{"id":2611,"date":"2019-08-04T19:58:10","date_gmt":"2019-08-04T16:58:10","guid":{"rendered":"http:\/\/blog.ulubat.org\/?p=2611"},"modified":"2019-08-31T13:04:13","modified_gmt":"2019-08-31T10:04:13","slug":"dislerinizi-fircalamak-sizi-alzheimera-karsi-koruyor-olabilir","status":"publish","type":"post","link":"https:\/\/blog.ulubat.org\/index.php\/genel\/dislerinizi-fircalamak-sizi-alzheimera-karsi-koruyor-olabilir\/","title":{"rendered":"Di\u015flerinizi F\u0131r\u00e7alamak Sizi Alzheimer\u2019a Kar\u015f\u0131 Koruyor Olabilir!"},"content":{"rendered":"\n

Alois Alzheimer, y\u00fczy\u0131l\u0131 a\u015fk\u0131n s\u00fcre \u00f6nce daha sonralar\u0131 kendi ad\u0131yla an\u0131lacak olan Alzheimer hastal\u0131\u011f\u0131n\u0131 \u201cyap\u0131\u015fkan plaklar\u0131n baz\u0131 beyin b\u00f6lgelerine ve n\u00f6ronlara verdi\u011fi hasar sonucu g\u00f6r\u00fclen demans\u201d<\/em> <\/strong>olarak tan\u0131mlad\u0131. O g\u00fcnden beri bilim insanlar\u0131 Alzheimer ara\u015ft\u0131rmalar\u0131nda bu \u201cyap\u0131\u015fkan plaklar\u201d\u0131n olu\u015fum sebebi ve tedavi y\u00f6ntemleri \u00fczerine yo\u011funla\u015fm\u0131\u015ft\u0131. Ancak bu y\u0131l\u0131n Ocak ay\u0131nda yay\u0131nlanan bir makale hastal\u0131\u011fa yeni bir bak\u0131\u015f a\u00e7\u0131s\u0131 kazand\u0131r\u0131yor; sonunda Alzheimer\u2019e neyin yol a\u00e7t\u0131\u011f\u0131n\u0131 biliyor olabiliriz.<\/strong><\/p>\n\n\n\n

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Sa\u011f elini kullanan bireyde Alzheimer’\u0131n beyin yar\u0131k\u00fcresine verdi\u011fi hasar<\/strong><\/em>
Kaynak:<\/em><\/strong> Jessica Wilson\/Science Photo Library <\/figcaption><\/figure>\n\n\n\n

Toplumlar\u0131n ya\u015flanmas\u0131 ile birlikte demans \u00e7ok h\u0131zl\u0131 bir \u015fekilde d\u00fcnya genelindeki \u00f6l\u00fcm sebepleri aras\u0131nda be\u015finci s\u0131raya y\u00fckseldi. 2018 y\u0131l\u0131 verilerine g\u00f6re d\u00fcnyada 50 milyon ki\u015fi demans hastas\u0131 ve her 3 saniyede yeni birine demans tan\u0131s\u0131 konulmakta.<\/strong> Alzheimer  hastal\u0131\u011f\u0131, demans\u0131n pek \u00e7ok tipinden en bilineni ve en \u00e7ok g\u00f6r\u00fcleni (t\u00fcm olgular\u0131n yakla\u015f\u0131k %50-70\u2019i).<\/p>\n\n\n\n

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En s\u0131k g\u00f6r\u00fclen 10 k\u00fcresel \u00f6l\u00fcm sebebi, 2016<\/em><\/strong>
Kaynak:<\/em><\/strong> https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/the-top-10-causes-of-death <\/figcaption><\/figure><\/div>\n\n\n\n

