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Related Experiment Video

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

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Gene-environment interaction in Alzheimer's disease.

Neeraj Kumar Singh¹, Neelam Chhillar, B D Banerjee

¹Department of Neurochemistry, Institute of Human Behaviour and Allied Sciences, Dilshad Garden, Delhi, India.

American Journal of Alzheimer'S Disease and Other Dementias

|August 21, 2012

Summary

Gene-environment interactions involving APOE ε4, lipids, and pesticides are crucial for Alzheimer's disease (AD) risk. These factors, including cholesterol and organochlorine pesticides, contribute to AD independently of APOE ε4 status.

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Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Published on: November 14, 2017

Area of Science:

Neuroscience
Genetics
Environmental Health

Background:

Alzheimer's disease (AD) etiology is complex, involving genetic and environmental factors.
The apolipoprotein E (APOE) ε4 allele is a known genetic risk factor for AD.
Gene-environment (GxE) interactions may play a significant role in AD pathogenesis.

Purpose of the Study:

To investigate GxE interactions in Alzheimer's disease.
To examine the roles of APOE genotypes, serum lipids, and organochlorine pesticides (OCPs) in AD etiology.
To determine if OCPs and lipids modify AD risk in the presence of APOE ε4.

Main Methods:

A case-control study design was employed.
APOE HhaI polymorphism was analyzed using PCR/PCR-RFLP.
Serum lipids and OCPs were quantified using autoanalyzer and gas chromatography (GC), respectively.

Main Results:

APOE ε4 allele frequency was significantly higher in AD cases compared to controls (p=0.000, OR=5.73).
Serum cholesterol, β-hexachlorocyclohexane, and dieldrin were identified as independent risk factors for AD.
Odds ratios for cholesterol, β-hexachlorocyclohexane, and dieldrin were 1.16, 11.38, and 10.45, respectively.

Conclusions:

GxE interactions are relevant to APOE ε4 allele status in Alzheimer's disease.
Environmental factors like OCPs and lipids contribute to AD risk, independent of APOE ε4.
Future AD research designs and analyses should account for GxE interactions.