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Full-Text Articles in Medicine and Health Sciences
Effects Of A Unilateral Injection Of Botulinum Neurotoxin Subtype-A In The Subthalamic Nucleus Of A Parkinsonian Rat Model, Olga Khazov
Electronic Thesis and Dissertation Repository
Dopaminergic degeneration in Parkinson’s disease (PD) leads to altered functional activity within the basal ganglia (BG) circuitry, including hyperactivity of the subthalamic nucleus (STN). Treatments restoring the BG functional circuitry often result in improvements in parkinsonian symptoms in patients and animal models. A recent study from our laboratory identified that infusing botulinum toxin (BoNT-A) into the internal globus pallidus provided a transient restoration of motor asymmetry and goal-directed locomotion in a rat model of PD. We hypothesized that infusions of BoNT-A into the STN in a parkinsonian rat model will improve motor asymmetry and locomotor abnormalities. Infusions of BoNT-A into …
A Synthetic Agonist To Vasoactive Intestinal Peptide Receptor-2 Induces Regulatory T Cell Neuroprotective Activities In Models Of Parkinson's Disease, R. Lee Mosley, Yaman Lu, Katherine E. Olson, Jatin Machhi, Wenhui Yan, Krista L. Namminga, Jenell R. Smith, Scott J. Shandler, Howard Gendelman
A Synthetic Agonist To Vasoactive Intestinal Peptide Receptor-2 Induces Regulatory T Cell Neuroprotective Activities In Models Of Parkinson's Disease, R. Lee Mosley, Yaman Lu, Katherine E. Olson, Jatin Machhi, Wenhui Yan, Krista L. Namminga, Jenell R. Smith, Scott J. Shandler, Howard Gendelman
Journal Articles: Pharmacology & Experimental Neuroscience
A paradigm shift has emerged in Parkinson's disease (PD) highlighting the prominent role of CD4+ Tregs in pathogenesis and treatment. Bench to bedside research, conducted by others and our own laboratories, advanced a neuroprotective role for Tregs making pharmacologic transformation of immediate need. Herein, a vasoactive intestinal peptide receptor-2 (VIPR2) peptide agonist, LBT-3627, was developed as a neuroprotectant for PD-associated dopaminergic neurodegeneration. Employing both 6-hydroxydopamine (6-OHDA) and α-synuclein (α-Syn) overexpression models in rats, the sequential administration of LBT-3627 increased Treg activity without altering cell numbers both in naïve animals and during progressive nigrostriatal degeneration. LBT-3627 administration was linked to …