Alzheimer, genellikle iki tip proteinin (amiloid ve tau)<\/em><\/strong> beyinde birikimini i\u00e7eriyor. Bunlar hastal\u0131\u011f\u0131n en erken fizyolojik i\u015faretleri, \u00f6zellikle amiloid proteininin defektif kontrol\u00fc sonucu beyinde biriken b\u00fcy\u00fck yap\u0131\u015fkan plaklar 1984\u2019ten beri hastal\u0131kla ilgili en kuvvetli hipotez.
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Alzheimer\u2019\u0131 anlamak ve tedavi etmek \u00fczere yap\u0131lan ara\u015ft\u0131rmalar\u0131n b\u00fcy\u00fck \u00e7o\u011funlu\u011funun merkezinde bu \u201camiloid hipotezi\u201d<\/em> var. Amiloid \u00fcretmek amac\u0131yla genetik olarak d\u00fczenlenmi\u015f fareler, amiloid proteini \u00fcretimini engelleyecek ya da yok edecek ila\u00e7lar ve tau dola\u015f\u0131kl\u0131klar\u0131n\u0131 y\u0131kmak i\u00e7in \u00e7ok b\u00fcy\u00fck mebla\u011flarda yat\u0131r\u0131mlar yap\u0131ld\u0131. \u00d6yleki ABD Ulusal Sa\u011fl\u0131k Enstit\u00fcleri (NIH) yaln\u0131zca 2018 y\u0131l\u0131nda Alzheimer ara\u015ft\u0131rmalar\u0131 i\u00e7in 1.9 milyar dolar harcad\u0131. Fakat son yap\u0131lan ara\u015ft\u0131rmaya g\u00f6re Alzheimer i\u00e7in geli\u015ftiren ila\u00e7lardaki ba\u015far\u0131s\u0131zl\u0131k oran\u0131 %99<\/em><\/strong>.
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Anla\u015f\u0131laca\u011f\u0131 gibi \u201camiloid hipotezi\u201d<\/em> tedavi i\u00e7in en uygun yakla\u015f\u0131m de\u011fildi. Bunun sonucunda baz\u0131 bilim insanlar\u0131 bu hipotezi sorgulamaya ba\u015flad\u0131. Ara\u015ft\u0131rmalar sonucunda bireylerde demans g\u00f6r\u00fclmeden de beyin plaklar\u0131 ve tau dola\u015f\u0131kl\u0131klar\u0131 oldu\u011fu tespit edildi ve \u201camiloidin Alzheimer hastal\u0131\u011f\u0131nda merkezi veya e\u015fsiz bir rol\u00fc oldu\u011fu\u201d<\/em> d\u00fc\u015f\u00fcncesi i\u00e7in yeterli kan\u0131t\u0131n olmad\u0131\u011f\u0131 ortaya \u00e7\u0131kt\u0131. 
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Alzheimer’e yol a\u00e7an amiloid plaklar\u0131
Kaynak: <\/strong><\/em>Juan Gaertner\/Science Photo Library <\/strong><\/figcaption><\/figure>\n\n\n\n

2016 y\u0131l\u0131nda ara\u015ft\u0131rmac\u0131lar amiloidin bakterilere kar\u015f\u0131 yap\u0131\u015fkan bir savunma olu\u015fturdu\u011funu ke\u015ffetti. Protein, bakterileri \u00f6ld\u00fcrebilecek antimikrobiyal bir bile\u015fik gibi davran\u0131yordu. Bilim insanlar\u0131, Alzheimer proteinleri \u00fcretmeye ko\u015fulland\u0131r\u0131lm\u0131\u015f fare beyinlerine bakteri enjekte ettiklerinde plaklar\u0131n gece boyunca bakterilerin etraf\u0131n\u0131 sard\u0131\u011f\u0131n\u0131 g\u00f6rd\u00fc.
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Bu s\u0131rada ekip h\u00e2l\u00e2 Alzheimer sonucu olu\u015fan beyin hasar\u0131n\u0131n sebebinin bakteri de\u011fil de amiloid plaklar\u0131 oldu\u011funu d\u00fc\u015f\u00fcn\u00fcyordu. Ara\u015ft\u0131rmadan sonra yap\u0131lan \u00e7al\u0131\u015fmalar mikroplar\u0131 inceledi ve Alzheimer hastalar\u0131n\u0131n beyinlerinde bulunan bir bakteri tespit etti. Fakat bakterinin hastal\u0131\u011fa m\u0131 yol a\u00e7t\u0131\u011f\u0131, yoksa Alzheimer ile olu\u015fan beyin hasar\u0131 sonucu kolayca beyne mi girdi\u011fi net de\u011fildi.
Bir\u00e7ok ara\u015ft\u0131rmac\u0131, Alzheimer i\u00e7in risk fakt\u00f6r\u00fc olarak bilinen ve di\u015f eti hastal\u0131klar\u0131n\u0131n ana sebebi olan Porphyromonas gingivalis<\/em><\/strong> <\/em>\u00fczerinde \u00e7al\u0131\u015f\u0131yor. \u015eimdiye kadar  P. gingivalis<\/em>\u2019in Alzheimer hastalar\u0131nda  beyin b\u00f6lgelerini istila etti\u011fini ve inflamasyona yol a\u00e7t\u0131\u011f\u0131n\u0131 buldu.\n\n<\/p>\n\n\n\n

