety profile in patients (including those with SAH), these data strongly support further studies to validate these findings in preclinical and clinical studies and to elucidate the mechanisms by which these agents might be acting.

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Parmentier-Batteur, Sophie, Georg Andrees Bohme, Dominique Lerouet, Li Zhou-Ding, Virginie Beray, Isabelle Margaill et Michel Plotkine. « Antisense Oligodeoxynucleotide to Inducible Nitric Oxide Synthase Protects against Transient Focal Cerebral Ischemia—Induced Brain Injury ». Journal of Cerebral Blood Flow & ; Metabolism 21, n^o 1 (janvier 2001) : 15–21. http://dx.doi.org/10.1097/00004647-200101000-00003.

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Nitric oxide (NO) has been suspected to mediate brain damage during ischemia. Here the authors studied the effects of an antisense oligodeoxynucleotide (ODN) directed against the inducible isoform of NO synthase (iNOS) in a model of transient focal cerebral ischemia in rats. Treatment consisted of seven intracerebroventricular injections of a phosphodiester/phosphorothioate chimera ODN (3 nmol each) at 12-hour intervals, and was initiated 12 hours before a 2-hour occlusion of the left middle cerebral artery and common carotid artery. Outcomes were measured three days after ischemia. When compared with animals treated with vehicle or an appropriate random non-sense control ODN sequence, the antisense treatment reduced the lesion volume by 30% and significantly improved recovery of sensorimotor functions, as assessed on a neuroscore. This effect was associated with a decrease in iNOS expression, as assessed by Western blot, a 39% reduction in iNOS enzymatic activity evaluated as Ca2+-independent NOS activity, and a 37% reduction in nitrotyrosine formation, reflecting protein nitration by NO-derived peroxynitrite. These findings provide new evidence that inhibition of iNOS may be of interest for the treatment of stroke.

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Haidar, Muhammad Ali, Zaynab Shakkour, Chloe Barsa, Maha Tabet, Sarin Mekhjian, Hala Darwish, Mona Goli et al. « Mitoquinone Helps Combat the Neurological, Cognitive, and Molecular Consequences of Open Head Traumatic Brain Injury at Chronic Time Point ». Biomedicines 10, n^o 2 (24 janvier 2022) : 250. http://dx.doi.org/10.3390/biomedicines10020250.

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Traumatic brain injury (TBI) is a heterogeneous disease in its origin, neuropathology, and prognosis, with no FDA-approved treatments. The pathology of TBI is complicated and not sufficiently understood, which is the reason why more than 30 clinical trials in the past three decades turned out unsuccessful in phase III. The multifaceted pathophysiology of TBI involves a cascade of metabolic and molecular events including inflammation, oxidative stress, excitotoxicity, and mitochondrial dysfunction. In this study, an open head TBI mouse model, induced by controlled cortical impact (CCI), was used to investigate the chronic protective effects of mitoquinone (MitoQ) administration 30 days post-injury. Neurological functions were assessed with the Garcia neuroscore, pole climbing, grip strength, and adhesive removal tests, whereas cognitive and behavioral functions were assessed using the object recognition, Morris water maze, and forced swim tests. As for molecular effects, immunofluorescence staining was conducted to investigate microgliosis, astrocytosis, neuronal cell count, and axonal integrity. The results show that MitoQ enhanced neurological and cognitive functions 30 days post-injury. MitoQ also decreased the activation of astrocytes and microglia, which was accompanied by improved axonal integrity and neuronal cell count in the cortex. Therefore, we conclude that MitoQ has neuroprotective effects in a moderate open head CCI mouse model by decreasing oxidative stress, neuroinflammation, and axonal injury.

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Zhao, Zaorui, Alan I. Faden, David J. Loane, Marta M. Lipinski, Boris Sabirzhanov et Bogdan A. Stoica. « Neuroprotective Effects of Geranylgeranylacetone in Experimental Traumatic Brain Injury ». Journal of Cerebral Blood Flow & ; Metabolism 33, n^o 12 (14 août 2013) : 1897–908. http://dx.doi.org/10.1038/jcbfm.2013.144.

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Geranylgeranylacetone (GGA) is an inducer of heat-shock protein 70 (HSP70) that has been used clinically for many years as an antiulcer treatment. It is centrally active after oral administration and is neuroprotective in experimental brain ischemia/stroke models. We examined the effects of single oral GGA before treatment (800 mg/kg, 48 hours before trauma) or after treatment (800 mg/kg, 3 hours after trauma) on long-term functional recovery and histologic outcomes after moderate-level controlled cortical impact, an experimental traumatic brain injury (TBI) model in mice. The GGA pretreatment increased the number of HSP70+ cells and attenuated posttraumatic α-fodrin cleavage, a marker of apoptotic cell death. It also improved sensorimotor performance on a beam walk task; enhanced recovery of cognitive/affective function in the Morris water maze, novel object recognition, and tail-suspension tests; and improved outcomes using a composite neuroscore. Furthermore, GGA pretreatment reduced the lesion size and neuronal loss in the hippocampus, cortex, and thalamus, and decreased microglial activation in the cortex when compared with vehicle-treated TBI controls. Notably, GGA was also effective in a posttreatment paradigm, showing significant improvements in sensorimotor function, and reducing cortical neuronal loss. Given these neuroprotective actions and considering its longstanding clinical use, GGA should be considered for the clinical treatment of TBI.

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Sutherland, Brad A., et Alastair M. Buchan. « Alteplase Treatment does not Increase Brain Injury After Mechanical Middle Cerebral Artery Occlusion in the Rat ». Journal of Cerebral Blood Flow & ; Metabolism 33, n^o 11 (21 août 2013) : e1-e7. http://dx.doi.org/10.1038/jcbfm.2013.148.

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Recanalization of an occluded vessel with recombinant tissue plasminogen activator is an effective strategy for treating acute ischemic stroke. Recombinant tissue plasminogen activator is administered as alteplase, a formulation containing many excipients including L-arginine, the substrate for nitric oxide production. Most studies fail to compare the effects of alteplase on brain injury to its L-arginine carrier solution. This study aimed to verify the previously reported detrimental effects of alteplase after cerebral ischemia and delineate the contribution of L-arginine. Male Wistar rats, subjected to 90 minutes of intraluminal middle cerebral artery occlusion (MCAO), were administered alteplase, the carrier solution or saline upon reperfusion. Neither alteplase nor the carrier affected cerebral blood flow (CBF) restoration throughout the first 60 minutes of reperfusion. Alteplase treatment was associated with increased mortality after MCAO. Twenty-four hours after MCAO, neurologic function and infarct volume did not differ between rats treated with alteplase, the carrier solution, or saline. Irrespective of treatment group, infarct volume was correlated with CBF during reperfusion, neuroscore, and peri-infarct depolarizations. These results suggest that alteplase treatment, independent of thrombolysis, does not cause increased ischemic injury compared with its appropriate carrier solution, supporting the continued use of alteplase in eligible ischemic stroke patients.

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Kyyriäinen, Jenni, Natallie Kajevu, Ivette Bañuelos, Leonardo Lara, Anssi Lipponen, Silvia Balosso, Elina Hämäläinen et al. « Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury ». International Journal of Molecular Sciences 22, n^o 19 (29 septembre 2021) : 10555. http://dx.doi.org/10.3390/ijms221910555.

