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Test Code (รหัสการทดสอบ):
092-10-0086

Order Name (ชื่อการทดสอบ):
APOE Alzheimer and Cardio report (WES add-on panel)

 
Specimen / Container (สิ่งส่งตรวจ/ภาชนะ):
Specimen: Not required

Document required: Consent for Genomic Medicine Testing
 
Turnaround Time (ระยะเวลารอผล):
Report within 2 weeks
 
Useful For (ประโยชน์การทดสอบ):
Healthy people who are interested to know about the risk of APOE gene for developing Alzheimer's and Cardiovascular Disease.
 
Methodology (วิธีการทดสอบ):
Data analysis using Whole Exome Sequencing (WES) data
 
Test List In Profile (การทดสอบใน Profile):
APOE Alzheimer and Cardio report
 
AliasesName (ชื่อเรียกอื่นๆ) :
whole exome sequencing, WES, APOE, Alzheimer, Cardio
 
 
 
Test Code (รหัสการทดสอบ):
092-10-0086

Order Name (ชื่อการทดสอบ):
APOE Alzheimer and Cardio report (WES add-on panel)

 
Patient Preparation (การเตรียมตัวผู้ป่วย):
Patient must has Whole exome sequencing (WES) before order this test
 
Collection Specimen Or Container (สิ่งส่งตรวจ/ภาชนะ):
Specimen: Not required

Document required: Consent for Genomic Medicine Testing
 
Specimen Testing Type (สิ่งส่งตรวจที่ใช้ในการทดสอบ):
Not required
 
Sub Mission Container (ภาชนะส่งตรวจ):
N/A
 
 
 
Test Code (รหัสการทดสอบ):
092-10-0086

Order Name (ชื่อการทดสอบ):
APOE Alzheimer and Cardio report (WES add-on panel)

 
Turnaround Time (ระยะเวลารอผล):
Report within 2 weeks
 
Performing Location (หน่วยงานที่ทำการทดสอบ):
Research and Development laboratory, Tel 14152
 
 
 
Test Code (รหัสการทดสอบ):
092-10-0086

Order Name (ชื่อการทดสอบ):
APOE Alzheimer and Cardio report (WES add-on panel)

 
 
Clinical Information (ข้อมูลทางคลินิก):
Apolipoprotein E (ApoE) is located on 19q13.2 and consists of 299 amino acids in length. It plays an important role in cholesterol transportation and metabolism. The three most common alleles of ApoE are e3 (Cys112/Arg158), e2 (Cys112/Cys158), and e4 (Arg112/Arg158). Among these three alleles, e3 is the wild-type and most commonly found. Mutations in ApoE might increase or decrease the risk of Alzheimer’s disease. Individuals with the APOE e3/e4 genotype have a three-to-four-fold relative risk, while individuals with the APOE e4/e4 genotype have a 15-fold relative risk compared to those with the APOE e3/e3 genotype. Other than the risk of late-onset Alzheimer's developing, these mutations are related to the age of onset of the disease. The average age of developing late-onset Alzheimer is 68 years at 94% for homozygous E4, 76 years at 47% frequency for heterozygous E4, and 84 years at 20% frequency for those who do not carry E4. Moreover, mutations in ApoE might increase or decrease the risk of cardiovascular disease.
 
Clinical Reference (เอกสารอ้างอิง):
1. Eichner JE, Dunn ST, Perveen G, Thompson DM, Stewart KE, Stroehla BC. Apolipoprotein E polymorphism and cardiovascular disease: a HuGE review. Am J Epidemiol. 2002 Mar 15;155(6):487-95. 
2. Schaefer EJ, Lamon-Fava S, Johnson S, Ordovas JM, Schaefer MM, Castelli WP, Wilson PW. Effects of gender and menopausal status on the association of apolipoprotein E phenotype with plasma lipoprotein levels. Results from the Framingham Offspring Study. Arterioscler Thromb. 1994 Jul;14(7):1105-13. 
3. Song Y, Stampfer MJ, Liu S. Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Ann Intern Med. 2004 Jul 20;141(2):137-47. 
4. Goldman JS, Hahn SE, Catania JW, LaRusse-Eckert S, Butson MB, Rumbaugh M, Strecker MN, Roberts JS, Burke W, Mayeux R, Bird T; American College of Medical Genetics and the National Society of Genetic Counselors. Genetic counseling and testing for Alzheimer disease: joint practice guidelines of the American College of Medical Genetics and the National Society of Genetic Counselors. Genet Med. 2011 Jun;13(6):597-605. 
5. Van Cauwenberghe C, Van Broeckhoven C, Sleegers K. The genetic landscape of Alzheimer disease: clinical implications and perspectives. Genet Med. 2016 May;18(5):421-30. 
6. Li Z, Shue F, Zhao N, Shinohara M, Bu G. APOE2: protective mechanism and therapeutic implications for Alzheimer's disease. Mol Neurodegener. 2020 Nov 4;15(1):63.