{"id":8452,"date":"2020-11-17T16:48:14","date_gmt":"2020-11-17T13:48:14","guid":{"rendered":"http:\/\/blog.ulubat.org\/?p=8452"},"modified":"2021-02-07T22:09:04","modified_gmt":"2021-02-07T19:09:04","slug":"insan-genom-serisi-1-alzheimer-beyni-nasil-degistiriyor","status":"publish","type":"post","link":"https:\/\/blog.ulubat.org\/index.php\/genel\/insan-genom-serisi-1-alzheimer-beyni-nasil-degistiriyor\/","title":{"rendered":"\u0130NSAN GENOM SER\u0130S\u0130 – 1: Alzheimer Beyni Nas\u0131l De\u011fi\u015ftiriyor?"},"content":{"rendered":"\n
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(Alzheimer hastas\u0131.)
(G\u00f6rsel Kayna\u011f\u0131: Pathdoc\/Shutterstock<\/a>)<\/figcaption><\/figure>\n\n\n\n

Giri\u015f<\/p>\n\n\n\n

Alzheimer yeti\u015fkinlerde\nen \u00e7ok g\u00f6r\u00fclen n\u00f6rodejeneratif hastal\u0131klardan biridir. 1906 y\u0131l\u0131nda Alman\nn\u00f6ropsikiyatr Alois Alzheimer\u2019\u0131n beyindeki Amiloid plaklar\u0131 ve n\u00f6rofibriller\nyumaklar\u0131 ke\u015ffetmesiyle ortaya \u00e7\u0131km\u0131\u015ft\u0131r. Genellikle 60-90 ya\u015f aral\u0131\u011f\u0131nda\ng\u00f6r\u00fcl\u00fcr ancak otuzlu ya\u015flarda da ortaya \u00e7\u0131kabilir. Hastal\u0131k ilerledik\u00e7e haf\u0131za\nve muhakemede azalma ve davran\u0131\u015f de\u011fi\u015fikli\u011fi g\u00f6r\u00fcl\u00fcr. Geli\u015fmi\u015f \u00fclkelerde\ng\u00f6r\u00fclme oran\u0131 %1.4\u2019t\u00fcr ve ABD\u2019de y\u0131lda 100 bin ki\u015fi bu hastal\u0131ktan dolay\u0131\n\u00f6lmektedir. T\u00fcrkiye\u2019deyse 600 bin hasta bulunuyor ve her \u00fc\u00e7 saniyede bir ki\u015fi\ndemansa (bunamaya) yakalan\u0131yor. Bu hastalar\u0131n da \u00fc\u00e7te ikisi Alzheimer oluyor.\n\u00dclkemizde 65 ya\u015ftan sonra her alt\u0131 kad\u0131ndan ve on bir erkekten biri Alzheimer\noluyor. Kad\u0131nlarda daha fazla g\u00f6r\u00fclmesinin nedeni hormonal fakt\u00f6rler, i\u015f\nalanlar\u0131, ya\u015fam s\u00fcresi, e\u011fitim seviyesi, stres, kalp hastal\u0131klar\u0131n\u0131n g\u00f6r\u00fclme\ns\u0131kl\u0131\u011f\u0131, depresyon ve uyku bozuklu\u011fu olabilir. <\/p>\n\n\n\n

Alzheimer\u2019da haf\u0131za ve\nmuhakemede zay\u0131flaman\u0131n yan\u0131 s\u0131ra konu\u015fma ve \u00fc\u00e7 boyutlu g\u00f6r\u00fc\u015fte bozukluk olur.\nHastal\u0131\u011f\u0131n son evrelerinde davran\u0131\u015fta sertlik, mutizm (sessizlik), yata\u011fa\nd\u00fc\u015fme, hal\u00fcsinasyon, n\u00f6bet, miyoklonus (kaslar\u0131n istemsiz sars\u0131lmas\u0131) olur ve\nParkinson semptomlar\u0131 g\u00f6r\u00fcl\u00fcr. Yetersiz beslenme, enfeksiyon ve kalp\nhastal\u0131klar\u0131 gibi nedenlerden dolay\u0131 \u00f6l\u00fcmle sonu\u00e7lan\u0131r. Tan\u0131s\u0131 da kesin olarak\nsadece postmortem konabilir. <\/p>\n\n\n\n