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We assessed the effect of antioxidant therapy using the Food and Drug Administration-approved respiratory drug N-acetylcysteine (NAC) or sulforaphane (SFN) as monotherapies or duotherapy in vitro in neuron-BV2 microglial co-cultures and validated the results in a lateral fluid-percussion model of TBI in rats. As in vitro measures, we assessed neuronal viability by microtubule-associated-protein 2 immunostaining, neuroinflammation by monitoring tumor necrosis factor (TNF) levels, and neurotoxicity by measuring nitrite levels. In vitro, duotherapy with NAC and SFN reduced nitrite levels to 40% (p < 0.001) and neuroinflammation to –29% (p < 0.001) compared with untreated culture. The treatment also improved neuronal viability up to 72% of that in a positive control (p < 0.001). The effect of NAC was negligible, however, compared with SFN. In vivo, antioxidant duotherapy slightly improved performance in the beam walking test. Interestingly, duotherapy treatment decreased the plasma interleukin-6 and TNF levels in sham-operated controls (p < 0.05). After TBI, no treatment effect on HMGB1 or plasma cytokine levels was detected. Also, no treatment effects on the composite neuroscore or cortical lesion area were detected. The robust favorable effect of duotherapy on neuroprotection, neuroinflammation, and oxidative stress in neuron-BV2 microglial co-cultures translated to modest favorable in vivo effects in a severe TBI model.

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Thal, Serge C., Sonja Sporer, Mariusz Klopotowski, Simone E. Thal, Johannes Woitzik, Robert Schmid-Elsaesser, Nikolaus Plesnila et Stefan Zausinger. « Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats ». Journal of Neurosurgery 111, n^o 5 (novembre 2009) : 988–94. http://dx.doi.org/10.3171/2009.3.jns08412.

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Object Global cerebral edema is an independent risk factor for early death and poor outcome after subarachnoid hemorrhage (SAH). In the present study, the time course of brain edema formation, neurological deficits, and neuronal cell loss were investigated in the rat filament SAH model. Methods Brain water content and neurological deficits were determined in rats randomized to sham (1-, 24-, or 48-hour survival), SAH by endovascular perforation (1-, 24-, or 48-hour survival), or no surgery (control). The neuronal cell count (CA1–3) was quantified in a separate set of SAH (6-, 24-, 48-, or 72-hour survival) and shamoperated animals. Results Brain water content increased significantly 24 (80.2 ± 0.4% [SAH] vs 79.2 ± 0.1% [sham]) and 48 hours (79.8 ± 0.2% [SAH] vs 79.3 ± 0.1% [sham]) after SAH. The neuroscore was significantly worse after SAH (33 ± 15 [24 hours after SAH] vs 0 ± 0 points [sham]) and correlated with the extent of brain edema formation (r = 0.96, p < 0.001). No hippocampal damage was present up to 72 hours after SAH. Conclusions Brain water content and neurological dysfunction reached a maximum at 24 hours after SAH. This time point, therefore, seems to be optimal to test the effects of therapeutic interventions on brain edema formation. Neuronal cell loss was not present in CA1–3 up to 72 hours of SAH. Therefore, morphological damage needs to be evaluated at later time points.

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Ravina, Kristine, Denise Briggs, Sezen Kislal, Zuha Warraich, Tiffany Nguyen, Rachel Lam, Thomas Zarembinski et Mehrdad Shamloo. « Intracerebral Delivery of Brain-Derived Neurotrophic Factor Using HyStem®-C Hydrogel Implants Improves Functional Recovery and Reduces Neuroinflammation in a Rat Model of Ischemic Stroke ». International Journal of Molecular Sciences 19, n^o 12 (28 novembre 2018) : 3782. http://dx.doi.org/10.3390/ijms19123782.

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Ischemic stroke is a leading cause of death and disability worldwide. Potential therapeutics aimed at neural repair and functional recovery are limited in their blood-brain barrier permeability and may exert systemic or off-target effects. We examined the effects of brain-derived neurotrophic factor (BDNF), delivered via an extended release HyStem®-C hydrogel implant or vehicle, on sensorimotor function, infarct volume, and neuroinflammation, following permanent distal middle cerebral artery occlusion (dMCAo) in rats. Eight days following dMCAo or sham surgery, treatments were implanted directly into the infarction site. Rats received either vehicle, BDNF-only (0.167 µg/µL), hydrogel-only, hydrogel impregnated with 0.057 µg/µL of BDNF (hydrogel + BDNFLOW), or hydrogel impregnated with 0.167 µg/µL of BDNF (hydrogel + BDNFHIGH). The adhesive removal test (ART) and 28-point Neuroscore (28-PN) were used to evaluate sensorimotor function up to two months post-ischemia. The hydrogel + BDNFHIGH group showed significant improvements on the ART six to eight weeks following treatment and their behavioral performance was consistently greater on the 28-PN. Infarct volume was reduced in rats treated with hydrogel + BDNFHIGH as were levels of microglial, phagocyte, and astrocyte marker immunoexpression in the corpus striatum. These data suggest that targeted intracerebral delivery of BDNF using hydrogels may mitigate ischemic brain injury and restore functional deficits by reducing neuroinflammation.

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Weyer, Vanessa, Máté E. Maros, Andrea Kronfeld, Stefanie Kirschner, Christoph Groden, Clemens Sommer, Yasemin Tanyildizi, Martin Kramer et Marc A. Brockmann. « Longitudinal imaging and evaluation of SAH-associated cerebral large artery vasospasm in mice using micro-CT and angiography ». Journal of Cerebral Blood Flow & ; Metabolism 40, n^o 11 (21 novembre 2019) : 2265–77. http://dx.doi.org/10.1177/0271678x19887052.

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Longitudinal in vivo imaging studies characterizing subarachnoid hemorrhage (SAH)-induced large artery vasospasm (LAV) in mice are lacking. We developed a SAH-scoring system to assess SAH severity in mice using micro CT and longitudinally analysed LAV by intravenous digital subtraction angiography (i.v. DSA). Thirty female C57Bl/6J-mice (7 sham, 23 SAH) were implanted with central venous ports for repetitive contrast agent administration. SAH was induced by filament perforation. LAV was assessed up to 14 days after induction of SAH by i.v. DSA. SAH-score and neuroscore showed a highly significant positive correlation (rsp = 0.803, p < 0.001). SAH-score and survival showed a negative significant correlation (rsp = −0.71, p < 0.001). LAV peaked between days 3–5 and normalized on days 7–15. Most severe LAV was observed in the internal carotid (Δmax = 30.5%, p < 0.001), anterior cerebral (Δmax = 21.2%, p = 0.014), middle cerebral (Δmax = 28.16%, p < 0.001) and basilar artery (Δmax = 23.49%, p < 0.001). Cerebral perfusion on day 5 correlated negatively with survival time (rPe = −0.54, p = 0.04). Arterial diameter of the left MCA correlated negatively with cerebral perfusion on day 3 (rPe = −0.72, p = 0.005). In addition, pseudoaneurysms arising from the filament perforation site were visualized in three mice using i.v. DSA. Thus, micro-CT and DSA are valuable tools to assess SAH severity and to longitudinally monitor LAV in living mice.

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Lipponen, Anssi, Teemu Natunen, Mika Hujo, Robert Ciszek, Elina Hämäläinen, Jussi Tohka, Mikko Hiltunen et al. « In Vitro and In Vivo Pipeline for Validation of Disease-Modifying Effects of Systems Biology-Derived Network Treatments for Traumatic Brain Injury—Lessons Learned ». International Journal of Molecular Sciences 20, n^o 21 (29 octobre 2019) : 5395. http://dx.doi.org/10.3390/ijms20215395.

