{"id":26088,"date":"2022-09-12T13:55:16","date_gmt":"2022-09-12T13:55:16","guid":{"rendered":"https:\/\/www.neuraxpharm.com\/sk\/?p=26088"},"modified":"2022-09-13T19:10:09","modified_gmt":"2022-09-13T19:10:09","slug":"je-alzheimerova-choroba-dedicna","status":"publish","type":"post","link":"https:\/\/www.neuraxpharm.com\/sk\/blog\/je-alzheimerova-choroba-dedicna","title":{"rendered":"Je Alzheimerova choroba dedi\u010dn\u00e1?"},"content":{"rendered":"

V\u0161etko, \u010do potrebujete vedie\u0165 o g\u00e9noch a ich vplyve pri Alzheimerovej chorobe<\/strong><\/p>\n

G\u00e9ny, tie mal\u00e9, nezn\u00e1me jednotky<\/h3>\n

Vedeck\u00e1 defin\u00edcia g\u00e9nu1<\/sup> by znela: \u201ekr\u00e1tky \u00fasek DNA preveden\u00fd na prote\u00edn\u201c. Pod\u013ea inej defin\u00edcie by to bola \u201etransmisie schopn\u00e1 jednotka biologickej dedi\u010dnosti\u201c. Tak\u017ee ke\u010f je g\u00e9n kr\u00e1tky \u00fasek DNA, cel\u00fa sekvenciu DNA patriacu \u017eiv\u00e9mu organizmu alebo konkr\u00e9tnemu druhu naz\u00fdvame gen\u00f3m. Keby to malo znie\u0165 viac eduka\u010dne a metaforicky, mohli by sme poveda\u0165, \u017ee g\u00e9ny s\u00fa postavy v na\u0161om pr\u00edbehu.<\/p>\n

DNA je kyselina nukleov\u00e1, ktor\u00e1 obsahuje genetick\u00e9 in\u0161trukcie pou\u017e\u00edvan\u00e9 pri v\u00fdvine a fungovan\u00ed \u017eiv\u00fdch organizmov.<\/p>\n

Jej hlavnou funkciou je uchov\u00e1vanie inform\u00e1ci\u00ed s cie\u013eom vytv\u00e1ra\u0165 bunky, prote\u00edny a in\u00e9 molekuly. V ka\u017edej \u013eudskej bunke sa nach\u00e1dza viac ne\u017e 22 000 g\u00e9nov zoskupen\u00fdch do 23 p\u00e1rov chromoz\u00f3mov s inform\u00e1ciami potrebn\u00fdmi pre n\u00e1\u0161 rast, v\u00fdvoj a fungovanie.2,3<\/sup><\/p>\n

DNA je okrem toho zodpovedn\u00e1 aj za dedi\u010dn\u00fa transmisiu, teda za genetick\u00e9 inform\u00e1cie, ktor\u00e9 odovzd\u00e1vaj\u00fa rodi\u010dia svojim de\u0165om. Ako sa v\u0161ak tieto genetick\u00e9 inform\u00e1cie pren\u00e1\u0161aj\u00fa z gener\u00e1cie na gener\u00e1ciu?<\/p>\n

V\u0161etci m\u00e1me dve k\u00f3pie ka\u017ed\u00e9ho g\u00e9nu \u2013 jeden zded\u00edme od matky a druh\u00fd od otca. Ka\u017ed\u00fa r\u00f4znu verziu g\u00e9nu naz\u00fdvame alela. G\u00e9n ABO napr\u00edklad4<\/sup> k\u00f3duje prote\u00edn \u013eudskej krvnej skupiny ABO, ktor\u00e1 m\u00e1 najmenej tri alely: A, B a O.<\/p>\n

Kombin\u00e1cia g\u00e9nov, ktor\u00e9 sme zdedili, sa naz\u00fdva genotyp, zatia\u013e \u010do fenotyp je v\u00fdsledkom toho, ako n\u00e1\u0161 organizmus reaguje na to, \u017ee je pren\u00e1\u0161a\u010dom t\u00fdchto g\u00e9nov v interakcii s prostred\u00edm.<\/p>\n

S\u00fa mut\u00e1cie dobr\u00e9 alebo zl\u00e9?<\/h3>\n

Gen\u00f3m v\u0161etk\u00fdch \u013eud\u00ed na svete je na 99,9 % podobn\u00fd. Hoci sa vonkaj\u0161\u00edm vzh\u013eadom m\u00f4\u017eeme v\u00fdrazne l\u00ed\u0161i\u0165, t\u00e1to odli\u0161nos\u0165 len sotva dosahuje 0,1 %.5<\/sup> Pre\u010do teda vyzer\u00e1me tak odli\u0161ne? Preto\u017ee mal\u00fd po\u010det g\u00e9nov zhroma\u017e\u010fuje mno\u017estvo genetick\u00fdch variantov zodpovedn\u00fdch za fenotypov\u00fa variabilitu, ktor\u00fa vid\u00edme.<\/p>\n

