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17. Elevation of brain magnesium with Swiss chard and buckwheat extracts in an animal model of reduced magnesium dietary intake.

Author

El-Khodor, Bassem F., James, Karma, Chang, Qing, Zhang, Wei, Loiselle, Yvette R., Panda, Chinmayee, and Hanania, Taleen

Subjects
BUCKWHEAT, PUBLIC health, MAGNESIUM, ANIMAL behavior, DIETARY supplements, CEREBROSPINAL fluid
Abstract

Inadequate dietary magnesium (Mg) intake is a growing public health concern. Mg is critical for diverse metabolic processes including energy production, macromolecule biosynthesis, and electrolyte homeostasis. Inadequate free Mg2+ ion concentration ([Mg2+]) in the brain is associated with several neurological and behavioral disorders. Elevating [Mg2+]in the brain using oral Mg supplementation has proven to be challenging due to the tight regulation of Mg2+ transport to the brain. This study explored the effect of short-term moderate reduction in dietary Mg intake (87% of normal Mg diet for 30 days) on [Mg2+] in the cerebrospinal fluid (CSF) ([Mg2+]CSF) and red blood cells (RBCs) ([Mg2+]RBC) in adult male rats. In addition, we investigated the effectiveness of magnesium-rich blend of Swiss chard and buckwheat extracts (SC/BW extract) in increasing brain [Mg2+] compared to various Mg salts commonly used as dietary supplements. Animals were assigned to either normal or low Mg diet for 30 - 45 days. Following this, animals maintained on low Mg diet were supplemented with various Mg compounds. [Mg2+]CSF and [Mg2+]RBC were measured at baseline and following Mg administration. Anxiety-like behavior and cognitive function were also evaluated. The present study showed that a short-term and moderate reduction in Mg dietary intake results in a significant decline in [Mg2+]CSF and [Mg2+]RBC and the emergence of anxiety-like behavior in comparison to animals maintained on normal Mg diet. Supplementation with SC/BW extract significantly elevated [Mg2+]CSF and improved animal performance in the novel object recognition test in comparison with animals maintained on reduced Mg intake and supplemented with various Mg compounds. These observations indicate that brain [Mg2+] is more sensitive to a short-term and moderate reduction in Mg dietary intake than previously thought and emphasizes the importance of dietary Mg in replenishing brain Mg2+ reserves. [ABSTRACT FROM AUTHOR]

Published
2022
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22. Aβ-accelerated neurodegeneration caused by Alzheimer’s-associated ACE variant R1279Q is rescued by angiotensin system inhibition in mice

Author

Cuddy, Leah K., primary, Prokopenko, Dmitry, additional, Cunningham, Eric P., additional, Brimberry, Ross, additional, Song, Peter, additional, Kirchner, Rory, additional, Chapman, Brad A., additional, Hofmann, Oliver, additional, Hide, Winston, additional, Procissi, Daniele, additional, Hanania, Taleen, additional, Leiser, Steven C., additional, Tanzi, Rudolph E, additional, and Vassar, Robert, additional

Published
2020
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28. Myelinated axons fail to develop properly in a genetically authentic mouse model of Charcot-Marie-Tooth disease type 2E

Author

Eunjoo Lancaster, Steven S. Scherer, Jian Li, Hanania Taleen, Mark A. Scheideler, and Ronald K.H. Liem

Subjects
0301 basic medicine, Male, Pathology, medicine.medical_specialty, Neurofilament, Nerve root, Intermediate Filaments, Sensory system, Biology, Nerve Fibers, Myelinated, Nerve conduction velocity, 03 medical and health sciences, Mice, 0302 clinical medicine, Developmental Neuroscience, Charcot-Marie-Tooth Disease, Neurofilament Proteins, medicine, Animals, Regeneration (biology), Wild type, Spinal cord, Mice, Mutant Strains, Mice, Inbred C57BL, Electrophysiology, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, nervous system, Neurology, Mutation, 030217 neurology & neurosurgery
Abstract

We have analyzed a mouse model of Charcot-Marie-Tooth disease 2E (CMT2E) harboring a heterozygous p.Asn98Ser (p.N98S) Nefl mutation, whose human counterpart results in a severe, early-onset neuropathy. Behavioral, electrophysiological, and pathological analyses were done on separate cohorts of Nefl N98S/+ mutant mice and their wild type Nefl +/+ littermates between 8 and 48 weeks of age. The motor performance of Nefl N98S/+ mice, as evidenced by altered balance and gait measures, was impaired at every age examined (from 6 to 25 weeks of age). At all times examined, myelinated axons were smaller and contained markedly fewer neurofilaments in Nefl N98S/+ mice, in all examined aspects of the PNS, from the nerve roots to the distal ends of the sciatic and caudal nerves. Similarly, the myelinated axons in the various tracts of the spinal cord and in the optic nerves were smaller and contained fewer neurofilaments in mutant mice. The myelinated axons in both the PNS and the CNS of mutant mice had relatively thicker myelin sheaths. The amplitude and the nerve conduction velocity of the caudal nerves were reduced in proportion with the diminished sizes of myelinated axons. Conspicuous aggregations of neurofilaments were only seen in primary sensory and motor neurons, and were largely confined to the cell bodies and proximal axons. There was evidence of axonal degeneration and regeneration of myelinated axons, mostly in distal nerves. In summary, the p.N98S mutation causes a profound reduction of neurofilaments in the myelinated axons of the PNS and CNS, resulting in substantially reduced axonal diameters, particularly of large myelinated axons, and distal axon loss in the PNS.

