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Custom Alzheimer's Disease Panel

Custom Alzheimer's Disease Panel

What is Alzheimer's disease?

Alzheimer's disease (AD), also known as primary dementia, is a degenerative disease of the central nervous system, mainly manifested as progressive memory disorder, cognitive dysfunction, personality change and language disorders and other neuropsychiatric symptoms. There are many factors in daily life that can cause Alzheimer's disease. Among them, age is the most important factor, and the prevalence of this disease increases with age. Followed by genetic factors. Genetic studies have found that there are three main causative genes: amyloid precursor protein gene (APP), presenilin-1 gene (PSEN1) and presenilin-2 gene (PSEN2). In addition, trace elements, vitamin deficiency, cerebral ischemia and hypoxia, brain injury, poisoning, metabolism and endocrine disorders and other reasons may cause this disease.

Disease-related gene description

There are three main causative genes associated with Alzheimer's disease: APP, PSEN1 and PSEN2. Amyloid-β peptide (Aβ) is formed by sequential cleavage of APP protein by β-secretase and γ-secretase. The main components of Aβ include Aβ40 and Aβ42, of which Aβ42 is more likely to aggregate and is cytotoxic. Aβ protein can induce oxidative stress in a variety of ways to cause free radical damage and metabolic disorders, resulting in the formation of more free radicals. Aβ protein can also induce inflammatory reaction, activate protein kinase and increase Tau protein abnormal phosphorylation, resulting in neurofibrillary tangle (NTF). These conditions, in turn, further lead to the formation and deposition of a large amount of Aβ protein, which leads to damage to synaptic function and irreversible damage to brain tissue. The PSEN1 and PSEN2 genes encode presenilins, which are considered to be the catalytic subunit of the γ-secretase complex. Both of these proteins have a key role in processing APP to release Aβ fragments. The PSEN1 mutation is the most common form of hereditary AD. In addition, many new genes have been shown to be associated with the disease, such as TREM2 and CD33. More genes related to AD can be found in the gene list.

CD-Genomic offers a custom Alzheimer's disease panel to help you analyze the SNP, CNV and InDels of genes associated with Alzheimer's disease. You can choose the genes of interest to detect. Amplicon sequencing technology based on NGS is used to detect genetic variation efficiently, quickly, and accurately.

Custom Alzheimer's disease panel offers but are not limited to:

  • Targeted sequencing technology by Illumina MiSeq/Ion PGM system provides ultra-deep sequencing to target specific genomic regions.
  • Every detected genetic variant will be further validated to ensure the validity of results.
  • Strict quality control throughout the pipeline workflow ensures the accuracy and repeatability of the sequencing.
  • Custom panel genes are constantly updated based on the frontiers of literature studies to target all relevant regions.
  • Customized Alzheimer’s disease panel only contains the genes you need, save your time and cost.
  • Precision bioinformatics pipelines ensure superior analytical performance.

Choose the genes that suit you from the Alzheimer’s disease gene list

ABCA7 APOE APP BACE1 BIN1
CASS4 CD2AP CD33 CELF1 CLU
CR1 CSF1R DNMT1 DSG2 EIF4G1
EPHA1 FERMT2 GBA GRN INPP5D
MAPT MEF2C MS4A NME8 PICALM
PRNP PSEN1 PSEN2 PTK2B SNCA
SNCB SORL1 TREM2 TYROBP ZCWPW1

Specimen requirements of our custom Alzheimer's disease panel

  • Specimen: blood, saliva or extracted DNA.
  • Volume: 3 mL blood, 2 mL saliva and 3ug DNA.
  • Collection: blood is collected by routine blood collection and saliva is collected by saliva collection kits (kits are available upon request). DNA samples are stored in TE buffer or equivalent.
  • Container: lavender-top (EDTA) tube or yellow-top (ACD) tube.
  • Storage/transport temperature: room temperature.

Gene panel workflow

Gene panel workflow

For more information about the Custom Alzheimer's Disease Panel or need other amplification requirements, please contact us.

References:

  1. Hardy J A, Higgins G A. Alzheimer's disease: the amyloid cascade hypothesis. Science, 1992, 256(5054): 184-186.s
  2. Guerreiro R, Wojtas A, et al. TREM2 variants in Alzheimer's disease. New England Journal of Medicine, 2013, 368(2): 117-127.
  3. Bagyinszky E, Youn Y C, et al. The genetics of Alzheimer's disease. Clinical interventions in aging, 2014, 9: 535.
  4. Karch C M, Goate A M. Alzheimer's disease risk genes and mechanisms of disease pathogenesis. Biological psychiatry, 2015, 77(1): 43-51.
* For Research Use Only. Not for use in diagnostic procedures.

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