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CALVIZIEGEN®

Cos’è Calviziegen

È un test genetico che analliza 6 variazioni genetiche (polimorfismi) in geni associati alla comparsa di Alopecia Androgenica, cioè alla caduta dei capelli in diverse aree del cuoio capelluto. Le variazioni testate si trovano nel gene del recettore per gli ormoni maschili androgeni, nel gene del recettore dell’ectodisplasina A2 e nella regione 20p.11 del cromosoma 20. La presenza di più variazioni genetiche aumenta la probabilità di andare incontro a Calvizie Androgenica. Il test permette di stimare il rischio globale di sviluppare l’Alopecia Androgenica ed il rischio di perdere i capelli entro 30, 50 e 70 anni di età in relazione alla media italiana.

Perchè dovrei fare il test Calviziegen?

L’alopecia androgenica, o calvizie comune, è la causa più frequente di perdita dei capelli e colpisce circa l’80% dei maschi e il 50% delle femmine. La predisposizione genetica aumenta la sensibilità del follicolo all’azione degli ormoni androgeni ed influenza la severità la calvizie e l&rsquoetà di comparsa. Anche il presentarsi di condizioni stressanti nel corso della vita può rendere manifesta la predisposizione genetica e accelerare la caduta dei capelli.

Conoscere la probabilità di andare incontro a calvizie androgenica può essere particolarmente utile a tutti quei soggetti che:

  • presentano casi di alopecia in famiglia e vogliono verifica la presenza di predisposizione genetica;
  • hanno un principio di alopecia e vogliono escludere una predisposizione genetica all’alopecia androgenica.

Una conoscenza precoce del rischio può permettere di discutere con lo specialista medico eventuali forme preventive.

Objectives: identify the presence of 6 genetic variants that are strongly associated with Androgenetic Alopecia. In addition, the test estimates the global risk of developing Androgenetic Alopecia and the risk of hair loss within the age of 30, 50 and 70 years in comparison to the Italian Average.

SNPs & GENES FUNCTION IN ANDROGENETIC ALOPECIA

Gene: AR; Androgen Receptor
Variation tested: rs6152 A>G, rs6625163 A>G, rs1041668 C>T
Chromosome location: Xq12
Total publications on the gene: 375
Meta-Analysis: 17
GWAS: 1

Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. The gene encoding androgen receptor (AR), alternatively known as the dihydrotestosterone receptor, is located on the X chromosome. The androgen receptor gene is more than 90 kb long and codes for a protein that has 3 major functional domains: the N-terminal domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid-hormone activated transcription factor. Upon binding the hormone ligand, the receptor dissociates from accessory proteins, translocates into the nucleus, dimerizes, and then stimulates transcription of androgen responsive genes. Transcription factor activity is modulated by bound coactivator and corepressor proteins. Transcription activation is down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3.
Two alternatively spliced variants encoding distinct isoforms have been described; this gene contains 2 polymorphic trinucleotide repeat segments that encode polyglutamine and polyglycine tracts in the N-terminal transactivation domain of its protein. The poly-Gln region of AR is highly polymorphic and the number of Gln varies in the population (from 17 to 26). A smaller size of the poly-Gln region may be associated with the development of prostate cancer. Expansion of the polyglutamine tract causes spinal bulbar muscular atrophy (Kennedy disease). The poly-Gly region of AR is polymorphic and ranges from 24 to 31 Gly. A poly-Gly region shorter or equal to 23 may be associated with the development of androgenetic alopecia.
Defects in AR are the cause of androgen insensitivity syndrome (AIS) [MIM:300068]; previously known as testicular feminization syndrome (TFM), an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [MIM:313200]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy; caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.
Defects in AR may play a role in metastatic prostate cancer.
Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [MIM:312300], also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.
In the Calviziegen 3 SNPs variations are tested in the AR gene that are strongly linked to the Androgenetic Alopecia.

Gene: EDA2R; ectodysplasin A2 receptor
Variation tested: rs1385699 C>T
Chromosome location: Xq12
Total publications on the gene: 1
Meta-Analysis: -
GWAS: -

EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that are encoded by the anhidrotic ectodermal dysplasia (EDA) gene. EDA protein belongs to the tumor necrosis factor family acts as a homotrimer and may be involved in cell-cell signaling during the development of ectodermal organs. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. The gene EDA2R encodes a receptor that specifically binds to EDA-A2 isoform. This protein is a type III transmembrane protein of the TNFR (tumor necrosis factor receptor) superfamily, and contains 3 cysteine-rich repeats and a single transmembrane domain but lacks an N-terminal signal peptide. Multiple alternatively spliced transcript variants have been found for this gene, but some variants lack sufficient support. The SNP rs1385699 C>T tested in the Calviziegen has been associated with Androgenetic Alopecia.

Chromosome: 20
Locus: 20P11.22
Variation tested: rs2180439 C>T , rs1160312 A>G
Total publications on the gene: 1
Meta-Analysis: -
GWAS: 1

A genome-wide association study for androgenic alopecia was conducted in 1,125 men and identified a newly associated locus at chromosome 20p11.22, confirmed in three independent cohorts (n = 1,650; OR = 1.60, P = 1.1 x 10(-14) for rs1160312). The one man in seven who harbors risk alleles at both 20p11.22 and AR (encoding the androgen receptor) has a sevenfold-increased odds of androgenic alopecia (OR = 7.12, P = 3.7 x 10(-15)). The 2 SNPs rs2180439 C>T , rs1160312 A>G tested in the Calviziegen test are associated with Androgenetic Alopecia.

Come avere la Nutrizione Personalizzata?

1. Ordina la consulenza genetica e ricevi il materiale per il prelievo orale 2. Spedisci il campione di saliva e cellule della bocca
4. Ordini i tuoi integratori personalizzati 3. Ricevi il Report Nutri-Genetico sulla tua pagina web personale (15 - 20 giorni) nutrimedigen.com

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L’offerta Calviziegen®

  • Test Calviziegen®: 175€

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