Annals of Indian Academy of Neurology
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ORIGINAL ARTICLE
Year : 2015  |  Volume : 18  |  Issue : 3  |  Page : 320-326

Effect of apolipoprotein E (APO E) polymorphism on leptin in Alzheimer's disease


1 Department of Neurochemistry, Institute of Human Behaviour and Allied Sciences, Delhi, India
2 Genetics and Molecular Medicine, Institute of Genomics and Integrated Biology, Delhi, India
3 Department of Neurology, Institute of Human Behaviour and Allied Sciences, Delhi, India
4 Department of Biostatistics, Institute of Human Behaviour and Allied Sciences, Delhi, India

Correspondence Address:
Rachna Agarwal
Department of Neurochemistry, Institute of Human Behaviour and Allied Sciences, Dilshad Garden, Delhi - 110 095
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.157255

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Background: Leptin, a 16 kDa peptide hormone synthesized and secreted specifically from white adipose cells protects neurons against amyloid β-induced toxicity, by increasing Apolipoprotein E (APO E)-dependent uptake of β amyloid into the cells, thereby, protect individuals from developing Alzheimer's disease (AD). The APO E ε4 allele is a known genetic risk factor for AD by accelerating onset. It is estimated that the lifetime risk of developing AD increases to 29% for carriers with one ε4 allele and 9% for those with no ε4 allele. Objectives: To determine the levels of serum leptin, cholesterol, low density lipoprotein (LDL-C), and high density lipoprotein (HDL-C) in the diagnosed cases of AD and the association of them with cognitive decline and Apolipoprotein E (APO E) genotypes in AD. Materials and Methods: Serum levels of serum leptin, cholesterol, LDL-C, and HDL-C along with APO E polymorphism were studied in 39 subjects with probable AD and 42 cognitive normal individuals. Results: AD group showed significantly lower levels of leptin (P = 0.00) as compared to control group. However, there was no significant difference in cholesterol, triglycerides, LDL-C, and HDL-C levels in AD and control groups. The frequency of ε4 allele in AD (38.5%) was found to be significantly higher than in control (10.3%). ε3 allele was more frequent than ε4 allele in AD and control group.


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