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We developed a pipeline for the discovery of transcriptomics-derived disease-modifying therapies and used it to validate treatments in vitro and in vivo that could be repurposed for TBI treatment. Desmethylclomipramine, ionomycin, sirolimus and trimipramine, identified by in silico LINCS analysis as candidate treatments modulating the TBI-induced transcriptomics networks, were tested in neuron-BV2 microglial co-cultures, using tumour necrosis factor α as a monitoring biomarker for neuroinflammation, nitrite for nitric oxide-mediated neurotoxicity and microtubule associated protein 2-based immunostaining for neuronal survival. Based on (a) therapeutic time window in silico, (b) blood-brain barrier penetration and water solubility, (c) anti-inflammatory and neuroprotective effects in vitro (p < 0.05) and (d) target engagement of Nrf2 target genes (p < 0.05), desmethylclomipramine was validated in a lateral fluid-percussion model of TBI in rats. Despite the favourable in silico and in vitro outcomes, in vivo assessment of clomipramine, which metabolizes to desmethylclomipramine, failed to demonstrate favourable effects on motor and memory tests. In fact, clomipramine treatment worsened the composite neuroscore (p < 0.05). Weight loss (p < 0.05) and prolonged upregulation of plasma cytokines (p < 0.05) may have contributed to the worsened somatomotor outcome. Our pipeline provides a rational stepwise procedure for evaluating favourable and unfavourable effects of systems-biology discovered compounds that modulate post-TBI transcriptomics.

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Edwards, Danielle N., Kathleen Salmeron, Douglas E. Lukins, Amanda L. Trout, Justin F. Fraser et Gregory J. Bix. « Integrin α5β1 inhibition by ATN-161 reduces neuroinflammation and is neuroprotective in ischemic stroke ». Journal of Cerebral Blood Flow & ; Metabolism 40, n^o 8 (1 octobre 2019) : 1695–708. http://dx.doi.org/10.1177/0271678x19880161.

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Stroke remains a leading cause of death and disability with limited therapeutic options. Endothelial cell β1 integrin receptors play a direct role in blood-brain barrier (BBB) dysfunction through regulation of tight junction proteins and infiltrating leukocytes, potentially mediated by β1 integrins. Following tandem transient common carotid artery/middle cerebral artery occlusion on wild-type mice, we administered the integrin a5b1 inhibitor, ATN-161, intraperitoneal (IP) injection at 1 mg/kg acutely after reperfusion, on post-stroke day (PSD)1 and PSD2. Systemic changes (heart rate, pulse distension, and body temperature) were determined. Additionally, infarct volume and edema were determined by 2,3-triphenyltetrazolium chloride and magnetic resonance imaging, while neurological changes were evaluated using an 11-point Neuroscore. Brain immunohistochemistry was performed for claudin-5, α5β1, IgG, and CD45 + cells, and quantitative polymerase chain reaction (qPCR) was performed for matrix metalloproteinase-9 (MMP-9), interleukin (IL)-1β, collagen IV, and CXCL12. ATN-161 significantly reduced integrin α5β1 expression in the surrounding peri-infarct region with no systemic changes. Infarct volume, edema, and functional deficit were significantly reduced in ATN-161-treated mice. Furthermore, ATN-161 treatment reduced IgG extravasation into the parenchyma through conserved claudin-5, collagen IV, CXCL12 while reducing MMP-9 transcription. Additionally, IL-1β and CD45 + cells were reduced in the ipsilateral cortex following ATN-161 administration. Collectively, ATN-161 may be a promising novel stroke therapy by reducing post-stroke inflammation and BBB permeability.

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Tettamanti, Mauro, Simone Beretta, Giuseppe Pignataro, Stefano Fumagalli, Carlo Perego, Luigi Sironi, Felicita Pedata et al. « Multicentre translational Trial of Remote Ischaemic Conditioning in Acute Ischaemic Stroke (TRICS) : protocol of multicentre, parallel group, randomised, preclinical trial in female and male rat and mouse from the Italian Stroke Organization (ISO) Basic Science network ». BMJ Open Science 4, n^o 1 (novembre 2020) : e100063. http://dx.doi.org/10.1136/bmjos-2020-100063.

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IntroductionMulticentre preclinical randomised controlled trials (pRCT) are emerging as a necessary step to confirm efficacy and improve translation into the clinic. The aim of this project is to perform two multicentre pRCTs (one in rats and one in mice) to investigate the efficacy of remote ischaemic conditioning (RIC) in an experimental model of severe ischaemic stroke.Methods and analysisSeven research laboratories within the Italian Stroke Organization (ISO) Basic Science network will participate in the study. Transient endovascular occlusion of the proximal right middle cerebral artery will be performed in two species (rats and mice) and in both sexes. Animals will be randomised to receive RIC by transient surgical occlusion of the right femoral artery, or sham surgery, after reperfusion. Blinded outcome assessment will be performed for dichotomised functional neuroscore (primary endpoint) and infarct volume (secondary endpoint) at 48 hours. A sample size of 80 animals per species will yield 82% power to detect a significant difference of 30% in the primary outcome in both pRCTs. Analyses will be performed in a blind status and according to an intention-to-treat paradigm. The results of this study will provide robust, translationally oriented, high-quality evidence on the efficacy of RIC in multiple species of rodents with large ischaemic stroke.Ethics and disseminationThis is approved by the Animal Welfare Regulatory Body of the University of Milano Bicocca, under project license from the Italian Ministry of Health. Trial results will be subject to publication according to the definition of the outcome presented in this protocol.Trial registration numberPCTE0000177.

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De Blasio, Daiana, Stefano Fumagalli, Luca Longhi, Franca Orsini, Alessandro Palmioli, Matteo Stravalaci, Gloria Vegliante et al. « Pharmacological inhibition of mannose-binding lectin ameliorates neurobehavioral dysfunction following experimental traumatic brain injury ». Journal of Cerebral Blood Flow & ; Metabolism 37, n^o 3 (20 juillet 2016) : 938–50. http://dx.doi.org/10.1177/0271678x16647397.

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Mannose-binding lectin is present in the contusion area of traumatic brain-injured patients and in that of traumatic brain-injured mice, where mannose-binding lectin-C exceeds mannose-binding lectin-A. The reduced susceptibility to traumatic brain injury of mannose-binding lectin double knock-out mice (mannose-binding lectin−/−) when compared to wild type mice suggests that mannose-binding lectin may be a therapeutic target following traumatic brain injury. Here, we evaluated the effects of a multivalent glycomimetic mannose-binding lectin ligand, Polyman9, following traumatic brain injury in mice. In vitro surface plasmon resonance assay indicated that Polyman9 dose-dependently inhibits the binding to immobilized mannose residues of plasma mannose-binding lectin-C selectively over that of mannose-binding lectin-A. Male C57Bl/6 mice underwent sham/controlled cortical impact traumatic brain injury and intravenous treatment with Polyman9/saline. Ex-vivo surface plasmon resonance studies confirmed that Polyman9 effectively reduces the binding of plasma mannose-binding lectin-C to immobilized mannose residues. In vivo studies up to four weeks post injury, showed that Polyman9 induces significant improvement in sensorimotor deficits (by neuroscore and beam walk), promotes neurogenesis (73% increase in doublecortin immunoreactivity), and astrogliosis (28% increase in glial fibrillary acid protein). Polyman9 administration in brain-injured mannose-binding lectin−/− mice had no effect on post-traumatic brain-injured functional deficits, suggestive of the specificity of its neuroprotective effects. The neurobehavioral efficacy of Polyman9 implicates mannose-binding lectin-C as a novel therapeutic target for traumatic brain injury.

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Fujimoto, Masashi, Masato Shiba, Fumihiro Kawakita, Lei Liu, Naoshi Shimojo, Kyoko Imanaka-Yoshida, Toshimichi Yoshida et Hidenori Suzuki. « Deficiency of tenascin-C and attenuation of blood-brain barrier disruption following experimental subarachnoid hemorrhage in mice ». Journal of Neurosurgery 124, n^o 6 (juin 2016) : 1693–702. http://dx.doi.org/10.3171/2015.4.jns15484.

