Pictured above: Dr. Sunday Bisong (IBRO Return Home Fellow 2016) with his students in front of his laboratory at the University of Calabar, Nigeria. Front row (left to right): Imeiba Ajiwhen (PhD student), Cecil Jones (undergraduate), Veronica Atta (undergraduate), Dr. Sunday Bisong, Udeme George (MSc student). Rear row (left to right): Mavis Otonkwe (undergraduate), Favour Abuo (MSc student).
IBRO Return Home Fellow, Sunday Agba Bisong, obtained his PhD at the University of Calabar (Nigeria) and pursued postdoctoral work at Dalhousie University (Canada) where he collaborated with Richard Brown, Professor of Psychology and Neuroscience. His time abroad was essential for gaining international experience and contacts, but Bisong really wanted to go back to Nigeria and establish his own lab and research team. In other words, he wanted to build capacity, skills and opportunities in the field of neuroscience at home. He got his chance in 2016 when he applied for and received an IBRO Return Home Fellowship. This initial support has allowed Bisong to start realizing his dream at his alma mater, the University of Calabar.
Bisong's current research focuses on the anti-oxidant effect of Rauwolfia vomitoria (R. vomitoria) on motor impairment and cognitive decline in Alzheimer's disease (AD). He shares his scientific research progress below.
SCIENTIFIC REPORT ON 2016 IBRO RETURN HOME FELLOWSHIP
Title of Research: Analysis of the Potentials of Rauwolfia Vomitoria in Prevention of Cognitive Decline in Some Pharmacological Mouse Models of Alzheimer's Disease
In a recently unpublished research (undergoing peer review), the aqueous root extract of Rauwolfia vomitoria (8mg/kg, administered for 12 days) prevented motor impairment and cognitive decline in a transgenic mouse model of Alzheimer’s disease (5xFAD). However, this study was done only on 6-month-old mice. Oxidative stress has been reported as one of the hallmarks of AD (Smith et al, 2000).
In spite of the difficulty in acquiring transgenic mouse models of AD, I was able to proceed with my research supported by IBRO Return Home funding. My research was organized into four batches: In one batch, treatment was started at one month of age through drinking water and then continued to 3 months of age when the mice were tested through the behavioural test battery to assay for cognitive impairment or otherwise. At the end of the behavioural tests, brain tissues were collected for immunohistochemistry of amyloid beta and tau proteins.
In other batches, treatment was started at one month of age through drinking water and then behavioural testing took place at 6 months of age, 9 months and 12 months of age, respectively. In a final batch, the pharmacological models of AD, scopolamine and ketamine models, were also treated with the RV extract and assessed for motor and cognitive decline at 3 months, 6 months, 9 months and 12 months of age.
Mice were organized into various groups: Control (Sham untreated, n=12); Oxidative induced (using 3-nitropropionic acid (3NP), n=12); Scopolamine model group (scopolamine model of AD, n=12); Ketamin model group (Ketamine model of AD, n=12); and Beta ameloid models: ß25-35 peptide administered i.c.v. 3 nmol/mouse (n=12), ß25-35 peptide administered i.c.v. 9 nmol/mouse (n=12) and ß1-28 peptide administered i.c.v. 3 nmol/mouse(n=12). This animal grouping above is repeated but with treatment of R. vomitoria 8mg/kg and 16 mg/kg p.o.
Abstract of completed research: Analysis of the Potentials of Rauwolfia Vomitoria in prevention of cognitive decline in an oxidative stress mouse model of Alzheimer's Disease.
Oxidative stress (OS) is implicated in Alzheimer’s disease. This study investigated the effect of oxidative stress on some neurobehavioural parameters and the anti-oxidant effect of aqueous root bark extract of Rauwolfia vormitoria (RV) and Vitamin E (Vit E) in mice. Fifty mice (17-27g body weight) were grouped into five (n=10 each): Group 1 was control (0.9% saline orally for 21 days), groups 2, 3, 4 & 5 had 3-nitropropionic acid (3-NP; 15mg/kg i.p. for 4 days) to induce OS. Groups 3 received RV (20mg/kg p.o.), group 4 received Vitamin E (100iu/kg p.o.) and group 5 received both RV and Vitamin E for 21 days.
At the end of the treatment neurobehavioral test: Morris water maze (MWM), Beam walking, Open field maze (OF) and elevated plus maze (EPM) were completed. Blood samples were obtained at the end of the behavioural tests for antioxidant assay. The LD50 was 739.81mg/kg. Catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSHP) concentrations were high while malondialdehyde (MDA) was lower (p<0.001) after treatment with RV and Vit E compared to control. Antioxidant levels were thus higher following RV, Vit E treatment (p<0.001), with RV +Vit E being synergistic (p<0.05) in their antioxidant activity. In the MWM test, 3-NP impaired memory was shown in lower retention quadrants duration and annulus crossings (p<0.01). Treatment with RV, Vit E and RV+Vit E improved memory. The beam walking test showed increase distance travelled, reversal and lower frequency of foot slips in RV (p<0.01) and RV+Vit E groups (p<0.05) compared to control and 3-NP groups, indicating improved motor coordination. The EPM test showed decreased anxiety as seen in increased time in the open arms and decreased stretch attend postures (SAP) at p<0.05 following treatment with RV, Vit E and RV + Vit E. Therefore, RV reduced oxidative stress, improved memory, motor coordination and reduced anxiety.
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