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Parkinson's Disease - Wiley Online Library

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Last Updated: 27 April 2022

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The understanding of Parkinson's disease through genetics and new therapies

Introduction Parkinson's disease is one of the most progressive neurodegenerative disorders that people suffer from for years. Although Lewy bodies are also present, the underlying cause of this disease is linked to a decrease in the number of dopaminergic neurons in the substantia n. . . . . This article examines both the origins, mechanism, and causes of Parkinson's disease in addition to new therapies for the disease prevention.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/brb3.2577


Role of upregulation of the KATP channel subunit SUR1 in dopaminergic neuron degeneration in Parkinson’s disease

In addition, the expression of the KATP channel subunit sulfonylurea receptor 1 is increased in Parkinson's disease's remaining n. . . . l dopaminergic neurons. The development of dopaminergic neuron degeneration was postponed due to interference with SUR1 expression by injection of lentivirus into the SN. In SynA53T+/+ mice, elevated expression of transcription factors FOXA1 and FOXA2 showed that elevated expression of transcription factors FOXA1 and FOXA2 might lead to the SUR1 subunit's upregulation. Our research revealed the SUR1 subunit's regulatory mechanism and the role of KATP channels in dopaminergic neuron degeneration, establishing a new target for PD drug therapy.

Source link: https://onlinelibrary.wiley.com/doi/10.1111/acel.13618


Engineered Exosomes with Independent Module/Cascading Function for the Therapy of Parkinson's Disease by Multi‐Step Targeting and Multi‐Stage Intervention Method

Exosome morphology and membrane damage are common in modern exosome engineering techniques, which are unable to adequately address disease treatment's diverse requirements. To build an engineered exosome nano-therapy platform with separate artificial module and natural module, herein, a scheme of "independence module/cascading function" is suggested. The first synthesized artificial module with movement/chemotaxis function is synthesized, and then it is controllably integrated with the natural exosome module in “one by one” mode using a "differentiated" conversion scheme.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/adma.202201406


Protective effect of Cistanoside A on dopaminergic neurons in Parkinson's disease via mitophagy

In the substantia n. . . . compacta, one of Parkinson's disease's most notable pathological signs is the absence of dopaminergic neurons. In the present study, an MPTP-stimulated mouse model of PD and MPP+ treatment PD model in a MES23. 5 neuronal cell model of PD was used to investigate the neuroprotective effects of CA on PD and its potential mechanism. CA improved mouse motor function and increased the number of tyrosine hydroxylase positive cells in SNc, according to the in vivo experiment findings.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/bab.2350


Neurophysiological mechanisms of gait disturbance in advanced Parkinson’s disease patients

This study explores the pathophysiologic causes of Parkinson's disease-related mobility in posture gait disturbances. According to musculoskeletal disorders, posturegait disorders contribute to the dysfunction of the entire neuraxis in comparison to the musculoskeletal system. Despite this, the impairment of these devices in PD could significantly undermine the ability to adapt and result in misadaptive changes in impairing posturegait control. The leading cause of PD is a deterioration of dopamine neurons. Inadequate DA supply in the striatum hinders the operation of intrinsic networks in the BG. GABAergic BG production to the cerebral cortex and brainstem also increases GABAergic BG production, resulting in functional disconnection of other structures from the BG. Patients with PD are unable to achieve habitually acquired automatized gait control due to the disconnection. In addition, Lewy body degeneration in most brain areas, particularly in cholinergic and other monoaminergic systems susceptible to neurodegeneration, can cause more disturbed posture control and alters non-motor symptoms of PD.

Source link: https://onlinelibrary.wiley.com/doi/10.1111/ncn3.12605


Regulation of Cdc42 signaling by the dopamine D2 receptor in a mouse model of Parkinson’s disease

The calcium putamen mainly contains MSNs that have the dopamine D1 receptor and the dopamine D2 receptor, which have both had significant effects on motor and cognition behavior. Nonetheless, the molecular mechanisms underlying spine loss and unusual behavior in dMSNs and iMSNs under parkinsonian condition are uncertain. Cell division control protein 42 signaling was significantly reduced in the caudate putamen in parkinsonian mice, according to the present study. We found that such a decrease under parkinsonian state was further reduced by conditional knockout of the D2R but not D1R. In addition, the thin spine loss in iMSNs and motor coordination and cognition that resulted from conditional D2R's conditional knockout of D2R were reversed by overexpression of constitutively active Cdc42 in the CPu. Overall, our findings show that poor Cdc42 signaling regulated by D2R plays a significant role in spine damage and behavioural abnormalities in PD.

Source link: https://onlinelibrary.wiley.com/doi/10.1111/acel.13588


Disrupted myelination network in the cingulate cortex of Parkinson's disease

Parkinson's disease's cognitive impairment has been shown by accumulating evidence that the cingulate cortex plays a significant role in cognitive impairment of Parkinson's disease. However, mechanistic studies of the cingulate cortex in PD pathogenesis are limited. Myelin genes and the oligodendrocyte transcription pathways were strongly downregulated, suggesting disturbed myelination in PD cingulate cortex. Myelinating oligodendrocytes were the primary cell type damaged in the PD cingulate cortex, according to cell type specific signatures. In addition, downregulation of myelination pathways in the cingulate cortex was presented and verified in another independent RNAseq cohort of dementia with Lewy bodies. Gene regulatory networks were further developed for 32 transcription factors and 466 target genes among differentially expressed genes using a tree-based machine learning algorithm, in conjunction with ATACseq results. In addition, the researchers have established a subset of DEGs by qPCRs in two PD mouse models.

Source link: https://onlinelibrary.wiley.com/doi/10.1049/syb2.12043


Parkinson's disease motor symptoms rescue by CRISPRa‐reprogramming astrocytes into GABAergic neurons

Abstract reprogramming based on genetic factors appears to be a promising approach to replace deficient cells in degenerative disorders such as Parkinson's disease. Both approaches were successful in reprogramming striatal astrocytes into triggered GABAergic neurons, according to single-cell transcriptome analysis of reprogrammed neurons in vivo. These GABAergic neurons integrate into striatal circuits, enhancing voluntary motor behavior aspects in a 6-OHDA Parkinson's disease model. Thus, the AAVdCAS scheme may lead to an alternative route for medical therapy of Parkinson's disease.

Source link: https://onlinelibrary.wiley.com/doi/10.15252/emmm.202114797


Synthesis of Evodileptin B, a Natural Anthranilate Derivative Isolated from Evodia lepta, and Evaluation of Its Therapeutic Potential against Parkinson's Disease

Evodileptin B is a natural anthranilate derivative isolated from the ethanol extract of Evodia lepta Merr. , a traditional medicinal plant of the family Rutaceae. The results revealed that evodilin B ameliorated MPP+-induced dopaminergic neurodegeneration in a dose-dependent manner. While not intended for the functional restoration of DA neurons, Evodileptin B therapy also significantly improved the DA neurotransmission-related behavioral abnormalities such as reduced locomotory and food sensing capability of worms under MPP+ exposure conditions, suggesting its potential use for the functional restoration of DA neurons.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/cbdv.202100808

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions