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Research in Parkinson's Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 4829

Special Issue Editor


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Guest Editor
Department of Neuroscience, San Raffaele Scientific Institute, Lombardy, Italy
Interests: Parkinson's disease; neurodegeneration; neurodegenerative diseases

Special Issue Information

Dear Colleague,

In recent years, therapeutic strategies for Parkinson’s disease (PD) have been developing in many different ways. In addition to the medication, surgery, rehabilitation, and other established therapies, various options with cell therapy and neurotrophic agents and so on are becoming a reality. The pathological condition of PD, animal model making, mechanisms to progress disease status, and mechanisms of therapeutic effects of each treatment are revealed synergistically. In this Special Issue, we are seeking novel research and/or review articles on:

  1. the pathological condition and disease progression of PD;
  2. the advancement of PD model animals;
  3. recent therapeutic strategy;
  4. mechanisms of therapeutic effects, and;
  5. attempts to overcome PD-associated complications, such as lumbago, abnormal posture, vesicorectal disorders, and psychological problems.

In this issue, we will overview the current status of PD treatment and neurobiology research to progress the clarification of the mechanisms of PD pathology and treatment.

Dr. Simone Bido
Guest Editor

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Keywords

  • abnormal posture
  • cell therapy
  • cerebral blood flow
  • dopamine
  • electrical stimulation
  • intractable pain, mitochondria
  • neuroprotection
  • neurotrophic factor
  • psychological disorders
  • rehabilitation
  • spinaal cord stimulation
  • spinal diseases
  • vagal nerve stimulation
  • vesicorectal disorder

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Published Papers (1 paper)

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Research

19 pages, 4883 KiB  
Article
Neuroprotective Effects of the DPP4 Inhibitor Vildagliptin in In Vivo and In Vitro Models of Parkinson’s Disease
by Ramesh Pariyar, Tonking Bastola, Dae Ho Lee and Jungwon Seo
Int. J. Mol. Sci. 2022, 23(4), 2388; https://doi.org/10.3390/ijms23042388 - 21 Feb 2022
Cited by 22 | Viewed by 4237
Abstract
Parkinson’s disease (PD) is characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Restoration of nigrostriatal dopamine neurons has been proposed as a potential therapeutic strategy for PD. Because currently used PD therapeutics only help relieve [...] Read more.
Parkinson’s disease (PD) is characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Restoration of nigrostriatal dopamine neurons has been proposed as a potential therapeutic strategy for PD. Because currently used PD therapeutics only help relieve motor symptoms and do not treat the cause of the disease, highly effective drugs are needed. Vildagliptin, a dipeptidyl peptidase 4 (DPP4) inhibitor, is an anti-diabetic drug with various pharmacological properties including neuroprotective effects. However, the detailed effects of vildagliptin against PD are not fully understood. We investigated the effects of vildagliptin on PD and its underlying molecular mechanisms using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model and a 1-methyl-4-phenylpyridium (MPP+)-induced cytotoxicity model. Vildagliptin (50 mg/kg) administration significantly attenuated MPTP-induced motor deficits as evidenced by rotarod, pole, and nest building tests. Immunohistochemistry and Western blot analysis revealed that vildagliptin increased tyrosine hydroxylase-positive cells in the SNpc and striatum, which was reduced by MPTP treatment. Furthermore, vildagliptin activated MPTP-decreased PI3k/Akt and mitigated MPTP-increased ERK and JNK signaling pathways in the striatum. Consistent with signaling transduction in the mouse striatum, vildagliptin reversed MPP+-induced dephosphorylation of PI3K/Akt and phosphorylation of ERK and JNK in SH-SY5Y cells. Moreover, vildagliptin attenuated MPP+-induced conversion of LC3B-II in SH-SY5Y cells, suggesting its role in autophagy inhibition. Taken together, these findings indicate that vildagliptin has protective effects against MPTP-induced motor dysfunction by inhibiting dopaminergic neuronal apoptosis, which is associated with regulation of PI3k/Akt, ERK, and JNK signaling transduction. Our findings suggest vildagliptin as a promising repurposing drug to treat PD. Full article
(This article belongs to the Special Issue Research in Parkinson's Disease)
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