Demans haf\u0131za, muhakeme ve di\u011fer zihinsel kabiliyetlerin zay\u0131flamas\u0131na verilen genel bir terimdir. Alzheimer ise demans\u0131n bir \u00e7e\u015fidi olup demans hastalar\u0131n\u0131n %60-80\u2019ini olu\u015fturur. Alzheimer ayn\u0131 zamanda demans\u0131n bir nedenidir. <\/p>\n\n\n\n

Wisconsin \u00dcniversitesi\nAlzheimer Ara\u015ft\u0131rma Merkezi\u2019nin yapt\u0131\u011f\u0131 bir \u00e7al\u0131\u015fmada insanlar\u0131n e\u011fitim\nd\u00fczeyiyle Alzheimer aras\u0131ndaki ili\u015fki incelenmi\u015ftir. Y\u00fcksek e\u011fitim seviyesine\nsahip ki\u015filerin beyninde Amiloid ve Tau proteinlerinin birikiminin di\u011fer\nbireylere g\u00f6re \u00e7ok daha az oldu\u011fu g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. Ayr\u0131ca Amerika Ulusal Sa\u011fl\u0131k\nEnstit\u00fcs\u00fc\u2019n\u00fcn destekledi\u011fi bir \u00e7al\u0131\u015fmada 10 y\u0131ll\u0131k s\u00fcreyle \u201cBilgisayarl\u0131 Bilgi \u0130\u015fleme\nH\u0131z\u0131\u201d egzersizi yapan bireyler incelenmi\u015ftir. Uygulaman\u0131n demans riskini %33\nazaltt\u0131\u011f\u0131 g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. Bu nedenle T\u00fcrk Alzheimer Derne\u011fi, G\u00fcnd\u00fcz Ya\u015fam Evleri\ndenilen bak\u0131m evlerinde Alzheimer hastalar\u0131 i\u00e7in bilgisayarl\u0131 dikkat ve bellek\negzersizleri yapmaktad\u0131r. Fiziksel aktivite ve beslenmenin de Alzheimer\u2019a iyi\ngeldi\u011fi g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. \u00d6zellikle her g\u00fcn meyve t\u00fcketenlerde hastal\u0131k riski \u00e7ok\nd\u00fc\u015fmektedir. G\u00fcnde 1-2 fincan kahve (ya da 3-4 fincan T\u00fcrk kahvesi) ve siyah\n\u00e7ikolata t\u00fcketimi de hastal\u0131\u011fa iyi gelmektedir. \u00c7ikolata Amiloid plaklar\u0131\nazalt\u0131r. \u0130\u00e7indeki Flavonoid de deney hayvanlar\u0131nda zihinsel i\u015flevlere iyi\ngelmi\u015ftir. <\/p>\n\n\n\n

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(Beyindeki amiloid plaklar. G\u00f6rsel Kayna\u011f\u0131: Nobeastsofierce\/Shutterstock)<\/a><\/figcaption><\/figure>\n\n\n\n