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OBJECT Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes brain edema and blood-brain barrier (BBB) disruption following experimental SAH. METHODS C57BL/6 wild-type (WT) or TNC knockout (TNKO) mice were subjected to SAH by endovascular puncture. Ninety-seven mice were randomly allocated to WT sham-operated (n = 16), TNKO sham-operated (n = 16), WT SAH (n = 34), and TNKO SAH (n = 31) groups. Mice were examined by means of neuroscore and brain water content 24–48 hours post-SAH; and Evans blue dye extravasation and Western blotting of TNC, matrix metalloproteinase (MMP)-9, and zona occludens (ZO)-1 at 24 hours post-SAH. As a separate study, 16 mice were randomized to WT sham-operated, TNKO sham-operated, WT SAH, and TNKO SAH groups (n = 4 in each group), and activation of mitogen-activated protein kinases (MAPKs) was immunohistochemically evaluated at 24 hours post-SAH. Moreover, 40 TNKO mice randomly received an intracerebroventricular injection of TNC or phosphate-buffered saline, and effects of exogenous TNC on brain edema and BBB disruption following SAH were studied. RESULTS Deficiency of endogenous TNC prevented neurological impairments, brain edema formation, and BBB disruption following SAH; it was also associated with the inhibition of both MMP-9 induction and ZO-1 degradation. Endogenous TNC deficiency also inhibited post-SAH MAPK activation in brain capillary endothelial cells. Exogenous TNC treatment abolished the neuroprotective effects shown in TNKO mice with SAH. CONCLUSIONS Tenascin-C may be an important mediator in the development of brain edema and BBB disruption following SAH, mechanisms for which may involve MAPK-mediated MMP-9 induction and ZO-1 degradation. TNC could be a molecular target against which to develop new therapies for SAH-induced brain injuries.

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Tomasevic, Gregor, Helmut L. Laurer, Gustav Mattiasson, Harryvan Steeg, Tadeusz Wieloch et Tracy K. McIntosh. « Delayed neuromotor recovery and increased memory acquisition dysfunction following experimental brain trauma in mice lacking the DNA repair gene XPA ». Journal of Neurosurgery 116, n^o 6 (juin 2012) : 1368–78. http://dx.doi.org/10.3171/2012.2.jns11888.

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Object This study investigates the outcome after traumatic brain injury (TBI) in mice lacking the essential DNA repair gene xeroderma pigmentosum group A (XPA). As damage to DNA has been implicated in neuronal cell death in various models, the authors sought to elucidate whether the absence of an essential DNA repair factor would affect the outcome of TBI in an experimental setting. Methods Thirty-seven adult mice of either wild-type (n = 18) or XPA-deficient (“knock-out” [n = 19]) genotype were subjected to controlled cortical impact experimental brain trauma, which produced a focal brain injury. Sham-injured mice of both genotypes were used as controls (9 in each group). The mice were subjected to neurobehavoral tests evaluating learning/acquisition (Morris water maze) and motor dysfunction (Rotarod and composite neuroscore test), pre- and postinjury up to 4 weeks. The mice were killed after 1 or 4 weeks, and cortical lesion volume, as well as hippocampal and thalamic cell loss, was evaluated. Hippocampal staining with doublecortin antibody was used to evaluate neurogenesis after the insult. Results Brain-injured XPA−/− mice exhibited delayed recovery from impairment in neurological motor function, as well as pronounced cognitive dysfunction in a spatial learning task (Morris water maze), compared with injured XPA+/+ mice (p < 0.05). No differences in cortical lesion volume, hippocampal damage, or thalamic cell loss were detected between XPA+/+ and XPA−/− mice after brain injury. Also, no difference in the number of cells stained with doublecortin in the hippocampus was detected. Conclusions The authors' results suggest that lack of the DNA repair factor XPA may delay neurobehavioral recovery after TBI, although they do not support the notion that this DNA repair deficiency results in increased cell or tissue death in the posttraumatic brain.

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Neuberger, Bruna, Fernanda Kulinski Mello, Michele Pereira Mallmann, Karine Gabriela da Costa Sobral, Michele Rechia Fighera, Luiz Fernando Freire Royes, Ana Flávia Furian, Tuane Bazanella Sampaio et Mauro Schneider Oliveira. « Beneficial Effects of Rosmarinic Acid In Vitro and In Vivo Models of Epileptiform Activity Induced by Pilocarpine ». Brain Sciences 13, n^o 2 (8 février 2023) : 289. http://dx.doi.org/10.3390/brainsci13020289.

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Epilepsy is characterized by a predisposition to generate recurrent and spontaneous seizures; it affects millions of people worldwide. Status epilepticus (SE) is a severe type of seizure. In this context, screening potential treatments is very important. In the present study, we evaluated the beneficial effects of rosmarinic acid (RA) in pilocarpine-induced in vitro and in vivo models of epileptiform activity. Using an in vitro model in combined entorhinal cortex–hippocampal from Wistar rats we evaluated the effects of RA (10 µg/mL) on the lactate release and a glucose fluorescent analogue, 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NDBG), after incubation in high potassium aCSF supplemented or not with pilocarpine. In the in vivo model, SE was induced in male C57BL/6 mice by pilocarpine. At 1, 24, and 48 h after the end of SE mice were treated with RA (30 mg/kg/v.o.). We evaluated the neuromotor impairment by neuroscore tests and protein carbonyl levels in the cerebral cortex. In both in vitro models, RA was able to decrease the stimulated lactate release, while no effect on 2-NBDG uptake was found. RA has beneficial effects in models of epileptiform activity in vivo and in vitro. We found that RA treatment attenuated SE-induced neuromotor impairment at the 48 h timepoint. Moreover, post-SE treatment with RA decreased levels of protein carbonyls in the cerebral cortex of mice when compared to their vehicle-treated counterparts. Importantly, RA was effective in a model of SE which is relevant for the human condition. The present data add to the literature on the biological effects of RA, which could be a good candidate for add-on therapy in epilepsy.

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Heiskanen, Mette, Olli Jääskeläinen, Eppu Manninen, Shalini Das Gupta, Pedro Andrade, Robert Ciszek, Olli Gröhn, Sanna-Kaisa Herukka, Noora Puhakka et Asla Pitkänen. « Plasma Neurofilament Light Chain (NF-L) Is a Prognostic Biomarker for Cortical Damage Evolution but Not for Cognitive Impairment or Epileptogenesis Following Experimental TBI ». International Journal of Molecular Sciences 23, n^o 23 (2 décembre 2022) : 15208. http://dx.doi.org/10.3390/ijms232315208.

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Plasma neurofilament light chain (NF-L) levels were assessed as a diagnostic biomarker for traumatic brain injury (TBI) and as a prognostic biomarker for somatomotor recovery, cognitive decline, and epileptogenesis. Rats with severe TBI induced by lateral fluid-percussion injury (n = 26, 13 with and 13 without epilepsy) or sham-operation (n = 8) were studied. During a 6-month follow-up, rats underwent magnetic resonance imaging (MRI) (day (D) 2, D7, and D21), composite neuroscore (D2, D6, and D14), Morris-water maze (D35–D39), and a 1-month-long video-electroencephalogram to detect unprovoked seizures during the 6th month. Plasma NF-L levels were assessed using a single-molecule assay at baseline (i.e., naïve animals) and on D2, D9, and D178 after TBI or a sham operation. Plasma NF-L levels were 483-fold higher on D2 (5072.0 ± 2007.0 pg/mL), 89-fold higher on D9 (930.3 ± 306.4 pg/mL), and 3-fold higher on D176 32.2 ± 8.9 pg/mL after TBI compared with baseline (10.5 ± 2.6 pg/mL; all p < 0.001). Plasma NF-L levels distinguished TBI rats from naïve animals at all time-points examined (area under the curve [AUC] 1.0, p < 0.001), and from sham-operated controls on D2 (AUC 1.0, p < 0.001). Plasma NF-L increases on D2 were associated with somatomotor impairment severity (ρ = −0.480, p < 0.05) and the cortical lesion extent in MRI (ρ = 0.401, p < 0.05). Plasma NF-L increases on D2 or D9 were associated with the cortical lesion extent in histologic sections at 6 months post-injury (ρ = 0.437 for D2; ρ = 0.393 for D9, p < 0.05). Plasma NF-L levels, however, did not predict somatomotor recovery, cognitive decline, or epileptogenesis (p > 0.05). Plasma NF-L levels represent a promising noninvasive translational diagnostic biomarker for acute TBI and a prognostic biomarker for post-injury somatomotor impairment and long-term structural brain damage.

