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Brain Sciences
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Molecular Mechanism and Pathology of Parkinson's Disease
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Molecular Mechanism and Pathology of Parkinson's Disease

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (10 February 2024) | Viewed by 7093

Special Issue Editor

Dr. Mohammed Emdadul Haque

E-Mail Website
Guest Editor
College of Medicine and Health Sciences United Arab Emirates University, Al-Ain United Arab Emirates, United Arab Emirates
Interests: molecular mechanism of neurodegeneration; cellular function of genes associated with Parkinson’s disease; identification of drug targets to treat neurodegeneration

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the progressive loss of a very specific type of neurons in the substantia nigra area (SNc), resulting in the depletion of dopamine in the striatum. The vast majority of PD cases are sporadic. However, several familial forms of PD-associated genes have been identified, including Synuclein, Parkin, Pink1, DJ-1 and LRRK2. In addition to these genes, there are several other genes and regulatory elements that potentiate the risk of developing PD in certain individuals.

We invite investigators to contribute original research and review articles that will stimulate the continuing efforts to understand the molecular pathways underlying dopaminergic neurodegeneration in sporadic or familial PD and the development of strategy to treat these conditions. We are also interested in articles describing the new model systems that recapitulate PD pathology. We also invite articles that cover early detection strategies and biomarkers for PD and its future direction. Potential topics include, but are not limited to:

  • Recent developments of PD research—familial and sporadic cases;
  • Advances in genetics of PD;
  • Latest technologies for clinical evaluation and measuring outcomes;
  • Role of mitochondria in neuro-degeneration;
  • Gene delivery in PD research;
  • Stem cells in PD therapy;
  • Potential screening tools for detecting PD;
  • Potential diagnostic approaches for detecting PD;
  • Potential therapeutic modalities for prevention and treatment of PD.

Dr. Mohammed Emdadul Haque
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Parkinson’s disease
  • neurodegeneration
  • parkin
  • α-synuclein
  • lewy body

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Published Papers (3 papers)