Alzheimer Geneti\u011fi<\/p>\n\n\n\n

Beynin hipokamp\u00fcs gibi limbik yap\u0131lar\u0131n\u0131 etkileyen Alzheimer\u2019la ilgili 1990\u2019larda d\u00f6rt gen belirlenmi\u015ftir. Bunlardan \u00fc\u00e7\u00fc otozomal bask\u0131nd\u0131r ve bunlar APP, PSEN1<\/em> ve PSEN2<\/em>\u2019dir. S\u0131ras\u0131yla \u03b2<\/a>-Amiloid \u00d6nc\u00fcl\u00fc Protein (\u03b2<\/a>APP ya da A\u03b2 peptidi), Presenilin 1 ve Presenilin 2 \u00fcretirler. D\u00f6rd\u00fcnc\u00fc gen APOE<\/em>\u2019dir ve plazma lipoproteinlerinin protein bile\u015feni olan Apolipoprotein E\u2019yi \u00fcretir. Ancak bu genin mutasyonu hastal\u0131\u011fa direkt olarak yol a\u00e7maz. Yine de Alzheimer\u2019\u0131n geli\u015fmesinde b\u00fcy\u00fck rol\u00fc vard\u0131r. Genin Epsilon 4 <\/em>aleli Alzheimer\u2019a duyarl\u0131l\u0131\u011f\u0131 artt\u0131r\u0131r ve hastal\u0131\u011f\u0131n daha erken ya\u015fta ba\u015flamas\u0131na neden olur. Epsilon 4, APOE<\/em> geninde ne kadar \u00e7ok bulunursa hastal\u0131k o kadar erken ba\u015flar. Bu d\u00f6rt proteinden Alzheimer i\u00e7in en \u00f6nemli olan \u03b2APP<\/a>\u2019dir ve Amiloid plaklar\u0131n birikiminden sorumludur. %20-70 kadar otozomal bask\u0131n Alzheimer hastas\u0131n\u0131n PSEN1, <\/em>%5\u2019ten az\u0131n\u0131n PSEN2 <\/em>ve %1-2\u2019sinin APP <\/em>mutasyonu vard\u0131r. Bununla birlikte beyinde birikip zihinsel fonksiyonlar\u0131 k\u00f6t\u00fc etkileyen TDP-43 proteini de Alzheimer\u2019la ili\u015fkilidir. Mitokondriyal DNA polimorfizmi de Alzheimer i\u00e7in bir risk fakt\u00f6r\u00fc olabilir. <\/p>\n\n\n\n

\u03b2APP; <\/a>beyin h\u00fccresinde endozom, lizozom, ER ve golgide\nbulunan transmembran bir proteindir. \u00dc\u00e7 farkl\u0131 proteaz taraf\u0131ndan par\u00e7alan\u0131r. Bunlar \u03b1-sekretaz<\/a>, \u03b2-sekretaz <\/a>ve\n\u03b3-sekretazd\u0131r<\/a>. \u03b2APP e\u011fer endozomal lizozom i\u00e7inde\npar\u00e7alan\u0131rsa 40 amino asitlik peptid olu\u015fur (A\u03b240<\/a>).\nBu peptidin i\u015flevi bilinmiyor ve beyne zarars\u0131z oldu\u011fu d\u00fc\u015f\u00fcn\u00fcl\u00fcyor ancak \u03b2APP\u2019nin\nER ya da cis<\/em>-Golgi i\u00e7inde\npar\u00e7alanmas\u0131 sonucu olu\u015fan 42 ya da 43 amino asitlik peptid (A\u03b242\/43) beyinde Amiloid\nplak olarak birikir. H\u00fccre membran\u0131nda bulunan \u03b2APP\u2019nin h\u00fccre d\u0131\u015f\u0131nda kalan k\u0131sm\u0131\nN-terminal u\u00e7tur. Geriye kalan k\u0131sm\u0131 da membrana g\u00f6m\u00fcl\u00fcd\u00fcr. \u03b1-sekretaz <\/a>bu peptidin N-terminal ucunda bulunan ve\nmembrandan 12-13 amino asitlik mesafede bulunan Lizin 16 – L\u00f6sitin 17 ba\u011f\u0131n\u0131\nkopar\u0131r. Bu sayede toksik A\u03b2 peptidi olu\u015fumunu engeller. \u03b2-sekretaz<\/a>\nise APP <\/em>geninde mutasyon varsa N-terminal\nucundan amino asit kopar\u0131rken toksik <\/a>A\u03b2 <\/a>olu\u015fturabilir. Mutasyon\nsonucunda Lizin-Metiyonin ba\u011f\u0131 yerine Asparajin-L\u00f6sitin ba\u011f\u0131 kopar\u0131l\u0131r. Buna\n\u0130sve\u00e7 mutasyonu denir. Neyse ki <\/a>\u03b1-sekretaz <\/a>\u03b2APP\u2019yi en \u00e7ok par\u00e7alayan\nproteazd\u0131r (%90). Bu sayede Alzheimer\u2019\u0131n ilerlemesi uzun zaman al\u0131r. \u03b1-sekretaz\nsonu\u00e7ta serbest APP\u03b1 ve membrana ba\u011fl\u0131 C83-terminal fragmenti olu\u015fturur. \u03b3-sekretaz\nda C-terminal ucunu membran i\u00e7inden kopar\u0131r ve bu \u015fekilde A\u03b240 <\/a>a\u00e7\u0131\u011fa \u00e7\u0131kar\u0131r. Ancak Alzheimer\u2019da \u03b3-sekretaz, <\/a>peptid zincirini C-terminal ucuna daha\nyak\u0131n kopar\u0131r ve sonu\u00e7ta A\u03b242 ve A\u03b243 olu\u015fur. MSS bunlar\u0131 temizleyemez ve bu\niki peptid Amiloid plak olu\u015fturur. APP,\nPSEN1 <\/em>ve PSEN2<\/em>\u2019de mutasyon olmas\u0131\nA<\/a>\u03b2<\/a>42\/43\u2019<\/em>\u00fcn \u00fcretimini artt\u0131r\u0131r. Bundan \u00f6t\u00fcr\u00fc\nAlzheimer\u2019\u0131n ilerlemesine neden olan sekretazlar \u03b2-sekretaz ve \u03b3-sekretazd\u0131r. <\/p>\n\n\n\n