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Mosnier, Hannah, Erin Kelly, Kamaya Lawrence, Sarah Cruickshank, Sarah Stacey, Adelina McCall, Sunny Dhatt, Erland Arning, Teodoro Bottiglieri et Nafisa Jadavji. « The Role of One-Carbon Metabolism After Ischemic Stroke in an Aged Mouse Model ». Current Developments in Nutrition 4, Supplement_2 (29 mai 2020) : 1226. http://dx.doi.org/10.1093/cdn/nzaa057_042.

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Abstract Objectives Nutrition is a modifiable risk factor for stroke, which is one of the leading causes of death and disability world-wide. In humans deficiencies in one-carbon metabolism, including the methyltetrahydrofolate reductase (MTHFR) polymorphism, have been linked to increased risk of stroke. The Mthfr+/− mice mouse model mimics the phenotype of the MTHFR677C – >T polymorphism. In our work using in vitro and in vivo models of ischemic stroke we have observed decreased recovery after stroke through reduced neuronal and astrocyte viability and increased apoptosis in MTHFR-deficient mice. In addition, we have previously shown dietary supplementation of one-carbon metabolites increases neuroplasticity and reduced oxidative stress after ischemic stroke. Using the MTHFR-deficient mouse model, the aim of this study was to investigate the impact of dietary supplementation with one-carbon metabolites on stroke outcome. Methods Male Mthfr+/− and wildtype littermate control mice were aged to 1.5-year-old and were placed on control diet (CD) 4-weeks prior to sensorimotor cortex damage using photothrombosis (PT), a model for ischemic stroke. Post-operatively, one group of Mthfr+/− and wildtype littermate mice were fed a supplemented diet (SD) containing 5-methylTHF, vitamin B12, and choline. Four weeks after PT damage and SD motor function was assessed and brain tissue was processed to assess lesion volume and investigate biochemical and molecular changes. Results Mthfr +/− mice fed a SD after PT did not have an impaired neuroscore compared to CD Mthfr+/− mice. When compared to CD, SD Mthfr+/− mice were able to stay on the accelerating rotarod longer and travelled further, they also used their impaired forepaw more. Total homocysteine levels in plasma and lesion volume were reduced in SD Mthfr+/+ and Mthfr+/− mice. In the brain, within the damage site, there were reduced levels of apoptotic cell death and an increased neuroprotective cellular response in SD treated Mthfr+/− mice. Conclusions This study reveals a critical role for one-carbon supplementation in supporting improvement of function after ischemic stroke. Our data suggests that in stroke affected patients, nutritional supplementation maybe an important component to post-operative care, in addition to pharmacological and rehabilitation therapies. Funding Sources NSERC.

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Schorr, Christian, Payman Goodarzi, Fei Chen et Tim Dahmen. « Neuroscope : An Explainable AI Toolbox for Semantic Segmentation and Image Classification of Convolutional Neural Nets ». Applied Sciences 11, n^o 5 (3 mars 2021) : 2199. http://dx.doi.org/10.3390/app11052199.

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Trust in artificial intelligence (AI) predictions is a crucial point for a widespread acceptance of new technologies, especially in sensitive areas like autonomous driving. The need for tools explaining AI for deep learning of images is thus eminent. Our proposed toolbox Neuroscope addresses this demand by offering state-of-the-art visualization algorithms for image classification and newly adapted methods for semantic segmentation of convolutional neural nets (CNNs). With its easy to use graphical user interface (GUI), it provides visualization on all layers of a CNN. Due to its open model-view-controller architecture, networks generated and trained with Keras and PyTorch are processable, with an interface allowing extension to additional frameworks. We demonstrate the explanation abilities provided by Neuroscope using the example of traffic scene analysis.

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Little, C. J. L., P. O. O. Julu, S. Hansen et S. W. J. Reid. « Real-time measurement of cardiac vagal tone in conscious dogs ». American Journal of Physiology-Heart and Circulatory Physiology 276, n^o 2 (1 février 1999) : H758—H765. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h758.

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Rapid changes in heart rate are caused by changes in parasympathetic tone. The NeuroScope is an electronic device designed to offer an objective real-time measure of instantaneous cardiac vagal tone by phase demodulation of a high-resolution time domain of R-R wave intervals. Data are displayed against an arbitrary but linear scale, the cardiac index of parasympathetic activity (CIPA). To validate this method, 10 conscious healthy dogs were each given six incremental doses of atropine (0.01 mg/kg) to a total dose of 0.06 mg/kg or equal volumes of saline. A dose-response curve was constructed. At the maximum dose of atropine, CIPA values fell to 1.3 ± 0.7% (SD) of baseline, whereas R-R intervals fell to 51.5 ± 11.5% of baseline, and standard deviation of the R-R wave interval fell to 10.6 ± 6.5% of baseline. These findings show that the NeuroScope can provide a specific real-time index of cardiac vagal tone in dogs without need for recourse to atropine.

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Hazan, Lynn, Michaël Zugaro et György Buzsáki. « Klusters, NeuroScope, NDManager : A free software suite for neurophysiological data processing and visualization ». Journal of Neuroscience Methods 155, n^o 2 (septembre 2006) : 207–16. http://dx.doi.org/10.1016/j.jneumeth.2006.01.017.

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Król, Dariusz, et Boguslaw Szlachetko. « Automatic Image and Speech Recognition Based on Neural Network ». Journal of Information Technology Research 3, n^o 2 (avril 2010) : 1–17. http://dx.doi.org/10.4018/jitr.2010040101.

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The objective of this paper is to present a real-time mechanism for recognition of different objects using Spatiognitron neural network technology. Spatiognitron is based on a biological neural structure and the theory described in this paper presents what are known as Time Delay Neural Networks (TDNN). These are fields which enable the recognition of different features in the input object. The approach was verified by qualitative recognition process tests in commercial car license plate recognition using a NeuroCar based system. A second set of tests was carried out in a laboratory environment using NeuroScope, an automatic speech recognition system.

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Potter, C. S., C. D. Gregory, H. D. Morris, Z. P. Liang et P. C. Lauterbur. « Toward a neuroscope : An application of high-performance computing for real-time evaluation of brain function using MRI ». Proceedings, annual meeting, Electron Microscopy Society of America 52 (1994) : 922–23. http://dx.doi.org/10.1017/s0424820100172346.

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Over the past few years, several laboratories have demonstrated that changes in local neuronal activity associated with human brain function can be detected by magnetic resonance imaging and spectroscopy. Using these methods, the effects of sensory and motor stimulation have been observed and cognitive studies have begun. These new methods promise to make possible even more rapid and extensive studies of brain organization and responses than those now in use, such as positron emission tomography.Human brain studies are enormously complex. Signal changes on the order of a few percent must be detected against the background of the complex 3D anatomy of the human brain. Today, most functional MR experiments are performed using several 2D slice images acquired at each time step or stimulation condition of the experimental protocol. It is generally believed that true 3D experiments must be performed for many cognitive experiments. To provide adequate resolution, this requires that data must be acquired faster and/or more efficiently to support 3D functional analysis.

