Emerging role of Nrf2 in Parkinson’s disease therapy: a critical reassessment DOI
Veerta Sharma,

Prateek Sharma,

Thakur Gurjeet Singh

et al.

Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)

Published: Dec. 19, 2024

Language: Английский

The neuroprotective effects of ferulic acid in toxin-induced models of Parkinson's disease: A review DOI

Samira Hassani,

Abolghasem Esmaeili

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 97, P. 102299 - 102299

Published: April 9, 2024

Language: Английский

Citations

12

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease DOI Creative Commons
Érica Novaes Soares, Ana Carla dos Santos Costa,

Gabriel de Jesus Ferrolho

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(6), P. 474 - 474

Published: March 7, 2024

Parkinson’s disease (PD) is a progressive neurodegenerative characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) the primary neurotransmitter involved in this disease, but cholinergic imbalance has been implicated. Current intervention PD focused on replenishing central DA, which provides remarkable temporary symptomatic relief does not address neuronal loss progression of disease. It well established nicotinic receptors (nAChRs) can regulate DA release nicotine itself may have neuroprotective effects. Recent studies identified nAChRs nonneuronal cell types, including glial cells, where they inflammatory responses. Given crucial role neuroinflammation dopaminergic degeneration involvement microglia astrocytes response, provide novel therapeutic target prevention and/or treatment PD. In review, following brief discussion PD, we focus cells and, specifically, their pathology treatment.

Language: Английский

Citations

11

Flavonoids as Potential Therapeutics Against Neurodegenerative Disorders: Unlocking the Prospects DOI
Md. Faysal,

Zerrouki Dehbia,

Mehrukh Zehravi

et al.

Neurochemical Research, Journal Year: 2024, Volume and Issue: 49(8), P. 1926 - 1944

Published: June 1, 2024

Language: Английский

Citations

11

Single-neuron neurodegeneration as a degenerative model for Parkinson’s disease DOI Creative Commons
Sandro Huenchuguala, Juan Segura‐Aguilar

Neural Regeneration Research, Journal Year: 2023, Volume and Issue: 19(3), P. 529 - 535

Published: July 28, 2023

Abstract The positive effect of levodopa in the treatment Parkinson’s disease, although it is limited time and has severe side effects, encouraged scientific community to look for new drugs that can stop neurodegenerative process or even regenerate neuromelanin-containing dopaminergic nigrostriatal neurons. Successful preclinical studies with coenzyme Q10, mitoquinone, isradipine, nilotinib, TCH346, neurturin, zonisamide, deferiprone, prasinezumab, cinpanemab prompted clinical trials. However, these failed after more than 50 years continues be key drug despite its effects 4–6 chronic treatment. lack translated successful results obtained investigations based on use neurotoxins do not exist human body as disease a big problem. In our opinion, cause failures lies experimental animal models involving body, such 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine 6-hydroxydopamine, induce very fast, massive expansive process, which contrasts extremely slow one exceedingly progress neurons idiopathic patients due (i) degenerative model neurotoxic an endogenous neurotoxin affects single neuron, (ii) event (iii) fact triggers produced inside fits this neuron at aminochrome, since generated within neurons, does all mechanisms involved disease. conclusion, hypothesis corresponds single-neuron neurodegeneration model, we must search molecules increase expression neuroprotective enzymes DT-diaphorase glutathione transferase M2-2. It been observed activation Kelch-like ECH-associated protein 1/nuclear factor (erythroid-derived 2)-like 2 pathway associated transcriptional genes.

Language: Английский

Citations

18

Advances in animal models of Parkinson's disease DOI Creative Commons

He Sui,

Qin Ru, Lin Chen

et al.

Brain Research Bulletin, Journal Year: 2024, Volume and Issue: 215, P. 111024 - 111024

Published: July 4, 2024

Parkinson's disease is a complex neurodegenerative characterized by progressive movement impairments. Predominant symptoms encompass resting tremor, bradykinesia, limb rigidity, and postural instability. In addition, it also includes series of non-motor such as sleep disorders, hyposmia, gastrointestinal dysfunction, autonomic dysfunction cognitive impairment. Pathologically, the manifests through dopaminergic neuronal loss presence Lewy bodies. At present, no significant breakthrough has been achieved in clinical treatment. Exploring treatment modalities necessitate establishment scientifically sound animal models. recent years, researchers have focused on replicating human disease, resulting various experimental models primarily drugs transgenic methods to mimic relevant pathologies identify more effective treatments. This review examines traditional neurotoxin well α-synuclein pre-formed fibrils models, non-human primate non-mammalian specie Additionally, introduces emerging including based optogenetics, induced pluripotent stem cells, gene editing, aiming provide reference for utilization research this field.