APP, <\/em>21.\nkromozomda oldu\u011fu i\u00e7in hastalar\u0131n %1\u2019i Down sendromludur. 40 ya\u015f\u0131ndan sonra neredeyse\nt\u00fcm Down sendromlu bireylerde Alzheimer belirtileri g\u00f6r\u00fcl\u00fcr. Hastal\u0131kta\nkortikal atrofi, n\u00f6ritik plaklar ve n\u00f6rofibriller yumaklar olu\u015fur. N\u00f6ritik\nplaklar A\u03b2<\/a>42\/43 ve Apolipoprotein E gibi bir\u00e7ok\nprotein i\u00e7erir. N\u00f6rofibriller yumaklar ise hiperfosforile Tau proteinleri\ni\u00e7erir. Asl\u0131nda Tau n\u00f6ronal b\u00fct\u00fcnl\u00fck, mikrot\u00fcb\u00fcl stabilitesi ve aksonal\ntransport i\u00e7in \u00f6nemlidir. Ancak hiperfosforile oldu\u011funda birikimi zararl\u0131d\u0131r.\nSerebral atardamar duvar\u0131nda da Amiloid birikir. Apolipoprotein E de Amiloid ve\nn\u00f6ritik plaklarda bulunan A\u03b2<\/a>\npeptidlerine ba\u011flan\u0131r. <\/p>\n\n\n\n

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(Haf\u0131zas\u0131 yok olmaya ba\u015flayan Alzheimer hastas\u0131 \u00e7izimi. G\u00f6rsel Kayna\u011f\u0131: Lightspring\/Shutterstock)<\/a><\/figcaption><\/figure>\n\n\n\n

Tau ne kadar Alzheimer\u2019da\nn\u00f6rodejenerasyona neden olsa da bu proteini kodlayan MAPT<\/em> genindeki mutasyon Alzheimer\u2019la ilgili de\u011fildir. Bu genin\nmutasyonu en s\u0131k g\u00f6r\u00fclen demanslardan biri olan Frontotemporal Demans\u2019a neden\nolur. <\/p>\n\n\n\n

Tau proteini Alzheimer\nilerledik\u00e7e entorhinal korteks ve hipokamp\u00fcsten ba\u015flayarak beyinde git gide\nbirikir. Bundan dolay\u0131 Tau\u2019nun birikme miktar\u0131 Alzheimer\u2019\u0131n a\u015famas\u0131 ve \u015fiddeti ile\norant\u0131l\u0131d\u0131r. Birka\u00e7 Tau proteininden olu\u015fan oligomerler beyindeki sinapslar\nboyunca ilerler ve bu noktalardan h\u00fccre fonksiyonunu bozmaya ba\u015flar. <\/p>\n\n\n\n

Tau\u2019nun ili\u015fkili oldu\u011fu\ndi\u011fer demanslar Kronik Travmatik Ensefalopati, Pick hastal\u0131\u011f\u0131, Frontotemporal\nDemans, Parkinsonism-17 (FTDP-17), Progresif Supran\u00fckleer Fel\u00e7 ve Kortikobazal\nDejenerasyon\u2019dur. Bu hastal\u0131klar\u0131n hepsi a\u011f\u0131r ve ilerleyicidir. Hepsinde anormal\nTau\u2019nun yap\u0131s\u0131 farkl\u0131d\u0131r. <\/p>\n\n\n\n