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Hrnkova, Miroslava, Zuzana Minichova, Norbert Zilka et Michal Novak. « P1-095 : Novel neurobehavioral scoring system (NeuroScale) for Axon transgenic rat model of neurofibrillary degeneration ». Alzheimer's & ; Dementia 2 (juillet 2006) : S123. http://dx.doi.org/10.1016/j.jalz.2006.05.470.

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Yamamoto, Jun, Mune-yoshi Takahashi, Minoru Tsukada et Yuichiro Anzai. « A New Multi-Unit Acquisition System for Free-Moving Animal Using Field Programmable Analog Array and on Chip MCU. Neuroscope 1. » Brain & ; Neural Networks 6, n^o 1 (1999) : 3–10. http://dx.doi.org/10.3902/jnns.6.3.

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I, D. V., et V. A. Aysina. « Early infantile epileptic encephalopathy type 54 : clinical and neurophysiological aspects ». Epilepsy and paroxysmal conditions 13, n^o 2 (21 juillet 2021) : 132–39. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2021.053.

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A clinical case of a boy aged 20 months old with early infantile epileptic encephalopathy (EIEE) type 54 due to mutated HNRNPU gene presumably suffering from genetic generalized epilepsy and impaired psychomotor development is described. Exome-wide sequencing was carried out by using NextSeq 500 (Illumina, USA). Video electroencephalographic (VEEG) monitoring was conducted by using NeuroScope NS425 (Biola, Russia). The patient was noted to suffer from neonatal delayed motor development and muscular hypotonia with atypical petit mal epilepsy with regional onset at the occipital-parietal-posterior temporal areas based on VEEG data developed at age of eight months as well as progressive psychoemotional disorders. Ethosuximide and valproic acid administered together were efficient in alleviating EIEE seizures that requires to be further followed up. The data obtained allow to identify a precise etiology of epilepsy and apply a differential approach to administer anti-epileptic agents.

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Korenova, Miroslava, Norbert Zilka, Zuzana Stozicka, Ondrej Bugos, Ivo Vanicky et Michal Novak. « NeuroScale, the battery of behavioral tests with novel scoring system for phenotyping of transgenic rat model of tauopathy ». Journal of Neuroscience Methods 177, n^o 1 (février 2009) : 108–14. http://dx.doi.org/10.1016/j.jneumeth.2008.09.027.

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Teoh, Jou Yin, et Kee Hean Lim. « Research beyond biomedical confines : towards better mental health and well-being for all ». Neuroscience Research Notes 2, n^o 4 (19 novembre 2019) : 1–4. http://dx.doi.org/10.31117/neuroscirn.v2i4.43.

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‘Working Together to Prevent Suicide’ is the theme of World Mental Health Day 2019. According to the World Health Organisation, suicide is the second leading cause of death for people aged 15-19 years old. One person dies of suicide every 40 seconds, with this form of death affecting people of all age groups in all countries. Hence in line with this year’s theme calling for a trans-sectoral and interdisciplinary approach to address this epidemic, we would like to invite all contributors and readers of Neuroscience Research Notes (NeurosciRN) to take a moment to reflect on how they - as researchers can contribute towards the facilitation, discussion and promotion of positive mental health, which in turn has been found to reduce suicide risk.

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Beard, Daniel J., Gina Hadley, Neal Thurley, David W. Howells, Brad A. Sutherland et Alastair M. Buchan. « The effect of rapamycin treatment on cerebral ischemia : A systematic review and meta-analysis of animal model studies ». International Journal of Stroke 14, n^o 2 (29 novembre 2018) : 137–45. http://dx.doi.org/10.1177/1747493018816503.

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Background Amplifying endogenous neuroprotective mechanisms is a promising avenue for stroke therapy. One target is mammalian target of rapamycin (mTOR), a serine/threonine kinase regulating cell proliferation, cell survival, protein synthesis, and autophagy. Animal studies investigating the effect of rapamycin on mTOR inhibition following cerebral ischemia have shown conflicting results. Aim To conduct a systematic review and meta-analysis evaluating the effectiveness of rapamycin in reducing infarct volume in animal models of ischemic stroke. Summary of review Our search identified 328 publications. Seventeen publications met inclusion criteria (52 comparisons: 30 reported infarct size and 22 reported neurobehavioral score). Study quality was modest (median 4 of 9) with no evidence of publication bias. The point estimate for the effect of rapamycin was a 21.6% (95% CI, 7.6%–35.7% p < 0.01) improvement in infarct volume and 30.5% (95% CI 17.2%–43.8%, p < 0.0001) improvement in neuroscores. Effect sizes were greatest in studies using lower doses of rapamycin. Conclusion Low-dose rapamycin treatment may be an effective therapeutic option for stroke. Modest study quality means there is a potential risk of bias. We recommend further high-quality preclinical studies on rapamycin in stroke before progressing to clinical trials.

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Merényi, Erzsébet, Joshua Taylor et Andrea Isella. « Deep data : discovery and visualization Application to hyperspectral ALMA imagery ». Proceedings of the International Astronomical Union 12, S325 (octobre 2016) : 281–90. http://dx.doi.org/10.1017/s1743921317000175.

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AbstractLeading-edge telescopes such as the Atacama Large Millimeter and sub-millimeter Array (ALMA), and near-future ones, are capable of imaging the same sky area at hundreds-to-thousands of frequencies with both high spectral and spatial resolution. This provides unprecedented opportunities for discovery about the spatial, kinematical and compositional structure of sources such as molecular clouds or protoplanetary disks, and more. However, in addition to enormous volume, the data also exhibit unprecedented complexity, mandating new approaches for extracting and summarizing relevant information. Traditional techniques such as examining images at selected frequencies become intractable while tools that integrate data across frequencies or pixels (like moment maps) can no longer fully exploit and visualize the rich information. We present a neural map-based machine learning approach that can handle all spectral channels simultaneously, utilizing the full depth of these data for discovery and visualization of spectrally homogeneous spatial regions (spectral clusters) that characterize distinct kinematic behaviors. We demonstrate the effectiveness on an ALMA image cube of the protoplanetary disk HD142527. The tools we collectively name “NeuroScope” are efficient for “Big Data” due to intelligent data summarization that results in significant sparsity and noise reduction. We also demonstrate a new approach to automate our clustering for fast distillation of large data cubes.

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Qu, Wenrui, Nai-Kui Liu, Xiangbing Wu, Ying Wang, Yongzhi Xia, Yan Sun, Yvonne Lai, Rui Li, Anantha Shekhar et Xiao-Ming Xu. « Disrupting nNOS–PSD95 Interaction Improves Neurological and Cognitive Recoveries after Traumatic Brain Injury ». Cerebral Cortex 30, n^o 7 (22 janvier 2020) : 3859–71. http://dx.doi.org/10.1093/cercor/bhaa002.

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Abstract Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI). However, directly inhibiting NMDARs or nNOS produces adverse side effects because they play key physiological roles in the normal brain. Since interaction of nNOS–PSD95 is a key step in NMDAR-mediated excitotoxicity, we investigated whether disrupting nNOS–PSD95 interaction with ZL006, an inhibitor of nNOS–PSD95 interaction, attenuates NMDAR-mediated excitotoxicity. In cortical neuronal cultures, ZL006 treatment significantly reduced glutamate-induced neuronal death. In a mouse model of controlled cortical impact (CCI), administration of ZL006 (10 mg/kg, i.p.) at 30 min postinjury significantly inhibited nNOS–PSD95 interaction, reduced TUNEL- and phospho-p38-positive neurons in the motor cortex. ZL006 treatment also significantly reduced CCI-induced cortical expression of apoptotic markers active caspase-3, PARP-1, ratio of Bcl-2/Bax, and phosphorylated p38 MAPK (p-p38). Functionally, ZL006 treatment significantly improved neuroscores and sensorimotor performance, reduced somatosensory and motor deficits, reversed CCI-induced memory deficits, and attenuated cognitive impairment. Histologically, ZL006 treatment significantly reduced the brain lesion volume. These findings collectively suggest that blocking nNOS–PSD95 interaction represents an attractive strategy for ameliorating consequences of TBI and that its action is mediated via inhibiting neuronal apoptosis and p38 MAPK signaling.