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Research

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19 pages, 5627 KiB  
Article
Akkermansia muciniphila Is Beneficial to a Mouse Model of Parkinson’s Disease, via Alleviated Neuroinflammation and Promoted Neurogenesis, with Involvement of SCFAs
by Chen-Meng Qiao, Wen-Yan Huang, Yu Zhou, Wei Quan, Gu-Yu Niu, Ting Li, Mei-Xuan Zhang, Jian Wu, Li-Ping Zhao, Wei-Jiang Zhao, Chun Cui and Yan-Qin Shen
Brain Sci. 2024, 14(3), 238; https://doi.org/10.3390/brainsci14030238 - 29 Feb 2024
Cited by 5 | Viewed by 2016
Abstract
Increasing evidence suggests that the gut microbiota may represent potential strategies for Parkinson’s disease (PD) treatment. Our previous research revealed a decreased abundance of Akkermansia muciniphila (Akk) in PD mice; however, whether Akk is beneficial to PD is unknown. To answer this question, [...] Read more.
Increasing evidence suggests that the gut microbiota may represent potential strategies for Parkinson’s disease (PD) treatment. Our previous research revealed a decreased abundance of Akkermansia muciniphila (Akk) in PD mice; however, whether Akk is beneficial to PD is unknown. To answer this question, the mice received MPTP intraperitoneally to construct a subacute model of PD and were then supplemented with Akk orally for 21 consecutive days. Motor function, dopaminergic neurons, neuroinflammation, and neurogenesis were examined. In addition, intestinal inflammation, and serum and fecal short-chain fatty acids (SCFAs) analyses, were assessed. We found that Akk treatment effectively inhibited the reduction of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and partially improved the motor function in PD mice. Additionally, Akk markedly alleviated neuroinflammation in the striatum and hippocampus and promoted hippocampal neurogenesis. It also decreased the level of colon inflammation. Furthermore, these aforementioned changes are mainly accompanied by alterations in serum and fecal isovaleric acid levels, and lower intestinal permeability. Our research strongly suggests that Akk is a potential neuroprotective agent for PD therapy. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathology of Parkinson's Disease)
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10 pages, 9772 KiB  
Article
The Cannabigerol Derivative VCE-003.2 Exerts Therapeutic Effects in 6-Hydroxydopamine-Lesioned Mice: Comparison with The Classic Dopaminergic Replacement Therapy
by Santiago Rodríguez-Carreiro, Elisa Navarro, Eduardo Muñoz and Javier Fernández-Ruiz
Brain Sci. 2023, 13(9), 1272; https://doi.org/10.3390/brainsci13091272 - 31 Aug 2023
Cited by 2 | Viewed by 1309
Abstract
(1) Background: A cannabigerol aminoquinone derivative, so-called VCE-003.2, has been found to behave as a neuroprotective agent (administered both i.p. and orally) in different experimental models of Parkinson’s disease (PD) in mice. These effects were exerted through mechanisms that involved the activation of [...] Read more.
(1) Background: A cannabigerol aminoquinone derivative, so-called VCE-003.2, has been found to behave as a neuroprotective agent (administered both i.p. and orally) in different experimental models of Parkinson’s disease (PD) in mice. These effects were exerted through mechanisms that involved the activation of a regulatory site within the peroxisome proliferator-activated receptor-γ (PPAR-γ). (2) Methods: We are now interested in comparing such neuroprotective potential of VCE-003.2, orally administered, with the effect of the classic dopaminergic replacement therapy with L-DOPA/benserazide in similar conditions, using 6-hydroxydopamine-lesioned mice. (3) Results: The oral administration of VCE-003.2 during 14 days at the dose of 20 mg/kg improved, as expected, the neurological status (measured in motor tests) in these mice. This correlated with a preservation of TH-labelled neurons in the substantia nigra. By contrast, the treatment with L-DOPA/benserazide (during 7 days at 2 mg/kg) was significantly less active in these experimental conditions, in concordance with their profile as a mere symptom-alleviating agent. (4) Conclusions: Our results confirmed again the therapeutic profile of VCE-003.2 in experimental PD and revealed a different and more relevant effect, as a disease modifier, compared to the classic symptom-alleviating L-DOPA treatment. This reinforces the interest in VCE-003.2 for a future clinical development in this disease. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathology of Parkinson's Disease)
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Review

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15 pages, 5109 KiB  
Review
The Role of Calcium and Iron Homeostasis in Parkinson’s Disease
by Ji Wang, Jindong Zhao, Kunying Zhao, Shangpeng Wu, Xinglong Chen and Weiyan Hu
Brain Sci. 2024, 14(1), 88; https://doi.org/10.3390/brainsci14010088 - 17 Jan 2024
Cited by 3 | Viewed by 3262
Abstract
Calcium and iron are essential elements that regulate many important processes of eukaryotic cells. Failure to maintain homeostasis of calcium and iron causes cell dysfunction or even death. PD (Parkinson’s disease) is the second most common neurological disorder in humans, for which there [...] Read more.
Calcium and iron are essential elements that regulate many important processes of eukaryotic cells. Failure to maintain homeostasis of calcium and iron causes cell dysfunction or even death. PD (Parkinson’s disease) is the second most common neurological disorder in humans, for which there are currently no viable treatment options or effective strategies to cure and delay progression. Pathological hallmarks of PD, such as dopaminergic neuronal death and intracellular α-synuclein deposition, are closely involved in perturbations of iron and calcium homeostasis and accumulation. Here, we summarize the mechanisms by which Ca2+ signaling influences or promotes PD progression and the main mechanisms involved in ferroptosis in Parkinson’s disease. Understanding the mechanisms by which calcium and iron imbalances contribute to the progression of this disease is critical to developing effective treatments to combat this devastating neurological disorder. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathology of Parkinson's Disease)
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