Bilimsel \u00c7al\u0131\u015fmalar<\/p>\n\n\n\n

Alzheimer ile ilgili \u00e7o\u011fu\n\u00e7al\u0131\u015fma hipokamp\u00fcs ve orta temporal lob \u00fczerinedir. 65 ya\u015f \u00fcst\u00fc Alzheimer\nhastalar\u0131nda komorbidite (birden fazla hastal\u0131k g\u00f6r\u00fclme durumu) s\u0131kt\u0131r. Beyin\nvolumetresini (diyabet, hipertansiyon, serebrovask\u00fcler hastal\u0131klar vb.) ve\nhipokamp\u00fcs boyutunu (hipokampal skleroz vb.) etkileyen hastal\u0131klar Alzheimer\u2019\u0131n\nyan\u0131nda geli\u015febilir. Bu durum hipokamp\u00fcs\u00fcn n\u00f6rodejenerasyonu \u00f6l\u00e7mede \u00f6nemli bir\nyap\u0131 oldu\u011funu g\u00f6sterir. Sadece hipokamp\u00fcs\u00fcn arkas\u0131nda bile Alzheimer\natrofisinden etkilenen bir\u00e7ok b\u00f6lge bulunmaktad\u0131r. Bu ay yay\u0131mlanan bir\n\u00e7al\u0131\u015fmada ge\u00e7 ba\u015flang\u0131\u00e7l\u0131 Alzheimer (LOAD) ile hastalar\u0131n daha gen\u00e7 oldu\u011fu\notozomal dominant Alzheimer (ADAD) korteks \u00f6rnekleri incelendi\u011finde etkilenen\nyerlerin ayn\u0131 ancak \u015fiddetlerinin farkl\u0131 oldu\u011fu g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. LOAD\u2019da atrofi en\n\u00e7ok temporal lobda bulunurken ADAD\u2019da en \u00e7ok pariyetal b\u00f6lgededir. Tau\u2019nun\nLOAD\u2019da temporal, oksipital, pariyetal ve frontal b\u00f6lgelere b\u00fcy\u00fck etkisi\nbulunurken LOAD\u2019a k\u0131yasla ADAD\u2019da precuneusa daha b\u00fcy\u00fck etkisi vard\u0131r. Amiloid\npatolojisi de en \u00e7ok ADAD\u2019da g\u00f6r\u00fclmektedir ve bazal ganglionu Amiloid\nizotoplar\u0131n\u0131 LOAD\u2019a g\u00f6re daha \u00e7ok almaktad\u0131r. <\/p>\n\n\n\n

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[D\u00fcnya Alzheimer g\u00fcn\u00fc (21 Eyl\u00fcl). G\u00f6rsel Kayna\u011f\u0131: awsome design studio\/Shutterstock<\/a>]<\/figcaption><\/figure>\n\n\n\n

ADAM transmembran proteinlerinden ADAM-10 ve ADAM-17 \u00fczerinde deney yap\u0131lm\u0131\u015ft\u0131r. ADAM proteinleri bir disintegrin ve metalloproteazd\u0131r. ADAM-17 bir T\u00fcm\u00f6r Nekroz Fakt\u00f6r\u00fc-\u03b1<\/a> D\u00f6n\u00fc\u015ft\u00fcr\u00fcc\u00fc Enzim\u2019dir (Tumor Necrosis Factor-\u03b1 Converting Enzyme) (TACE). Bu enzim \u03b1-sekretaz\u0131n <\/a>yapt\u0131\u011f\u0131 gibi Lizin 16 \u2013 L\u00f6sitin ba\u011flar\u0131n\u0131 kopar\u0131r. ADAM-10\u2019un da h\u00fccrede \u00e7ok olmas\u0131 Protein Kinaz C (PKC) ba\u011fl\u0131 \u03b1-sekretaz\u0131n etkinli\u011fini artt\u0131r\u0131r. ADAM10 ve ADAM17 enzimleri peptidleri par\u00e7alar. B\u00f6lgeleri prodomain, metalloprotez, disintegrin, \u00e7oklu sistein b\u00f6lgesi, transmembran b\u00f6lge ve sitoplazmik k\u0131s\u0131md\u0131r. Aktiviteleri prodomain taraf\u0131ndan sa\u011flan\u0131r. <\/p>\n\n\n\n

