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Handley, R.R., Reid, S.J., Brauning, R., Maclean, P., Mears, E.R., Fourie, I., Patassini, S., Cooper, G.J.S., Rudiger, S.R., McLaughlan, C.J., Verma, P.J., Gusella, J.F., MacDonald, M.E., Waldvogel, H.J., Bawden, C.S., Faull, R.L.M. and Snell, R.G. (2017) Brain Urea Increase Is an Early Huntington’s Disease Pathogenic Event Observed in a Prodromal Transgenic Sheep Model and HD Cases. Proceedings of the National Academy of Sciences of the United States of America, 114, E11293-E11302.
https://doi.org/10.1073/pnas.1711243115
has been cited by the following article:
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TITLE:
Studies on Parkinson’s-Disease-Linked Genes, Brain Urea Levels and Histopathology in Rotenone Induced Parkinson’s Disease Rat Model
AUTHORS:
Suchitra Kavuri, Senthilkumar Sivanesan, Mathew D. Howell, Rajagopalan Vijayaraghavan, Jayakumar Rajadas
KEYWORDS:
Parkinson’s Disease, Rotenone Intraperitoneal and Oral, Brain Urea, Al-pha-Synuclein, Beclin-1, AMP-Activated Protein Kinase, Brain and Liver Pa-thology
JOURNAL NAME:
World Journal of Neuroscience,
Vol.10 No.4,
November
27,
2020
ABSTRACT: Parkinson’s disease (PD) is a debilitating neurological disorder that
affects the aged population globally. This
study aimed to explore how oral- and intraperitoneal-rotenone-induced PD
alters brain urea levels, histopathology, and key Parkinsonism-related genes in the striatum. Hematoxylin and
eosin staining was performed for histopathology assessment and real-time
polymerase chain reaction was performed for gene expression. Rotenone 3 mg/kg
body weight (Rot-3-ip) for 21 days and rotenone 50 mg/kg body weight
(Rot-50-po) for 28 days significantly (p Snca, Becn1 and Prkaa1 gene expression in the striatum. Lewy bodies were visible in
both Rot-3-ip and Rot-50-po rat brains. There were contrasting features in brain and liver
histopathology between the oral and intraperitoneal rotenone treatment groups. However, there was no significant (p
can have different impacts on the pathological sequence of events based
on the molecular approach.