Hlavn\u00fdm zdrojom genetickej variability je mut\u00e1cia6<\/sup>. Je z\u00e1kladnou vlastnos\u0165ou DNA, v\u010faka ktorej m\u00f4\u017ee prebieha\u0165 evol\u00facia, v ktorej zohr\u00e1vaj\u00fa \u00falohu pr\u00edrodn\u00fd v\u00fdber a osud. Hoci je frekvencia alebo miera mut\u00e1ci\u00ed ve\u013emi n\u00edzka (r\u00e1dovo 10 \u2013 5 na osobu alebo \u017eiv\u00fd organizmus a gener\u00e1ciu), rekurentnou mut\u00e1ciou g\u00e9nu m\u00f4\u017ee v popul\u00e1cii d\u00f4js\u0165 k substit\u00facii jednej alely za in\u00fa.<\/p>\n

Mut\u00e1cia m\u00e1 tzv. pre-adapta\u010dn\u00fd charakter, \u010do znamen\u00e1, \u017ee k nej doch\u00e1dza n\u00e1hodne a bez toho, aby sme vedeli, \u010di bude pre organizmus u\u017eito\u010dn\u00e1 alebo \u0161kodliv\u00e1. Ke\u010f k nej v\u0161ak d\u00f4jde, je zap\u00edsan\u00e1 do jeho gen\u00f3mu.<\/p>\n

Je Alzheimerova choroba dedi\u010dn\u00e1?<\/h3>\n

V\u00e4\u010d\u0161ina z n\u00e1s Alzheimerovu chorobu pozn\u00e1 alebo o nej po\u010dula. Ide o typ neurodegenerat\u00edvneho ochorenia, ktor\u00e9 sp\u00f4sobuje najm\u00e4 probl\u00e9my s pam\u00e4\u0165ou a spr\u00e1van\u00edm. Pr\u00edznaky sa obvykle objavia okolo 65. roku a \u010dasom sa zhor\u0161uj\u00fa, a\u017e s\u00fa nakoniec tak\u00e9 z\u00e1va\u017en\u00e9, \u017ee zasahuj\u00fa do vykon\u00e1vania ka\u017edodenn\u00fdch \u00faloh, v d\u00f4sledku \u010doho je postihnut\u00fd \u010dlovek z\u00e1visl\u00fd od in\u00fdch \u013eud\u00ed.<\/p>\n

Vieme v\u0161ak naozaj, \u010do sa deje vn\u00fatri organizmu a ak\u00e9 s\u00fa mo\u017en\u00e9 pr\u00ed\u010diny? V mozgu postihnutom Alzheimerovou chorobou doch\u00e1dza k po\u0161kodeniu neur\u00f3nov akumul\u00e1ciou prote\u00ednov (amyloidov a tau prote\u00ednov), p\u00f4soben\u00edm ktor\u00fdch sa medzi nimi str\u00e1caj\u00fa spojenia7<\/sup>, a\u017e nakoniec zanikn\u00fa.<\/p>\n

V 95 % pr\u00edpadov je Alzheimerova choroba d\u00f4sledkom kombin\u00e1cie genetick\u00fdch faktorov8<\/sup> a faktorov prostredia a \u017eivotn\u00e9ho \u0161t\u00fdlu, ktor\u00e9 na \u010dloveka za\u010dn\u00fa \u010dasom p\u00f4sobi\u0165. Zvy\u0161n\u00fdch 5 % pr\u00edpadov, definovan\u00fdch ako skor\u00e1 alebo dedi\u010dn\u00e1 Alzheimerova choroba9<\/sup>, sa spravidla vyvinie pred 65. rokom, pri\u010dom zhor\u0161ovanie stavu je agres\u00edvnej\u0161ie a\/alebo r\u00fdchlej\u0161ie, preva\u017ene kv\u00f4li mut\u00e1ci\u00e1m v g\u00e9noch: amyloidov\u00fd prekurzorov\u00fd prote\u00edn (APP), presenil\u00edn-1 (PSEN1) a\/alebo presenil\u00edn-2 (PSEN2).<\/p>\n