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Ahnstedt, Hilda, Maryam Mostajeran, Frank W. Blixt, Karin Warfvinge, Saema Ansar, Diana N. Krause et Lars Edvinsson. « U0126 Attenuates Cerebral Vasoconstriction and Improves Long-Term Neurologic Outcome after Stroke in Female Rats ». Journal of Cerebral Blood Flow & ; Metabolism 35, n^o 3 (mars 2015) : 454–60. http://dx.doi.org/10.1038/jcbfm.2014.217.

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Sex differences are well known in cerebral ischemia and may impact the effect of stroke treatments. In male rats, the MEK1/2 inhibitor U0126 reduces ischemia-induced endothelin type B (ETB) receptor upregulation, infarct size and improves acute neurologic function after experimental stroke. However, responses to this treatment in females and long-term effects on outcome are not known. Initial experiments used in vitro organ culture of cerebral arteries, confirming ERK1/2 activation and increased ETB receptor-mediated vasoconstriction in female cerebral arteries. Transient middle cerebral artery occlusion (tMCAO, 120 minutes) was induced in female Wistar rats, with U0126 (30 mg/kg intraperitoneally) or vehicle administered at 0 and 24 hours of reperfusion, or with no treatment. Infarct volumes were determined and neurologic function was assessed by 6-point and 28-point neuroscores. ETB receptor-mediated contraction was studied with myograph and protein expression with immunohistochemistry. In vitro organ culture and tMCAO resulted in vascular ETB receptor upregulation and activation of ERK1/2 that was prevented by U0126. Although no effect on infarct size, U0126 improved the long-term neurologic function after experimental stroke in female rats. In conclusion, early prevention of the ERK1/2 activation and ETB receptor-mediated vasoconstriction in the cerebral vasculature after ischemic stroke in female rats improves the long-term neurologic outcome.

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Ito, Eiji, Masazumi Fujii, Yuichiro Hayashi, Jiang Zhengang, Tetsuya Nagatani, Kiyoshi Saito, Yugo Kishida, Kensaku Mori et Toshihiko Wakabayashi. « Magnetically Guided 3-Dimensional Virtual Neuronavigation for Neuroendoscopic Surgery ». Operative Neurosurgery 66, suppl_2 (1 juin 2010) : ons342—ons353. http://dx.doi.org/10.1227/01.neu.0000369659.19479.af.

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Abstract OBJECTIVE The authors have developed a novel intraoperative neuronavigation with 3-dimensional (3D) virtual images, a 3D virtual navigation system, for neuroendoscopic surgery. The present study describes this technique and clinical experience with the system. METHODS Preoperative imaging data sets were transferred to a personal computer to construct virtual endoscopic views with image segmentation software. An electromagnetic tracker was used to acquire the position and orientation of the tip of the neuroendo-scope. Virtual endoscopic images were interlinked to an electromagnetic tracking system and demonstrated on the navigation display in real time. Accuracy and efficacy of the 3D virtual navigation system were evaluated in a phantom test and on 5 consecutive patients undergoing neuroendoscopic surgery. RESULTS Virtual navigation views were consistent with actual endoscopic views and trajectory in both phantom testing and clinical neuroendoscopic surgery. Anatomic structures that can affect surgical approaches were adequately predicted with the virtual navigation system. The virtual semitransparent view contributed to a clear understanding of spatial relationships between surgical targets and surrounding structures. Surgical procedures in all patients were performed while confirming with virtual navigation. In neurosurgery with a flexible neuroscope, virtual navigation also demonstrated anatomic structures in real time. CONCLUSION The interactive method of intraoperative visualization influenced the decision-making process during surgery and provided useful assistance in identifying safe approaches for neuroendoscopic surgery. The magnetically guided navigation system enabled navigation of surgical targets in both rigid and flexible endoscopic surgeries.

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England, Timothy J., William H. Hind, Nadiah A. Rasid et Saoirse E. O'Sullivan. « Cannabinoids in Experimental Stroke : A Systematic Review and Meta-Analysis ». Journal of Cerebral Blood Flow & ; Metabolism 35, n^o 3 (mars 2015) : 348–58. http://dx.doi.org/10.1038/jcbfm.2014.218.

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Cannabinoids (CBs) show promise as neuroprotectants with some agents already licensed in humans for other conditions. We systematically reviewed CBs in preclinical stroke to guide further experimental protocols. We selected controlled studies assessing acute administration of CBs for experimental stroke, identified through systematic searches. Data were extracted on lesion volume, outcome and quality, and analyzed using random effect models. Results are expressed as standardized mean difference (SMD) with 95% confidence intervals (CIs). In all, 144 experiments (34 publications) assessed CBs on infarct volume in 1,473 animals. Cannabinoids reduced infarct volume in transient (SMD −1.41 (95% CI −1.71), −1.11) P<0.00001) and permanent (−1.67 (−2.08, −1.27), P<0.00001) ischemia and in all subclasses: endocannabinoids (−1.72 (−2.62, −0.82), P=0.0002), CB1/CB2 ligands (−1.75 (−2.19, −1.31), P<0.00001), CB2 ligands (−1.65 (−2.09, −1.22), P<0.00001), cannabidiol (−1.20 (−1.63, −0.77), P<0.00001), Δ9-tetrahydrocannabinol (−1.43 (−2.01, −0.86), P<0.00001), and HU-211 (−2.90 (−4.24, −1.56), P<0.0001). Early and late neuroscores significantly improved with CB use (−1.27 (−1.58, −0.95), P<0.00001; −1.63 (−2.64, −0.62), P<0.002 respectively) and there was no effect on survival. Statistical heterogeneity and publication bias was present, median study quality was 4 (range 1 to 6/8). Overall, CBs significantly reduced infarct volume and improve functional outcome in experimental stroke. Further studies in aged, female and larger animals, with other co-morbidities are required.

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Raghupathi, Ramesh, Seamus C. Fernandez, Hisayuki Murai, Stephen P. Trusko, Richard W. Scott, Walter K. Nishioka et Tracy K. McIntosh. « BCL-2 Overexpression Attenuates Cortical Cell Loss after Traumatic Brain Injury in Transgenic Mice ». Journal of Cerebral Blood Flow & ; Metabolism 18, n^o 11 (novembre 1998) : 1259–69. http://dx.doi.org/10.1097/00004647-199811000-00013.

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The proto-oncogene, BCL-2, has been suggested to participate in cell survival during development of, and after injury to, the CNS. Transgenic (TG) mice overexpressing human Bcl-2 (n = 21) and their wild-type (WT) littermates (n = 18) were subjected to lateral controlled cortical impact brain injury. Lateral controlled cortical impact brain injury resulted in the formation of a contusion in the injured cortex at 2 days, which developed into a well-defined cavity by 7 days in both WT and TG mice. At 7 days after injury, brain-injured TG mice had a significantly reduced cortical lesion (volume = 1.99 mm3) compared with that of the injured WT mice (volume = 5.1 mm3, P <0.01). In contrast, overexpression of BCL-2 did not affect the extent of hippocampal cell death after lateral controlled cortical impact brain injury. Analysis of motor function revealed that both brain-injured WT and TG mice exhibited significant right-sided deficits at 2 and 7 days after injury ( P < 0.05 compared with the uninjured controls). Although composite neuroscores (sum of scores from forelimb and hind limb flexion, lateral pulsion, and inclined plane tests) were not different between WT and TG brain-injured mice, TG mice had a slightly but significantly reduced deficit in the inclined plane test ( P < 0.05 compared to the WT mice). These data suggest that the cell death regulatory gene, BCL-2, may play a protective role in the pathophysiology of traumatic brain injury.