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Alzheimer’l\u0131 beyin h\u00fccresi, TEM
Kaynak: <\/strong><\/em>Thomas DEERINCK, NCMIR \/ Science Photo Library <\/figcaption><\/figure>\n\n\n\n

Tamam\u0131yla Yeni Bir Hipotez<\/strong><\/h2>\n\n\n\n

Cortexyme* ve \u00e7e\u015fitli \u00fcniversitelerden ara\u015ft\u0131rmac\u0131lar 54 ki\u015fiyle yapt\u0131klar\u0131 \u00e7al\u0131\u015fmada Alzheimer\u2019l\u0131 insanlar\u0131n beyinlerindeki hipokamp\u00fcs b\u00f6lgesinden al\u0131nan \u00f6rneklerin y\u00fczde 96 ila 99\u2019unda P. gingivalis\u2019in<\/em> bu dokulardan beslenmek \u00fczere kulland\u0131\u011f\u0131 iki toksik enzim bulduklar\u0131n\u0131 bildirdiler. Bu protein y\u0131k\u0131c\u0131 enzimler \u201cgingipainler\u201d <\/em><\/strong>olarak adland\u0131r\u0131ld\u0131 ve beyin dokular\u0131nda olduk\u00e7a y\u00fcksek seviyelerde bulundu. Bu da daha fazla tau dola\u015f\u0131kl\u0131\u011f\u0131 ve bili\u015fsel zay\u0131flama demek.
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Alzheimer olmayan insanlar\u0131n beyinlerinden ald\u0131klar\u0131 \u00f6rnekleri de inceleyen ara\u015ft\u0131rmac\u0131lar baz\u0131lar\u0131nda P. gingivalis<\/em> ve protein k\u00fcmelerinin d\u00fc\u015f\u00fck seviyelerde de olsa bulunduklar\u0131n\u0131 g\u00f6rd\u00fcler. Alzheimer semptomlar\u0131 ba\u015flamadan 10 ila 20 y\u0131l \u00f6nce tau ve amiloid proteinlerinin k\u00fcmelenebildi\u011fi zaten biliniyordu. Ara\u015ft\u0131rmac\u0131lar bu \u00e7al\u0131\u015fmayla P. gingivalis\u2019in<\/em> beyne girmesinin Alzheimer i\u00e7in bir sonu\u00e7 de\u011fil de sebep oldu\u011funu g\u00f6stermi\u015f oldu.
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Di\u015f eti hastal\u0131\u011f\u0131na yol a\u00e7an Porphyromonas gingivalis bakterisi<\/em><\/strong>
Kaynak:<\/em><\/strong> A. Dowsett, Public Health England\/Science Photo Library <\/figcaption><\/figure><\/div>\n\n\n\n