Odhaduje sa, \u017ee genetika sa na riziku Alzheimerovej choroby podie\u013ea v rozsahu 60 \u2013 80 %10<\/sup> a okrem interakci\u00ed medzi g\u00e9nmi a medzi g\u00e9nmi a prostred\u00edm ide zrejme o kombin\u00e1ciu be\u017en\u00fdch a zriedkav\u00fdch alel s jednozna\u010dn\u00fdm n\u00edzkym a\u017e stredn\u00fdm vplyvom na riziko ochorenia.<\/p>\n

Mo\u017eno si kladiete ot\u00e1zku, ak\u00e1 je \u00farove\u0148 poznania v r\u00e1mci s\u00fa\u010dasn\u00e9ho genetick\u00e9ho v\u00fdskumu. V kontexte s\u00fa\u010dasnej hum\u00e1nnej genetiky umo\u017enil vznik nov\u00fdch techn\u00edk celog\u00e9nov\u00e9 skr\u00edningov\u00e9 \u0161t\u00fadie (GWAS), ktor\u00e9 identifikovali viac ne\u017e 80 g\u00e9nov11\u201313<\/sup> spojen\u00fdch s Alzheimerovou chorobou, z ktor\u00fdch najv\u00fdznamnej\u0161\u00ed je g\u00e9n APOE objaven\u00fd takmer pred 30 rokmi14,15<\/sup>. Napriek tomu tieto sign\u00e1ly predstavuj\u00fa sotva 31 % genetick\u00fdch vari\u00e1ci\u00ed ochorenia, \u010do znamen\u00e1, \u017ee v\u00e4\u010d\u0161ina genetick\u00e9ho rizika zost\u00e1va st\u00e1le nejasn\u00e116<\/sup>.<\/p>\n

Poznanie rizika Alzheimerovej choroby pomocou predik\u010dnej medic\u00edny<\/h3>\n

V s\u00fa\u010dasnosti je mo\u017en\u00e9 vizualizova\u0165 zdravie \u010dloveka pre\u010d\u00edtan\u00edm jeho gen\u00f3mu. Medic\u00edna mala doteraz prevent\u00edvny, diagnostick\u00fd a terapeutick\u00fd charakter, ale s v\u00fdvojom genomiky m\u00f4\u017ee by\u0165 aj predikt\u00edvna a personalizovan\u00e1.<\/p>\n

Anal\u00fdzou DNA \u010dloveka m\u00f4\u017eeme z\u00edska\u0165 \u00fadaje o existencii jednej alebo viacer\u00fdch mut\u00e1ci\u00ed v gen\u00f3me, ktor\u00e9 s ur\u010ditou pravdepodobnos\u0165ou znamenaj\u00fa, \u017ee dan\u00e1 osoba m\u00e1 predispoz\u00edciu alebo n\u00e1chylnos\u0165 na to, \u017ee v bud\u00facnosti sa u nej vyskytne nejak\u00e9 ochorenie17<\/sup>, napr\u00edklad rakovina. A to nielen u nej, ale aj v jej rodine.<\/p>\n

Personalizovan\u00e1 a presn\u00e1 medic\u00edna by neexistovala bez toho, aby sme poznali svoj gen\u00f3m. Na z\u00e1klade genetick\u00fdch vari\u00e1ci\u00ed, ktor\u00fdch je pacient s ur\u010dit\u00fdm ochoren\u00edm nosite\u013eom, vieme predv\u00edda\u0165, ak\u00fd druh lie\u010dby by mu mal by\u0165 podan\u00fd18<\/sup>. Generick\u00e1 lie\u010dba zostane bokom a prijme sa rozhodnutie s ve\u013ekou presnos\u0165ou vybra\u0165 tie najvhodnej\u0161ie formy lie\u010dby, ktor\u00e9 kore\u0161ponduj\u00fa s jednotliv\u00fdmi genotypmi.<\/p>\n

V medic\u00edne je to u\u017e pri niektor\u00fdch ochoreniach realitou, no my v centre Ace na\u010falej pracujeme na tom, aby sme v bl\u00edzkej bud\u00facnosti dok\u00e1zali predv\u00edda\u0165 aj vznik Alzheimerovej choroby.<\/p>\n