Language: Английский

Citations

9

Targets to Search for New Pharmacological Treatment in Idiopathic Parkinson’s Disease According to the Single-Neuron Degeneration Model DOI Creative Commons
Sandro Huenchuguala, Juan Segura‐Aguilar

Biomolecules, Journal Year: 2024, Volume and Issue: 14(6), P. 673 - 673

Published: June 8, 2024

One of the biggest problems in treatment idiopathic Parkinson’s disease is lack new drugs that slow its progression. L-Dopa remains star drug this disease, although it induces severe side effects. The failure clinical studies with depends on use preclinical models based neurotoxins do not represent what happens since they induce rapid and expansive neurodegeneration. We have recently proposed a single-neuron degeneration model for requires years to accumulate enough lost neurons onset motor symptoms. This excessive formation aminochrome during neuromelanin synthesis surpass neuroprotective action enzymes DT-diaphorase glutathione transferase M2-2, which prevent neurotoxic effects aminochrome. Although an effect, stereotaxic injection endogenous neurotoxin cannot be used generate animal. Therefore, aim review evaluate strategies pharmacologically increasing expression DT diaphorase GSTM2-2 molecules vesicular monoamine transporter 2, such as pramipexole.

Language: Английский

Citations

7

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease DOI Open Access
Érica Novaes Soares, Ana Carla dos Santos Costa,

Gabriel de Jesus Ferrolho

et al.

Published: Jan. 31, 2024

Parkinson’s disease (PD) is a progressive neurodegenerative characterized by resting tremor, bradykinesia, rigidity, postural instability, that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) the primary neurotransmitter involved in this disease, but cholinergic imbalance has been implicated. Current intervention PD focused on replenishing central DA, which provides remarkable temporary symptomatic relief does not address neuronal losss and progression of disease. It well established nicotinic receptors (nAChRs) can regulate DA release nicotine itself may have neuroprotective effects. Recent studies identified nAChRs nonneuronal cell types including glial cells, where they inflammatory responses. Given crucial role neuroinflammation dopaminergic degeneration, involvement microglia astrocytes response, provide novel therapeutic target prevention and/or treatment PD. In review, following brief discussion PD, we focus cells specifically their pathology treatment.

Language: Английский

Citations

5

To what extent may aminochrome increase the vulnerability of dopaminergic neurons in the context of Parkinson's disease DOI Creative Commons
Abdeslam Chagraoui, Youssef Anouar, Philippe De Deurwaerdère

et al.

The International Journal of Biochemistry & Cell Biology, Journal Year: 2024, Volume and Issue: 168, P. 106528 - 106528

Published: Jan. 19, 2024

Language: Английский

Citations

4

Biofilm proficient Bacillus subtilis prevents neurodegeneration in Caenorhabditis elegans Parkinson’s disease models via PMK-1/p38 MAPK and SKN-1/Nrf2 signaling DOI Creative Commons

Marcos Francisco,

Roberto Grau

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: March 21, 2025

Parkinson's disease (PD) is a no-curable neurodegenerative of pandemic distribution for which only palliative treatments are available. A hallmark PD injury to dopaminergic neurons in the substantia nigra pars compacta. Here, we report that Caenorhabditis elegans colonized by biofilm-forming Bacillus subtilis resistant caused treatment with PD-related neurotoxin 6-hydroxydopamine (6-OHDA). Biofilm-forming B. subtilis-colonized C. display dopamine-dependent behaviors indistinguishable from those 6-OHDA-untreated worms gut commensal E. coli OP50. In model strains early neuron decay or overexpressing human alpha-synuclein, colonization had neuroprotective effects and prevents alpha-synulcein aggregation, respectively. The subtilis-controlled insulin/IGF-1 signaling (ILS), whose downregulation aging-related PD, not involved protecting against 6-OHDA-related injury. We demonstrate activates PMK-1 (p38 MAPK)/SKN-1 (Nrf2) signaling, protects 6-OHDA-induced

Language: Английский

Citations

0

Molecular Mechanisms of Ferroptosis and Their Involvement in Acute Kidney Injury DOI Creative Commons
Jie Liu, Xiao Han, Jia Zu Zhou

et al.

Journal of Inflammation Research, Journal Year: 2023, Volume and Issue: Volume 16, P. 4941 - 4951

Published: Nov. 1, 2023

Abstract: Ferroptosis is a novel way of regulating cell death, which occurs in process that closely linked to intracellular iron metabolism, lipid amino acid and multiple signaling pathways. The latest research shows ferroptosis plays key role the pathogenesis acute kidney injury (AKI). may be an important target for treating AKI caused by various reasons, such as ischemia-reperfusion injury, rhabdomyolysis syndrome, sepsis, nephrotoxic drugs. This paper provides review on regulatory mechanisms its AKI, help provide new ideas treatment future research. Keywords: ferroptosis, iron, peroxidation, molecular mechanism,

Language: Английский

Citations

7