Bu sene yap\u0131lan bir di\u011fer\n\u00e7al\u0131\u015fmada farelerin korteksinde DLGAP2 <\/em>\u00fcretiminin\nazalmas\u0131 sonucu plak ve yumaklar\u0131n artt\u0131\u011f\u0131 ve zihinsel i\u015flevlerin h\u0131zla\nzay\u0131flad\u0131\u011f\u0131 g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. Bunun nedeni DLGAP2\u2019<\/em>nin\ndendritler i\u00e7in \u00f6nemli bir protein olmas\u0131d\u0131r. Dendritlerin hem \u015feklini hem de\nsay\u0131s\u0131n\u0131 d\u00fczenler. <\/p>\n\n\n\n

TNF-\u03b1\n<\/a>ile ilgili bu ay yay\u0131nlanan bir\n\u00e7al\u0131\u015fmada bu sitokinin seviyesinin de\u011fi\u015fmesinin Alzheimer\u2019\u0131n \u015fiddetini\nartt\u0131rd\u0131\u011f\u0131 g\u00f6r\u00fclm\u00fc\u015ft\u00fcr. TNF-\u03b1 SSS\u2019de artt\u0131k\u00e7a n\u00f6ron kayb\u0131na neden olur. Hafif\nbili\u015fsel bozukluk ve Alzheimer\u2019da SSS\u2019de TNF-\u03b1 resept\u00f6rleri (TNFR1 ve TNFR2)\nsay\u0131s\u0131 bu nedenle artar. TNFR1\u2019in inflamatuvar i\u015flevi ve TNFR2\u2019nin\nn\u00f6roprotektif etkisi vard\u0131r. <\/p>\n\n\n\n

Video: Alzheimer Beyni Nas\u0131l De\u011fi\u015ftiriyor? (How Alzheimer\u2019s Changes The Brain)<\/a><\/p>\n\n\n\n

Tan\u0131 \u0130\u00e7in Testler<\/p>\n\n\n\n

Hen\u00fcz Tau ve Amiloid\nplaklar\u0131n \u00f6l\u00e7\u00fcm\u00fc i\u00e7in bir kan testi yoktur ancak bu konuda \u00e7al\u0131\u015fmalar\ns\u00fcrmektedir. Bilgisayarl\u0131 tomografi ve MR\u2019la bile g\u00f6r\u00fcnt\u00fcleme yap\u0131lamaz. Ancak\nPET analizi her iki proteinin de miktar\u0131n\u0131 \u00f6l\u00e7ebilir. Ancak ne kadar Amiloid\nPET analizi G\u0131da ve \u0130la\u00e7 \u0130daresi (FDA) onayl\u0131 olsa da Amiloid birikiminden\ndemans\u0131n a\u015famas\u0131n\u0131 g\u00f6steremez. Bununla birlikte Tau PET analizi ileride\nAlzheimer\u2019\u0131n a\u015famalar\u0131n\u0131 kesin olarak tespit edebilir. FDA taraf\u0131ndan ilk\nonaylanan Tau PET izotopu da F-18\nFlortaucipir<\/em>\u2019dir. <\/p>\n\n\n\n

65 ya\u015f sonras\u0131 koku\nduyusunda azalma Alzheimer\u2019\u0131n g\u00f6stergesi olabilir ve testinin yap\u0131lmas\u0131\nkolayd\u0131r. Entorhinal korteks kal\u0131nl\u0131\u011f\u0131n\u0131n MR ile \u00f6l\u00e7\u00fclmesine k\u0131yasla koku testi\ndaha g\u00fcvenilirdir ancak Amiloid PET testi kadar g\u00fcvenilir de\u011fildir. Ne var ki\nkoku testi PET analizlerine g\u00f6re \u00e7ok ucuzdur. <\/p>\n\n\n\n

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(Alzheimer hastal\u0131\u011f\u0131. G\u00f6rsel Kayna\u011f\u0131: DedMityay\/Shutterstock<\/a>)<\/figcaption><\/figure>\n\n\n\n