Published
2018

31. Biomarker Analysis of Orally Dosed, Dual Active, Matrix Metalloproteinase (MMP)-2 and MMP-9 Inhibitor, AQU-118, in the Spinal Nerve Ligation (SNL) Rat Model of Neuropathic Pain

Author

Kwan, Mei, primary, Choo, Anthony, additional, Hanania, Taleen, additional, Ghavami, Afshin, additional, Beltran, Jose, additional, Shea, John, additional, Barboza, Amidi, additional, Hu, Andrew, additional, Fowler, Marcie, additional, Neelagiri, Venugopal, additional, and Sucholeiki, Irving, additional

Published
2019
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35. Effect of a novel, orally active matrix metalloproteinease-2 and-9 inhibitor in spinal and trigeminal rat models of neuropathic pain

Author

Henry, Michael A., Fairchild, Dara D., Patil, Mayur J., Hanania, Taleen, Hain, Heather S., Davis, Scott F., Malekiani, Sam A., Hu, Andrew, Sucholeiki, Roy, Nix, Darrell, and Sucholeiki, Irving

Subjects
Indoles, Cyclohexanecarboxylic Acids, Administration, Oral, Thiophenes, Matrix Metalloproteinase Inhibitors, Article, Rats, Rats, Sprague-Dawley, Disease Models, Animal, Spinal Nerves, Hyperalgesia, Animals, Matrix Metalloproteinase 2, Neuralgia, Trigeminal Nerve, Amines, Gabapentin, Propionates, gamma-Aminobutyric Acid
Abstract

To study the effects of a novel matrix metalloproteinase-2 (MMP-2) and MMP-9 inhibitor, AQU-118, on mechanical allodynia in the spinal nerve ligation (SNL) model of neuropathic pain and the chronic constriction injury of the infraorbital nerve (CCI-IoN) model of neuropathic orofacial pain.Five groups of SNL rats were given daily oral doses of AQU-118 (5, 10, 20 mg/kg), gabapentin (100 mg/kg), or vehicle (0.5% methylcellulose) and then paw withdrawal threshold was measured with von Frey filaments (VF). Three groups of CCI-IoN rats were given daily oral doses of either AQU-118 (40 mg/kg), gabapentin (100 mg/kg), or vehicle (0.5% methylcellulose) and then mechanical allodynia was measured with facial VF and non-reflex-based orofacial stimulation test (OFST) assay. Naïve rats were also tested for the effect of AQU-118 (40 mg/kg) on basal sensitivity to mechanical stimulation/locomotive activity.Mechanical allodynia in SNL rats was attenuated by gabapentin (100 mg/kg) and AQU-118 (in a dose-dependent manner). Mechanical allodynia in CCI-IoN rats was also attenuated (in an equipotent manner) by both AQU-118 (40 mg/ kg) and gabapentin (100 mg/kg) as measured by both facial VF and OFST assay. Upon cessation of either AQU-118 or gabapentin, VF-related responses in both models and OFST assay times reverted to levels observed in vehicle-treated rats. No statistically significant change was observed in locomotive activity/paw withdrawal threshold by AQU-118 (40 mg/kg) in naïve rats.The results demonstrated that oral AQU-118 attenuates mechanical allodynia in both neuropathic pain models and with efficacies that mirror gabapentin at the 40 mg/kg dose used in the CCI-IoN model but without effect on basal sensitivity to mechanical stimulation/locomotive activity. These findings support a possible role for MMP-2/-9 in the etiology of neuropathic pain and also suggest that inhibition strategies represent a viable treatment option.

Published
2015

37. Comprehensive Analysis of Two Shank3 and the Cacna1c Mouse Models of Autism Spectrum Disorder

Author

Kabitzke, Patricia, primary, Brunner, Daniela, additional, He, Dansha, additional, Fazio, Pamela A., additional, Cox, Kimberly, additional, Sutphen, Jane, additional, Thiede, Lucinda, additional, Sabath, Emily, additional, Hanania, Taleen, additional, Alexandrov, Vadim, additional, Rasmusson, Randall, additional, Spooren, Will, additional, Ghosh, Anirvan, additional, Feliciano, Pamela, additional, Biemans, Barbara, additional, Benedetti, Marta, additional, and Clayton, Alice Luo, additional

Published
2016
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40. SEP-363856, a Novel Psychotropic Agent with a Unique, Non-D2Receptor Mechanism of Action▪

Author

Dedic, Nina, Jones, Philip G., Hopkins, Seth C., Lew, Robert, Shao, Liming, Campbell, John E., Spear, Kerry L., Large, Thomas H., Campbell, Una C., Hanania, Taleen, Leahy, Emer, and Koblan, Kenneth S.