Ekip, P. gingivalis\u2019in<\/em> yol a\u00e7t\u0131\u011f\u0131 di\u015f eti hastal\u0131\u011f\u0131na sahip farelerde beyin enfeksiyonu, amiloid \u00fcretimi, tau protein dola\u015f\u0131kl\u0131klar\u0131 ve normalde Alzheimer\u2019da etkilenen beyin b\u00f6lgelerinde ve sinirlerde hasar tespit ettiler, bu da P. gingivalis\u2019in<\/em> Alzheimer\u2019a sebep oldu\u011fu olgusunu g\u00fc\u00e7lendirdi. \u00c7al\u0131\u015fma b\u00fcy\u00fck \u00e7o\u011funlukla Koch post\u00fclatlar\u0131na uysa da gelecekteki \u00e7al\u0131\u015fmalarda daha \u00e7ok insan denekle \u00e7al\u0131\u015fman\u0131n gerekece\u011fi de bir ger\u00e7ek.
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P. gingivalis\u2019in<\/em> beyne nas\u0131l ula\u015ft\u0131\u011f\u0131n\u0131 bilmesek de bunun i\u00e7in birka\u00e7 rota olu\u015fturmak m\u00fcmk\u00fcn. A\u011fz\u0131m\u0131z normal olarak \u00e7e\u015fitli ve nispeten dengeli bir bakteri toplulu\u011funa ev sahipli\u011fi yapar. Fakat dental plaklar di\u015f etlerinin alt\u0131na yerle\u015fti\u011finde  P. gingivalis<\/em> gibi bakterilerin \u00fcreyebilece\u011fi ve toksin salabilece\u011fi inflamasyon cepleri olu\u015fturur. Olu\u015fan bu inflamasyon kronik di\u015f eti iltihab\u0131 (periodontit) ve di\u015f kayb\u0131na sebep olabilir. Baz\u0131 \u00e7al\u0131\u015fmalar g\u00f6steriyor ki a\u011fz\u0131nda daha az di\u015fi bulunan insanlarda demans g\u00f6r\u00fclmesi daha olas\u0131. P. gingivalis<\/em> taraf\u0131ndan \u00fcretilen toksinler ve yol a\u00e7t\u0131\u011f\u0131 inflamasyon, a\u011fz\u0131n koruyucu katman\u0131na hasar vererek bakterinin kana kar\u0131\u015fmas\u0131n\u0131 ve di\u011fer organlara ula\u015fmas\u0131n\u0131 olas\u0131 hale getirir. Di\u015f eti hastal\u0131klar\u0131na sahip olmasan\u0131z bile yemek yeme veya yanl\u0131\u015f di\u015f f\u0131r\u00e7alama gibi sebeplerle koruyucu katman\u0131n zedelenmesi bakterilerin a\u011f\u0131zdan kana ge\u00e7mesine davetiye \u00e7\u0131karabilir.
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Gingipain R2 (rgpB) ve n\u00f6ronlar, Alzheimer’l\u0131 beyin hipokamp\u00fcs\u00fc<\/em><\/strong>
Kaynak:<\/em><\/strong> https:\/\/advances.sciencemag.org\/content\/advances\/5\/1\/eaau3333\/F2.large.jpg?width=800&height=600&carousel=1
<\/figcaption><\/figure>\n\n\n\n