Tedavi<\/p>\n\n\n\n

Hastal\u0131\u011f\u0131n kesin bir\ntedavisi olmasa da \u03b1-sekretaz<\/a>\u0131n Amiloid plak\nbirikimini engellemesi tedavi i\u00e7in kullan\u0131\u015fl\u0131 olabilir. Bu da deneysel olarak\nforbol esterler ve muskarinik agonistler gibi PKC aktivat\u00f6rleri ile\nyap\u0131lm\u0131\u015ft\u0131r. ADAM-10 ve ADAM-17 proteinleri bu deneyler i\u00e7inde yer al\u0131r. <\/p>\n\n\n\n

Son y\u0131llarda a\u015f\u0131\ngeli\u015ftirmeye y\u00f6nelik umutlar tam s\u00f6nerken Nature dergisinde yay\u0131mlanan bir\nyaz\u0131da Aduconumab<\/em> molek\u00fcl\u00fcn\u00fcn beyinde\nbiriken Amiloid plaklar\u0131n\u0131 b\u00fcy\u00fck \u00f6l\u00e7\u00fcde azaltt\u0131\u011f\u0131 belirtildi. Ba\u015far\u0131s\u0131z olan\na\u015f\u0131lardan di\u011fer bir fark\u0131 da hastal\u0131\u011f\u0131n gidi\u015fat\u0131n\u0131 yava\u015flatmas\u0131d\u0131r. Bu a\u015f\u0131n\u0131n\nyan etkileri de vard\u0131r ancak bunlar tolere edilebilir. \u00d6n\u00fcm\u00fczdeki y\u0131llarda bu molek\u00fcl\nile ilgili yeni verilerin \u00e7\u0131kmas\u0131 bekleniyor.<\/p>\n\n\n\n

Bilgi Kaynak\u00e7as\u0131<\/p>\n\n\n\n

  1. T\u00fcrkiye Alzheimer Derne\u011fi. 29.08.2020. https:\/\/www.alzheimerdernegi.org.tr\/2020\/08\/29\/turkiyede-600-000-aile-alzheimer-hastaligi-ile-mucadele-ediyor\/#:~:text=Alzheimer%27in%20kad%C4%B1nlarda%20daha%20%C3%A7ok,11%27de%201%20olarak%20g%C3%B6zlenmekte<\/a>. <\/li>
  2. T\u00fcrkiye Alzheimer Derne\u011fi. https:\/\/www.alzheimerdernegi.org.tr\/2020\/08\/29\/gelismis-ulkelerde-alzheimer-hastaligi-azalirken-turkiyede-artiyor\/<\/a> <\/li>
  3. Genetics In Medicine. Thompson and Thompson. \u201cCase 4: Alzheimer Disease (Cerebral Neuronal Dysfunction and Death, MIM 104300)\u201d 398-399. Eight Edition (2016).<\/li>
  4. Genetics In Medicine. Thompson and Thompson. \u201cChapter 12 \u2013 The Molecular, Biochemical and Cellular Basis Of Genetic Disease\u201d 242-246. Eight Edition (2016). <\/li>
  5. Genetics In Medicine. Thompson and Thompson. \u201cChapter 8 \u2013 Complex Inheritance Of Common Multifactorial Disorders\u201d 150-152. Eight Edition (2016). <\/li>
  6. Bright Focus Foundation. James M. Ellison MD. \u201cTAU Protein And Alzheimer\u2019s Disease: What\u2019s The Connection?\u201d 06.05.2019, 09.11.2020. https:\/\/www.brightfocus.org\/alzheimers-disease\/article\/tau-protein-and-alzheimers-disease-whats-connection<\/a> <\/li>
  7. BrainFacts.org. Mehta, Aalok. \u201cAlzheimer\u2019s Disease and Dementia Today\u201d <\/a>14.02.2012. https:\/\/www.brainfacts.org\/archives\/2012\/alzheimers-disease-today<\/a> <\/li>
  8. ScienceDirect. Dincer et al., \u201cComparing cortical signatures of atrophy between late-onset and autosomal dominant Alzheimer disease\u201d Neuroimage: Clinical. <\/em>(2020). <\/li>
  9. ScienceDirect. Tousseyn et al., \u201cCHAPTER 52 \u2013 The Molecular and Genetic Basis of Neurodegenerative Diseases\u201d Modern Surgical Pathology (Second Edition). <\/em>(2) 2039-2068. (2009).<\/li>
  10. ScienceDirect. Heinrikson, R.L.. \u201cSecretases\u201d Encyclopedia of Biological Chemistry. <\/em>199-202. (2013). <\/li>
  11. ScienceDirect. Marr, Robert A.. \u201cChapter 4 – The Amyloid \u03b2 Precursor Protein and Cognitive Function in Alzheimer\u2019s Disease\u201d Genes, Environment and Alzheimer\u2019s Disease. <\/em>97-133. (2016). <\/li>
  12. ScienceDirect. Ouellette et al.. \u201cCross-Species Analyses Identify Dlgap2 as a Regulator of Age-Related Cognitive Decline and Alzheimer\u2019s Dementia\u201d Cell Reports. <\/em>(32):9. Eyl\u00fcl 2020.<\/li>
  13. Frontiers In Cell and Developmental Biology. Kato, Takashi. Hagiyama, Man. Ito, Akihiko. \u201cRenal ADAM10 and 17: Their Physiological and Medical Meanings\u201d 06.11.2018. https:\/\/www.frontiersin.org\/articles\/10.3389\/fcell.2018.00153\/full<\/a> <\/li>
  14. ScienceDirect. Zhao, Aonan. Li, Yuanyuan. Deng, Yulei. \u201cTNF receptors are associated with tau pathology and conversion to Alzheimer\u2019s dementia in subjects with mild cognitive impairment\u201d Neuroscience Letters. <\/em>(738). Kas\u0131m 2020. <\/li>
  15. Alzheimer\u2019s Association. \u201cDementia vs. Alzheimer\u2019s Disease: What Is The Difference?\u201d <\/a>https:\/\/www.alz.org\/alzheimers-dementia\/difference-between-dementia-and-alzheimer-s<\/a> <\/li>
  16. T\u00fcrk N\u00f6ropsikyatri Derne\u011fi.
    21 Eyl\u00fcl D\u00fcnya Alzheimer G\u00fcn\u00fc – T\u00fcrk N\u00f6ro-Psikiyatri Derne\u011fi (turknoropsikiyatri.org)<\/a> <\/li><\/ol>\n\n\n\n