Abstract

For the past 50 years, the clinical efficacy of antipsychotic medications has relied on blockade of dopamine D2receptors. Drug development of non-D2compounds, seeking to avoid the limiting side effects of dopamine receptor blockade, has failed to date to yield new medicines for patients. In this work, we report the discovery of SEP-363856 (SEP-856), a novel psychotropic agent with a unique mechanism of action. SEP-856 was discovered in a medicinal chemistry effort utilizing a high throughput, high content, mouse-behavior phenotyping platform, in combination with in vitro screening, aimed at developing non-D2(anti-target) compounds that could nevertheless retain efficacy across multiple animal models sensitive to D2-based pharmacological mechanisms. SEP-856 demonstrated broad efficacy in putative rodent models relating to aspects of schizophrenia, including phencyclidine (PCP)-induced hyperactivity, prepulse inhibition, and PCP-induced deficits in social interaction. In addition to its favorable pharmacokinetic properties, lack of D2receptor occupancy, and the absence of catalepsy, SEP-856’s broad profile was further highlighted by its robust suppression of rapid eye movement sleep in rats. Although the mechanism of action has not been fully elucidated, in vitro and in vivo pharmacology data as well as slice and in vivo electrophysiology recordings suggest that agonism at both trace amine-associated receptor 1 and 5-HT1Areceptors is integral to its efficacy. Based on the preclinical data and its unique mechanism of action, SEP-856 is a promising new agent for the treatment of schizophrenia and represents a new pharmacological class expected to lack the side effects stemming from blockade of D2signaling.

Published
2019
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41. In vivo phenotypic drug discovery: applying a behavioral assay to the discovery and optimization of novel antipsychotic agents

Author

Shao, Liming, primary, Campbell, Una C., additional, Fang, Q. Kevin, additional, Powell, Noel A., additional, Campbell, John E., additional, Jones, Philip G., additional, Hanania, Taleen, additional, Alexandrov, Vadim, additional, Morganstern, Irene, additional, Sabath, Emily, additional, Zhong, Hua M., additional, Large, Thomas H., additional, and Spear, Kerry L., additional

Published
2016
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42. Comprehensive Analysis of the 16p11.2 Deletion and Null Cntnap2 Mouse Models of Autism Spectrum Disorder

Author

Brunner, Daniela, primary, Kabitzke, Patricia, additional, He, Dansha, additional, Cox, Kimberly, additional, Thiede, Lucinda, additional, Hanania, Taleen, additional, Sabath, Emily, additional, Alexandrov, Vadim, additional, Saxe, Michael, additional, Peles, Elior, additional, Mills, Alea, additional, Spooren, Will, additional, Ghosh, Anirvan, additional, Feliciano, Pamela, additional, Benedetti, Marta, additional, Luo Clayton, Alice, additional, and Biemans, Barbara, additional

Published
2015
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47. The potent and selective α 4 β 2*/ α 6*‐nicotinic acetylcholine receptor partial agonist 2‐[5‐[5‐(( S )Azetidin‐2‐ylmethoxy)‐3‐pyridinyl]‐3‐isoxazolyl]ethanol demonstrates antidepressive‐like behavior in animal models and a favorable ADME‐tox profile

Author

Yu, Li‐Fang, primary, Brek Eaton, J., additional, Zhang, Han‐Kun, additional, Sabath, Emily, additional, Hanania, Taleen, additional, Li, Guan‐Nan, additional, Breemen, Richard B., additional, Whiteaker, Paul, additional, Liu, Qiang, additional, Wu, Jie, additional, Chang, Yong‐Chang, additional, Lukas, Ronald J., additional, Brunner, Dani, additional, and Kozikowski, Alan P., additional

Published
2014
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50. SAHA Enhances Synaptic Function and Plasticity In Vitro but Has Limited Brain Availability In Vivo and Does Not Impact Cognition

Author

Hanson, Jesse E., primary, La, Hank, additional, Plise, Emile, additional, Chen, Yung-Hsiang, additional, Ding, Xiao, additional, Hanania, Taleen, additional, Sabath, Emily V., additional, Alexandrov, Vadim, additional, Brunner, Dani, additional, Leahy, Emer, additional, Steiner, Pascal, additional, Liu, Lichuan, additional, Scearce-Levie, Kimberly, additional, and Zhou, Qiang, additional

Published
2013
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