Kan-beyin bariyeri beyni mikroplara kar\u015f\u0131 koruyabilir fakat P. gingivalis<\/em> l\u00f6kositlere ve kan damarlar\u0131n\u0131n i\u00e7inde bulunan koruyucu katmandaki h\u00fccrelere sald\u0131r\u0131r, b\u00f6ylelikle beyne ula\u015fabilir. Bir di\u011fer yol ise a\u011fza yak\u0131n kranial sinirleri istila edip bir h\u00fccreden di\u011ferine ge\u00e7erek y\u0131llar s\u00fcren periyotta beyne ula\u015fmas\u0131 olabilir.
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P. gingivalis\u2019in<\/em> beyne ula\u015ft\u0131ktan sonra demansa yol a\u00e7abilmesi i\u00e7in iki olas\u0131 se\u00e7enek var. Bunlardan ilki  beynin var olan enfeksiyonu kontrol alt\u0131na almak i\u00e7in amiloid sal\u0131n\u0131m\u0131n\u0131 tetiklemesi ve bunun sonucunda n\u00f6ronlar\u0131n \u00f6lebilecek olmas\u0131. \u0130kincisi ise P. gingivalis\u2019in<\/em> direkt olarak beyne hasar vermesi. Alzheimer hastal\u0131\u011f\u0131n\u0131n artm\u0131\u015f imm\u00fcn tepkiyle n\u00f6ronlar\u0131 korumaya \u00e7al\u0131\u015f\u0131rken \u00f6ld\u00fcrmesi ve bu y\u00fczden inflamasyonla yak\u0131ndan ili\u015fkili olmas\u0131 halihaz\u0131rda bilinen bir ger\u00e7ek. P. gingivalis<\/em> ise di\u015f eti inflamasyonlar\u0131ndaki ana sebep olmas\u0131 nedeniyle beyin \u00fczerinde ayn\u0131 etkiyi yap\u0131yor olabilir. 
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Baz\u0131 bilim insanlar\u0131n\u0131n bakteriyel enfeksiyonlar\u0131n direkt olarak Alzheimer\u2019a yol a\u00e7mas\u0131 konusunda \u015f\u00fcpheleri var; onlara g\u00f6re Alzheimer\u2019da hayati rol oynayan etmenler genlerimiz. Asl\u0131nda bakteriyel hipotez genetik kan\u0131tlarla \u00e7eli\u015fmiyor aksine insan v\u00fccudunun inflamasyona yatk\u0131nl\u0131\u011f\u0131 ve buna kar\u015f\u0131 g\u00f6sterilen immun tepki olduk\u00e7a fazla genetik varyasyona sahip oldu\u011fundan P. gingivalis\u2019in<\/em> beyne ne kadar hasar verebilece\u011fini etkiliyor.
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Alzheimer\u2019\u0131n en b\u00fcy\u00fck genetik risk fakt\u00f6r\u00fc ApoE immun protein varyasyonlar\u0131d\u0131r. Ge\u00e7en y\u0131l \u0130sve\u00e7\u2019te bir ekip, P. gingivalis<\/em> taraf\u0131ndan sal\u0131nan gingipainlerin<\/em> ApoE proteinini \u00e7e\u015fitli par\u00e7alanma b\u00f6lgeleri i\u00e7eren amino asitler arac\u0131l\u0131\u011f\u0131yla daha k\u00fc\u00e7\u00fck par\u00e7ac\u0131klara ay\u0131rd\u0131\u011f\u0131n\u0131 ve bu par\u00e7ac\u0131klar\u0131n sinirlere zarar verebilece\u011fini ortaya \u00e7\u0131kard\u0131. ApoE proteininin varyantlar\u0131ndan biri olan ApoE4\u2019\u00fcn ise bu par\u00e7alanma b\u00f6lgelerini i\u00e7eren amino asitleri daha fazla i\u00e7erdi\u011fi ve genetik olarak ApoE4\u2019e sahip ki\u015filerin gingipainlerin etkisine daha h\u0131zl\u0131 bir \u015fekilde yan\u0131t verdi\u011fi b\u00f6ylelikle Alzheimer\u2019\u0131n bu ki\u015filerde daha h\u0131zl\u0131 geli\u015fti\u011fi ortaya \u00e7\u0131kt\u0131.
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Kaynak: <\/em><\/strong>https:\/\/www.roche.com\/dam\/jcr:fee71abd-0cde-4672-b684-20c438641c5a\/Alzheimer%E2%80%99s_Hero.jpg<\/figcaption><\/figure>\n\n\n\n

