Association between MDR1 gene polymorphisms and Parkinson's disease in Asian and Caucasian populations: a meta-analysis

Ahmed, Shiek S. S. J.; Husain, Rahat; Kumar, Suresh; Veerabathiran, Ramakrishnan

doi:10.1016/j.jns.2016.07.041

Cited by 29 publications

(11 citation statements)

References 38 publications

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“…SLC6A3 is a genetic modifier of the treatment response to l -DOPA in PD [97]. The multidrug resistance gene ( MDR1 ) C1236T polymorphism may also influence PD pharmacotherapy [98] as well as SNPs in genes encoding the dopamine transporter (DAT; SLC6A3) and the vesicular monoamine transporter 2 (VMAT2; SLC18A2) [99]. Consequently, the personalized treatment of PD patients requires the implementation of pharmacogenetic procedures in order to optimize therapeutics (improving efficacy and safety) [9].…”

Section: Pharmacogenomicsmentioning

confidence: 99%

Parkinson’s Disease: From Pathogenesis to Pharmacogenomics

Cacabelos

2017

IJMS

451

300

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Parkinson’s disease (PD) is the second most important age-related neurodegenerative disorder in developed societies, after Alzheimer’s disease, with a prevalence ranging from 41 per 100,000 in the fourth decade of life to over 1900 per 100,000 in people over 80 years of age. As a movement disorder, the PD phenotype is characterized by rigidity, resting tremor, and bradykinesia. Parkinson’s disease -related neurodegeneration is likely to occur several decades before the onset of the motor symptoms. Potential risk factors include environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular damage, and genomic defects. Parkinson’s disease neuropathology is characterized by a selective loss of dopaminergic neurons in the substantia nigra pars compacta, with widespread involvement of other central nervous system (CNS) structures and peripheral tissues. Pathogenic mechanisms associated with genomic, epigenetic and environmental factors lead to conformational changes and deposits of key proteins due to abnormalities in the ubiquitin–proteasome system together with dysregulation of mitochondrial function and oxidative stress. Conventional pharmacological treatments for PD are dopamine precursors (levodopa, l-DOPA, l-3,4 dihidroxifenilalanina), and other symptomatic treatments including dopamine agonists (amantadine, apomorphine, bromocriptine, cabergoline, lisuride, pergolide, pramipexole, ropinirole, rotigotine), monoamine oxidase (MAO) inhibitors (selegiline, rasagiline), and catechol-O-methyltransferase (COMT) inhibitors (entacapone, tolcapone). The chronic administration of antiparkinsonian drugs currently induces the “wearing-off phenomenon”, with additional psychomotor and autonomic complications. In order to minimize these clinical complications, novel compounds have been developed. Novel drugs and bioproducts for the treatment of PD should address dopaminergic neuroprotection to reduce premature neurodegeneration in addition to enhancing dopaminergic neurotransmission. Since biochemical changes and therapeutic outcomes are highly dependent upon the genomic profiles of PD patients, personalized treatments should rely on pharmacogenetic procedures to optimize therapeutics.

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Section: Pharmacogenomicsmentioning

confidence: 99%

Parkinson’s Disease: From Pathogenesis to Pharmacogenomics

Cacabelos

2017

IJMS

451

300

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“…To define the relationship between selected SNP (rs1800629) predispositions with Mg risk, this case-control study was performed with participants from the south Indian population. To acquire more strong and conclusive results, we additionally executed a meta-analysis from Asian and Caucasian ethnic background by considering the available studies on the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) [12].…”

Section: Introductionmentioning

confidence: 99%

Genetic predisposition of TNFα gene polymorphism in South-Indian Migraineurs and meta-analysis

Kesavan,

Satheesh,

Husain

et al. 2021

Front. Biosci. (Elite Ed)

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Introduction 3. Methodology 3.1 Stage 1: case-control study 3.2 Meta-analysis 4. Results 4.1 Geographical attribute 4.2 Genotypic frequencies of rs1800629 SNP among South-Indian Migraineurs 4.3 Literature search and study characteristics 4.4 Meta-analysis of rs1800629 polymorphism with Mg risk 5. Discussion 6. Conclusions 7. Author contributions 8. Ethics approval and consent to participate 9. Acknowledgment 10. Funding 11. Conflict of interest 12. References

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“…1D) that we were able to reveal is consistent with elevated ceramide glucosyltransferase activity. This gene has been suggested as an overlap between immune system neutrophil lipid regulation and neural glial regulation [14,21], and linked with a multidrug resistance protein [29], a gene known and described to have a role in Parkinson's disease [1]. Elevated 2-hydroxy ceramide at day 8 could be related to the neurological injury noted in the patient as 2-hydroxy ceramide is known to be critical for myelin sheath stability of oligodendrocytes [30].…”

Section: Discussionmentioning

confidence: 99%

Multi-Omic integration after carbon monoxide toxicity in a child reveals gene transcripts related to Parkinson and Multiple Sclerosis

Leimanis-Laurens

Prokop

Nedveck

et al. 2020

Preprint

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Background This report highlights the unique transcriptomic and lipidomic changes noted in a 4-year-old African American female patient exposed to a house fire. She required admission to the pediatric Intensive care unit due to organ failure that resulted from CO and cyanide toxicity. Patient was neurologically intact initially but later developed neurological symptoms consistent with Parkinsonism, a transient state resembling Parkinson’s Disease. Results An integrative omics-based approach was used to examine both gene expression and the lipidome of the patient which was then compared to 4 control patients. Total blood RNA from a PaxGene®collection system was correlated to plasma-based metabolomics measured over three time points and correlated with the clinical condition of the patient. We see significant elevation of the Parkinson’s associated gene ( SELENOT ) on day one. This gene plays a crucial role in the protection of dopaminergic neurons against oxidative stress in Parkinson's disease. The Multiple Sclerosis linked gene DDX39B which mediates ATP hydrolysis during pre-mRNA splicing was increased on day 8. We noted increased UGCG gene expression which correlated with increased ceramide lipids on lipidome analysis. The elevated ratio of hexosylceramide to its ceramide precursor is indicative of an elevated UGCG mediated ceramide glucosyltransferase activity. This correlation of clinical symptoms with both increased gene activity and lipid dyshomeostasis is unique, highlighting the potential of personalized omics. ConclusionsIn clinical practice, the ability to predict and quantify neurological injury using gene expression has the potential to make meaningful changes to management. This report shows the potential for real time transcriptomics and metabolomics to modify not only initial therapy, but the eventual physical rehabilitation of patients exposed to neurotoxins.

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Association between MDR1 gene polymorphisms and Parkinson's disease in Asian and Caucasian populations: a meta-analysis

Cited by 29 publications

References 38 publications

Parkinson’s Disease: From Pathogenesis to Pharmacogenomics

Parkinson’s Disease: From Pathogenesis to Pharmacogenomics

Genetic predisposition of TNFα gene polymorphism in South-Indian Migraineurs and meta-analysis

Multi-Omic integration after carbon monoxide toxicity in a child reveals gene transcripts related to Parkinson and Multiple Sclerosis

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