Related Experiment Video

Updated: May 1, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
08:09

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

6.9K

The relationship between monoamine oxidase B (MAOB) A644G polymorphism and Parkinson disease risk: a meta-analysis

Ying Liu, Zhiyun Wang, Benshu Zhang1

  • 1Benshu Zhang, 153 Anshan Rd.,, Tianjin 30052, China, +86 022 23626407, drliuying@126.com.

Annals of Saudi Medicine
|March 25, 2014
PubMed
Abstract

Insights

The Monoamine oxidase B (MAOB) A644G polymorphism is linked to an increased risk of developing Parkinson disease (PD). This meta-analysis confirms a significant association, suggesting its role in PD development.

Area of Science:

  • Genetics
  • Neuroscience
  • Epidemiology

Background:

  • Parkinson disease (PD) is a neurodegenerative disorder with complex etiology.
  • The role of specific genetic polymorphisms, such as Monoamine oxidase B (MAOB) A644G, in PD susceptibility has been investigated.
  • Previous studies on the MAOB A644G polymorphism and PD risk yielded inconsistent results.

Purpose of the Study:

  • To conduct a comprehensive meta-analysis.
  • To assess the association between the MAOB A644G polymorphism and Parkinson disease risk.
  • To clarify the conflicting findings from individual studies.

Main Methods:

  • A systematic meta-analysis was performed on published case-control studies.
  • Studies published up to March 2013 were included.
  • Fixed-effects models were used to derive pooled odds ratios (OR) and 95% confidence intervals (CI).

Main Results:

  • Twenty studies comprising 2846 cases and 3508 controls were analyzed.
  • The MAOB A644G polymorphism showed a significant association with PD risk in a recessive model (OR=1.32, 95% CI 1.18-1.47).
  • Subgroup analyses by ethnicity and gender also indicated significant associations.

Conclusions:

  • The MAOB A644G polymorphism is suggested to be associated with the development of Parkinson disease.
  • This meta-analysis provides stronger evidence for the genetic contribution of MAOB A644G to PD.
  • Further research may explore the functional implications of this polymorphism in PD pathogenesis.

More Related Videos

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease15:09

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

16.2K
Targeted Next-generation Sequencing and Bioinformatics Pipeline to Evaluate Genetic Determinants of Constitutional Disease09:34

Targeted Next-generation Sequencing and Bioinformatics Pipeline to Evaluate Genetic Determinants of Constitutional Disease

Published on: April 4, 2018

36.1K

Related Concept Videos

Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of...
28
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
28
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
1.4K
Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
2.0K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
2.2K
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
159