P. gingivalis<\/em> ve gingipainlerin<\/em> etkilerinin ortaya \u00e7\u0131kmas\u0131yla birlikte Alzheimer ile ilgili tedavi aray\u0131\u015flar\u0131ndaki bak\u0131\u015f a\u00e7\u0131s\u0131 da de\u011fi\u015fti. Ara\u015ft\u0131rmac\u0131lar gingipainleri bloke edecek molek\u00fcller \u00fczerinde \u00e7al\u0131\u015farak P. gingivalis arac\u0131l\u0131 beyin infeksiyonlar\u0131n\u0131 ve inflamasyonlar\u0131n\u0131  azaltmay\u0131, amiloid proteini \u00fcretimini engellemeyi hatta hasarl\u0131 n\u00f6ronlar\u0131 kurtarmay\u0131 ama\u00e7l\u0131yor.
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Bireysel olarak di\u015f, di\u015f eti ve a\u011f\u0131z sa\u011fl\u0131\u011f\u0131m\u0131za dikkat etmek en basit Alzheimer\u2019dan korunma yollar\u0131ndan biri olabilir. Fakat unutulmamal\u0131d\u0131r ki Alzheimer olduk\u00e7a kompleks bir hastal\u0131kt\u0131r ve b\u00f6yle bir hastal\u0131\u011f\u0131 dar bir \u00e7er\u00e7eveye oturtmak olduk\u00e7a zordur. Bilim \u00e7evrelerince bu yeni \u00e7al\u0131\u015fman\u0131n sevin\u00e7le kar\u015f\u0131lanmas\u0131n\u0131n sebeplerinden biri en ba\u015fta bahsedildi\u011fi gibi y\u00fczy\u0131l\u0131 a\u015fk\u0131n s\u00fcredir var olan bu hastal\u0131\u011fa tam anlam\u0131yla bir tedavi y\u00f6ntemi geli\u015ftirmek i\u00e7in yeni bir bak\u0131\u015f a\u00e7\u0131s\u0131na ve umuda sahip olunmas\u0131 olabilir.
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*Cortexyme, Alzheimer ve di\u011fer n\u00f6rodejeneratif hastal\u0131klar i\u00e7in yeni tedavi y\u00f6ntemleri geli\u015ftiren bir kurulu\u015ftur.<\/em><\/strong><\/p>\n\n\n\n

Kaynak\u00e7a:<\/h2>\n\n\n\n
  1. https:\/\/www.newscientist.com\/article\/2191814-we-may-finally-know-what-causes-alzheimers-and-how-to-stop-it\/<\/strong><\/a> <\/li>
  2. KELE\u015e, E , \u00d6ZALEVL\u0130, S . “Alzheimer Hastal\u0131\u011f\u0131 ve Tedavi Yakla\u015f\u0131mlar\u0131”. \u0130zmir Katip \u00c7elebi \u00dcniversitesi Sa\u011fl\u0131k Bilimleri Fak\u00fcltesi Dergisi 3 (2018): 39-42<\/strong><\/li>
  3. https:\/\/www.alz.co.uk\/research\/world-report-2018<\/strong><\/a>, World Alzheimer Report 2018<\/strong><\/li>
  4. “Alzheimer\u2019s disease drug-development pipeline: few candidates, frequent failures”  <\/strong>https:\/\/doi.org\/10.1186\/alzrt269<\/strong><\/a><\/li>
  5. “Porphyromonas gingivalis in Alzheimer\u2019s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors”<\/strong> DOI: 10.1126\/sciadv.aau3333<\/a><\/strong> <\/li>
  6. \u201cPotentially modifiable risk factors for dementia in identical twins\u201d, <\/strong>https:\/\/doi.org\/10.1016\/j.jalz.2006.01.002<\/strong><\/a><\/li>
  7. https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/the-top-10-causes-of-death<\/strong><\/li><\/ol>\n","protected":false},"excerpt":{"rendered":"

    Alois Alzheimer, y\u00fczy\u0131l\u0131 a\u015fk\u0131n s\u00fcre \u00f6nce daha sonralar\u0131 kendi ad\u0131yla an\u0131lacak olan Alzheimer hastal\u0131\u011f\u0131n\u0131 \u201cyap\u0131\u015fkan plaklar\u0131n baz\u0131 beyin b\u00f6lgelerine ve<\/p>\n","protected":false},"author":153,"featured_media":2621,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[1,25,165],"tags":[57,346,349,348,347,345],"acf":[],"views":1384,"_links":{"self":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2611"}],"collection":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/users\/153"}],"replies":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/comments?post=2611"}],"version-history":[{"count":17,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2611\/revisions"}],"predecessor-version":[{"id":3126,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2611\/revisions\/3126"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media\/2621"}],"wp:attachment":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media?parent=2611"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/categories?post=2611"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/tags?post=2611"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}