Literat\u00fara:<\/p>\n

    \n
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  2. Human Genome Project FAQ. Accessed April 13, 2022. https:\/\/www.genome.gov\/human-genome-project\/Completion-FAQ<\/li>\n
  3. \u00bfCu\u00e1ntos genes tenemos los humanos? – Gen-\u00c9tica. Accessed April 13, 2022. https:\/\/montoliu.naukas.com\/2020\/11\/30\/cuantos-genes-tenemos-los-humanos\/<\/li>\n
  4. The ABO blood group – Blood Groups and Red Cell Antigens – NCBI Bookshelf. Accessed April 13, 2022. https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK2267\/<\/li>\n
  5. Human Genomic Variation. Accessed April 13, 2022. https:\/\/www.genome.gov\/dna-day\/15-ways\/human-genomic-variation<\/li>\n
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  7. Alzheimer\u2019s & Dementia | Alzheimer\u2019s Association. Accessed April 13, 2022. https:\/\/www.alz.org\/alzheimer_s_dementia<\/li>\n
  8. Schellenberg GD, D\u2019Souza I, Poorkaj P. The genetics of Alzheimer\u2019s disease. Curr Psychiatry Rep<\/em>. 2000;2(2):158-164. Accessed August 29, 2016. http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/11122949<\/li>\n
  9. Campion D, Dumanchin C, Hannequin D, et al. Early-onset autosomal dominant Alzheimer disease: prevalence, genetic heterogeneity, and mutation spectrum. Am J Hum Genet<\/em>. 1999;65(3):664-670. doi:10.1086\/302553<\/li>\n
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  11. de Rojas I, Moreno-Grau S, Tesi N, et al. Common variants in Alzheimer\u2019s disease and risk stratification by polygenic risk scores. Nat Commun<\/em>. 2021;12(1):3417. doi:10.1038\/s41467-021-22491-8<\/li>\n
  12. Bellenguez C, K\u00fc\u00e7\u00fckali F, Jansen IE, et al. New insights into the genetic etiology of Alzheimer\u2019s disease and related dementias. Nat Genet 2022<\/em>. Published online April 4, 2022:1-25. doi:10.1038\/s41588-022-01024-z<\/li>\n
  13. Wightman DP, Jansen IE, Savage JE, et al. A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer\u2019s disease. Nat Genet<\/em>. 2021;53(9):1276-1282. doi:10.1038\/S41588-021-00921-Z<\/li>\n
  14. Soininen HS, Scbeltens P. Early diagnostic indices for the prevention of Alzheimer\u2019s disease. Ann Med<\/em>. 1998;30(6):553-559. doi:10.3109\/07853899809002604<\/li>\n
  15. Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. JAMA<\/em>. 1997;278(16):1349-1356. http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/9343467<\/li>\n
  16. PG R, KB H, K B, et al. Assessment of the genetic variance of late-onset Alzheimer\u2019s disease. Neurobiol Aging<\/em>. 2016;41. doi:10.1016\/J.NEUROBIOLAGING.2016.02.024<\/li>\n
  17. Gibson G. On the utilization of polygenic risk scores for therapeutic targeting. Barsh GS, ed. PLOS Genet<\/em>. 2019;15(4):e1008060. doi:10.1371\/journal.pgen.1008060<\/li>\n
  18. Escott-Price V, Schmidt KM. Probability of Alzheimer\u2019s disease based on common and rare genetic variants. Alzheimer\u2019s Res Ther<\/em>. 2021;13(1):1-9. doi:10.1186\/S13195-021-00884-7\/FIGURES\/3<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    V 95 % pr\u00edpadov je Alzheimerova choroba d\u00f4sledkom kombin\u00e1cie genetick\u00fdch faktorov a faktorov prostredia a \u017eivotn\u00e9ho \u0161t\u00fdlu, ktor\u00e9 na \u010dloveka za\u010dn\u00fa \u010dasom p\u00f4sobi\u0165. Zvy\u0161n\u00fdch 5 % pr\u00edpadov, definovan\u00fdch ako skor\u00e1 alebo dedi\u010dn\u00e1 Alzheimerova choroba, sa spravidla vyvinie pred 65. rokom, pri\u010dom zhor\u0161ovanie stavu je agres\u00edvnej\u0161ie a\/alebo r\u00fdchlej\u0161ie, preva\u017ene kv\u00f4li mut\u00e1ci\u00e1m v g\u00e9noch.<\/p>\n","protected":false},"author":1390,"featured_media":26089,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[89],"tags":[],"class_list":["post-26088","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-alzheimerova-choroba"],"yoast_head":"\nJe Alzheimerova choroba dedi\u010dn\u00e1? - Neuraxpharm SK<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.neuraxpharm.com\/sk\/blog\/je-alzheimerova-choroba-dedicna\" \/>\n<meta property=\"og:locale\" content=\"sk_SK\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Je Alzheimerova choroba dedi\u010dn\u00e1?\" \/>\n<meta property=\"og:description\" content=\"V 95 % pr\u00edpadov je Alzheimerova choroba d\u00f4sledkom kombin\u00e1cie genetick\u00fdch faktorov a faktorov prostredia a \u017eivotn\u00e9ho \u0161t\u00fdlu, ktor\u00e9 na \u010dloveka za\u010dn\u00fa \u010dasom p\u00f4sobi\u0165. 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