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Maklygina, Yuliya, Igor Romanishkin, Aleksej Skobeltsin, Dina Farrakhova et Victor Loschenov. « Phototherapy of Brain Tumours Using a Fibre Optic Neurosystem ». Photonics 8, n^o 11 (21 octobre 2021) : 462. http://dx.doi.org/10.3390/photonics8110462.

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In this work, a new approach was tested to assess the cellular composition of tissues by time-resolved methods of fluorescence analysis of exogenous and endogenous fluorophores. First of all, the differences in fluorescence kinetics of endogenous fluorophores (coenzymes NADH and FAD) in tumour and immunocompetent cells were determined. After that, differences in fluorescence kinetics of photosensitizer 5 ALA-induced protoporphyrin IX were established due to its different metabolism in cells of different phenotypes. Kinetics of photoluminescence of NADH and FAD coenzymes as well as photosensitizer were studied by means of two different methods: time-resolved spectroscopy based on a streak-camera and fibre optic neuroscopy, which served to perform process monitoring and regular fluorescence diagnosis of the probed region. Time-resolved fluorescence microscopy (FLIM) was used as a control technique. Time-resolved spectroscopic fluorescence lifetime analysis was performed on sexually mature female rats induced with glioma C6 brain tumour under in vivo conditions; thus, under conditions where the immune system actively intervenes in the process of oncogenesis. In this regard, the aim of the study was to recognize the cellular composition of the brain tumour tissue, namely the ratio of cancer and immunocompetent cells and their mutual localization. Understanding the role of the immune system thus provides new ways and approaches for further diagnosis and therapy, making tumour-associated immune cells a prime target for modern therapies.

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Maklygina, Yuliya, Igor Romanishkin, Aleksej Skobeltsin, Dina Farrakhova, Sergej Kharnas, Lina Bezdetnaya et Victor Loschenov. « Changes in Spectral Fluorescence Properties of a Near-Infrared Photosensitizer in a Nanoform as a Coating of an Optical Fiber Neuroport ». Photonics 8, n^o 12 (6 décembre 2021) : 556. http://dx.doi.org/10.3390/photonics8120556.

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In this work, we tested a new approach to assess the presence of inflammatory process in the implant area using spectral methods and the technique of fiber fluorescence analysis of photosensitizers in nanoform. First of all, the spectral characteristics of the photosensitizer when interacting with the porous surface of the implant, based on hydroxyapatite under in vitro and in vivo conditions, were determined. Thus, it was shown that spectral characteristics of photosensitizers can be used for judgement on the process of inflammation in the implant area and thus on the local presence of the immunocompetent cells. The analysis was performed at a sufficient depth in the biotissue by using the near-infrared spectral region, as well as two different methods: fiber-based laser spectroscopy and fiber-optic neuroscopy, which served to monitor the process and regular fluorescence diagnosis of the studied area. Fluorescence spectroscopic analysis was performed on experimental animals in vivo, i.e., under conditions of active immune system intervention, as well as on cell cultures in vitro in order to judge the role of the immune system in the interaction with the implant in comparison. Thus, the aim of the study was to determine the relationship between the fluorescence signal of nanophotosensitizers in the near infrared spectral region and its parameters with the level of inflammation and the type of surface with which the photosensitizer interacts in the implant area. Thus, fiber-optic control opens up new approaches for further diagnosis and therapy in the implant area, making immune cells a prime target for advanced therapies.

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Davis, Kyle W., Colleen G. Bilancia, Megan Martin, Rena Vanzo, Megan Rimmasch, Yolanda Hom, Mohammed Uddin et Moises A. Serrano. « NeuroSCORE is a genome-wide omics-based model that identifies candidate disease genes of the central nervous system ». Scientific Reports 12, n^o 1 (31 mars 2022). http://dx.doi.org/10.1038/s41598-022-08938-y.

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AbstractTo identify candidate disease genes of central nervous system (CNS) phenotypes, we created the Neurogenetic Systematic Correlation of Omics-Related Evidence (NeuroSCORE). We identified five genome-wide metrics highly associated with CNS phenotypes to score 19,601 protein-coding genes. Genes scored one point per metric (range: 0–5), identifying 8298 scored genes (scores ≥ 1) and 1601 “high scoring” genes (scores ≥ 3). Using logistic regression, we determined the odds ratio that genes with a NeuroSCORE from 1 to 5 would be associated with known CNS-related phenotypes compared to genes that scored zero. We tested NeuroSCORE using microarray copy number variants (CNVs) in case–control cohorts and aggregate mouse model data. High scoring genes are associated with CNS phenotypes (OR = 5.5, p < 2e-16), enriched in case CNVs, and mouse ortholog genes that cause behavioral and nervous system abnormalities. We identified 1058 high scoring genes with no disease association in OMIM. Transforming the logistic regression results indicates high scoring genes have an 84–92% chance of being associated with a CNS phenotype. Top scoring genes include GRIA1, MAP4K4, SF1, TNPO2, and ZSWIM8. Finally, we interrogated CNVs in the Clinical Genome Resource, finding the majority of clinically significant CNVs contain high scoring genes. These findings can direct future research and improve molecular diagnostics.

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Huie, J. Russell, Jessica L. Nielson, Jorden Wolfsbane, Clark R. Andersen, Heidi M. Spratt, Douglas S. DeWitt, Adam R. Ferguson et Bridget E. Hawkins. « Data-driven approach to integrating genomic and behavioral preclinical traumatic brain injury research ». Frontiers in Bioengineering and Biotechnology 10 (10 janvier 2023). http://dx.doi.org/10.3389/fbioe.2022.887898.

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Understanding recovery from TBI is complex, involving multiple systems and modalities. The current study applied modern data science tools to manage this complexity and harmonize large-scale data to understand relationships between gene expression and behavioral outcomes in a preclinical model of chronic TBI (cTBI). Data collected by the Moody Project for Translational TBI Research included rats with no injury (naïve animals with similar amounts of anesthetic exposure to TBI and sham-injured animals), sham injury, or lateral fluid percussion TBI, followed by recovery periods up to 12 months. Behavioral measures included locomotor coordination (beam balance neuroscore) and memory and cognition assessments (Morris water maze: MWM) at multiple timepoints. Gene arrays were performed using hippocampal and cortical samples to probe 45,610 genes. To reduce the high dimensionality of molecular and behavioral domains and uncover gene–behavior associations, we performed non-linear principal components analyses (NL-PCA), which de-noised the data. Genomic NL-PCA unveiled three interpretable eigengene components (PC2, PC3, and PC4). Ingenuity pathway analysis (IPA) identified the PCs as an integrated stress response (PC2; EIF2-mTOR, corticotropin signaling, etc.), inflammatory factor translation (PC3; PI3K-p70S6K signaling), and neurite growth inhibition (PC4; Rho pathways). Behavioral PCA revealed three principal components reflecting the contribution of MWM overall speed and distance, neuroscore/beam walk, and MWM platform measures. Integrating the genomic and behavioral domains, we then performed a ‘meta-PCA’ on individual PC scores for each rat from genomic and behavioral PCAs. This meta-PCA uncovered three unique multimodal PCs, characterized by robust associations between inflammatory/stress response and neuroscore/beam walk performance (meta-PC1), stress response and MWM performance (meta-PC2), and stress response and neuroscore/beam walk performance (meta-PC3). Multivariate analysis of variance (MANOVA) on genomic–behavioral meta-PC scores tested separately on cortex and hippocampal samples revealed the main effects of TBI and recovery time. These findings are a proof of concept for the integration of disparate data domains for translational knowledge discovery, harnessing the full syndromic space of TBI.

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