    G\u00f6rsel Kaynak\u00e7as\u0131<\/p>\n\n\n\n

    1. Nobeastsofierce\/Shutterstock<\/a> <\/li>
    2. Pathdoc\/Shutterstock<\/a> <\/li>
    3. Lightspring\/Shutterstock<\/a> <\/li>
    4. awsome design studio\/Shutterstock<\/a> <\/li>
    5. DedMityay\/Shutterstock<\/a> <\/li><\/ol>\n\n\n\n

      Video Kayna\u011f\u0131<\/p>\n\n\n\n

      1. National Institute of Health. 13.11.2020. “Video: How Alzheimer’s Changes the Brain”
        Video: How Alzheimer’s Changes the Brain | National Institute on Aging (nih.gov)<\/a> <\/li><\/ol>\n","protected":false},"excerpt":{"rendered":"

        Giri\u015f Alzheimer yeti\u015fkinlerde en \u00e7ok g\u00f6r\u00fclen n\u00f6rodejeneratif hastal\u0131klardan biridir. 1906 y\u0131l\u0131nda Alman n\u00f6ropsikiyatr Alois Alzheimer\u2019\u0131n beyindeki Amiloid plaklar\u0131 ve n\u00f6rofibriller<\/p>\n","protected":false},"author":267,"featured_media":8460,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[1,25,165],"tags":[715,1402,1410,57,1365,1389,1384,1382,157,1393,250,1379,70,74,894,893,1374,58,1405,274,1391,332,1376,1386,1396,865,1407,1395,149,1228,115,810,1187,249,990,92,1177,1363,848,621,674,174,1237,1401,1399,1377,1387,1394,1248,1408,1369,1368,220,297,1378,1371,1398,1390,1406,1397,1403,1366,1385,1383,1400,996,1229,1404,1380,1381,1388,1370,1219,345,1226,84,1142,1392,1372,987,1364,59,60,68],"acf":[],"views":842,"_links":{"self":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/8452"}],"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\/267"}],"replies":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/comments?post=8452"}],"version-history":[{"count":8,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/8452\/revisions"}],"predecessor-version":[{"id":9779,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/8452\/revisions\/9779"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media\/8460"}],"wp:attachment":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media?parent=8452"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/categories?post=8452"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/tags?post=8452"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}