Demencije i hipokampus
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1 Gyrus 2 (2014) Demencije i hipokampus Dinko Smilović Medicinski fakultet Sveučilišta u Zagrebu U bolesti, osim hipokampusa, najveći gubitci moždane mase se nalaze u temporalnom i parijetalnom režnju, te djelovima frontalnog režnja i cingularnog girusa, te se prikazuju CT-om i MRI-om. Demencija (latinski de bez i ment um ) je bolest gdje dolazi do ozbiljnog gubitka globalne kognitivne sposobnosti u prijašnje zdrave osobe, tj. do većeg gubitka nego što bi se očekivalo normalnim starenjem. Ono može biti statično, kao kod globalnih oštećenja mozga ili progresivno, kao kod većine demencija. Iako je demencija češća u starije populacije (iznad 65 godina) može se javiti prije tog razdoblja, te se tada naziva demencija ranog nastupa. Demencija sama po sebi nije jedna bolest, već ne-specifični sindrom te može zahvaćati pamćenje, pažnju, jezik i sposobnost rješavanja problema. Za dijagnozu demencije simptomi moraju biti prisutni barem 6 mjeseci, te se moraju isključiti ostali uzrozi, što se može pomoću memo-vi- TAMINS-testa (Vesna Brinar i sur. 2009). Demencija se susreće u bolestima poput Alzheimerove demencije, vaskularne demencije, frontotemporalne demencije, semantičke demencije, Parkinsonove demencije i demencije sa Lewisovim tjelešcima. Već duže vrijeme se govori o povezanosti atrofije hipokampusa i demencija, koja je najizraženija u Alzheimerovoj bolesti. Hipokampus je veoma važan u funkciji pamćenja i dugoročnog zapamćivanja informacija, te je manjak funkcije hipokampusa odgovoran za smetnje pamćenja u ljudi oboljelih od demencija. Hipokampalna atrofija se često zapaža u ljudi oboljelih od demencija, te se mislilo da je specifična za Alzheimerovu bolest, no novija istraživanja pokazuju da se pojavljuje u svih demencija. Volumen hipokampusa je u prosjeku 25-42% manji u Alzheimerovoj bolesti, 21% vaskularnoj demenciji (Vijayakumar i Vijayakumar 2013), 15% u blagom kognitivnom oštećenju, 13% u pseudodemenciji (Dolek i sur. 2012) i 16-21% u frontotemporalnoj demenciji (Frisoni i sur. 1999) mjereno klasičnom metodom MRI uređajem. Novijom metodom mjerenja magnetskog transfera MRI-om se mogu bolje predočiti razlike u gubitku volumena u Alzheimerovoj bolesti i ostalim demencijama te ih tako lakše razlikovati (Hanyu i sur. 2000). Brzina kojom hipokampus atrofira se može koristiti kao rani marker u dijagnostici demencija ako se prati kroz minimalno 6 godina ( Heijer i sur. 2006). Slika 1. Desetogodišnje praćenje hipokampalnog volumena na MRI-u, (pribavljeno s adrese : content/133/4/1163/f2.expansion.html) Najpoznatija i najčešća demencija današnjice je Alzheimerova bolest, koja čini 60-80% dij- 64
2 agnosticiranih demencija te je ujedno i bolest koja u najvećoj mjeri uzrokuje propadanje hipokampusa.. Bolest najčešće nastaje sporadično (95%), te se etiologija objašnjava genskom interakcijom (APP, PSEN1, PSEN2, APOE 4) sa okolišnim čimbenicima poput stresa. Slika 2. Prikaz progresije Alzheimerove bolesti, primjetite veliko smanjenje hipokampusa (pribavljeno s adrese: en.wikipedia.org/wiki/file:alzheimer %27s_disease_brain_comparison.jpg) U bolesti se javljaju plakovi koji sadržavaju izvanstanične depozite većinom beta-amiloida te se talože u krvnim žilama mozga i moždanih ovojnica i dok ih se dovoljno nakupi postaju toksični za neurone. Također se javljaju neurofibrilarne petlje hiperfosforiliranog tau-proteina zbog povećanog ulaska kalcija u stanice. U bolesti dolazi do propadanja kolinergičkih neurona i acetilkolin-sintetizirajućeg enzima acetilkolin-transferaze u hipokampusu, Meynertovoj bazalnoj jezgri i septalno-hipokampalnom putu. Bolest se iskazuje kao retrogradni gubitak pamćenja, s time da se starija sjećanja, semantička i implicitna memorija manje oštećuju od recentnijih sjećanja. Kasnije se javlja dezorijentacija u vremenu i prostoru, poremećaji govora, te se u velikom broju slučaja javlja depresija, nemir i agitiranost. Progresijom počinju dominirati psihički poremećaji karakterizirani halucinacijama, deluzijama i paranoidnim idejama te bolesnici postaju vezani uz postelju i inkontinentni. U bolesti, osim hipokampusa, najveći gubitci moždane mase se nalaze u temporalnom i parijetalnom režnju, te djelovima frontalnog režnja i cingularnog girusa, te se prikazuju CT-om i MRI-om. U likvoru se mogu naći markeri za razlikovanje AD od ostalih demencija, a to su niska razina beta-amiloida 1-42 i visoke razine T-tau i P-tau proteina. Atrofija hipokampusa je zaslužna za početne simptome bolesti, najprominentniji je gubitak recentnog sjećanja (Brinar i sur. 2009). Vaskularna demencija je druga najčešća demencija. Uzrokovana je problemima u opskrbi mozga krvlju, a tipično se iskazuje brojnim mikro infaktima u mozgu, uzrokovanim dugotrajnom arterijskom hipertenzijom ili dijabetesom, hipoksijama. Često se javljaju u a. cerebri anterior ili a. cerebri posterior. U bolesti dominiraju simptomi subkortikalne demencije, što se iskazuje smanjenom pozornošću i inicijativom uz dominantnu psihomotoričku usporenost, nerijetko sa patološkim smijehom ili plačem. Simptomi nastupaju naglo, fluktuiraju te je progresija sporija nego u Alzheimerovoj demenciji (Brinar i sur. 2009). Slika 3. Prikaz mikro infakta na MRI analizi mozga (pribavljeno s adrese: dementia_pictures_slideshow/article.htm) Smatra se ireverzibilnim oblikom demencije, no veoma je važna rana detekcija i točna dijagnoza jer se dio progresije bolesti može prevenirati. 80% oboljelih ima hipertenziju, a ostali rizični čimbenici su pušenje, dob, hiperkolesterolemija i dijabetes mellitus. Dokazano je da u vaskularnoj demenciji, dementivnost korelira sa hipokampalnom atrofijom (Fein i sur. 2000), te da je bolji prediktor nego sam prediktor progresije bolesti od broja infarkta u mozgu (Gainotti i sur. 2004). Gubitak piramidnih neurona u hipokampusu u vaskularnoj demenciji je veoma sličan kao i u Alzheimerovoj bolesti, te se te dvije bolesti često međusobno krivo dijagnosticiraju (Kril i sur. 2002). 65
3 Parkinsonova bolest je degenerativna bolest koja počinje sa gubitkom dopaminergičkih neurona u substanciji nigri. Bolest se pojavljuje sporadično, no 20% bolesnika ima pozitivnu obiteljsku anamnezu u prvom koljenu. Bolest ima 6 stadija, a u 5. i 6. dolazi do propadanja raznih moždanih struktura, uključujući i hipokampus (Bruck i sur. 2004), dok neki autori tvrde da hipokampus ostaje očuvan (Apostolova i sur. 2010). Parkinsonova bolest može biti udružena sa demencijom te tada dolazi do dvostruko veće brzine atrofije hipokampusa tokom bolesti (Camicioli i sur. 2003). Patološka karakteristika bolesti je pojava Lewyjevih tjelešaca, koje su eozinofilne citoplazmatske inkluzije, te su građene od alfa-sinukleina (Brinar i sur. 2009). Frontotemporalna lobarna demencija je demencija koja primarno počinje u frontalnom režnju mozga, te kasnije može preći na temporalni režanj. (Slika 4. Izgled mozga osobe umrle od frontotemporalne demencije, preuzeto s adrese: Od kognitivnih funkcija bolest smanjuje socijalno ponašanje, regulacije emocija, sposobnost fokusiranja te uzrokuje semantičku demenciju i primarnu progresivnu afaziju (Brinar i sur. 2009). Također, za razliku od ostalih demencija, obično se javlja u mlađih ljudi, te se u 30-60% oboljelih javlja naslijeđem, što se povezuje sa mutacijom tau-proteinskog gena na kromosomu 17. Govorni poremećaji mogu biti nefluentna afazija, zbog oštećenja frontalnog režnja, te fluentna afazija, zbog oštećenja temporalnog režnja. Hipokampus tokom bolesti atrofira bilateralno, a u semantičkoj demenciji, podvrsti frontotemporalne lobarne demencije, lijevi hipokampus je manji nego u ljudi oboljelih od Alzheimerove bolesti (Pol i sur. 2006), te promjene u njemu nisu difuzne nego više lokalizirane anteriorno (Laakso i sur. 2000). Iako za većinu demencija još uvijek ne postoji lijek koji bi izliječio bolesti, neki od lijekova na tržištu (npr. Donepezil - reverzibilan i viksokospecifičan inhibitor kolinesteraze) u mozgu mogu usporiti hipokampalnu atrofiju te posljedično i sve jači gubitak pamćenja u bolesnika (Hashimoto i sur. 2005). Neki autori navode da bi se razvojem novih lijekova za sprečavanje atrofije hipokampusa ublažila progresija bolesti i pomoglo u kvalitetnijem liječenju svih oblika demencije (Dhikava i Anandb 2007). Hipokampus je jedna od najvažnijih struktura mozga, koja nam omogućava dugoročno pamćenje i nas ostvaruje kao osobe s poviješću, iskustvima te znanjima koja se povećavaju kako živimo. Njegova disfunkcija nam oduzima taj dio osobnosti i uzrokuje stagnaciju u našem pamćenju te našem napretku kao socijalne i profesionalne osobe. Sve demencije dovode do atrofije hipokampusa i to čini jedan od najozbiljnijih čimbenika u patogenezi bolesti, uzrokujući velike štete za osobe oboljele od njih, te za ljude koji za njih brinu pa i za cijelo društvo. Pošto cijela svjetska populacija stari, za očekivati je da će se incidencija demencija tokom vremena povećavati te one postaju jedan od najvećih zdravstvenih problema današnjice. Pošto se ne očekuje da će se u skoro vrijeme razviti lijekovi koji će izliječiti demencije, razvojem lijekova koji bi čuvali funkciju hipokampusa i zaustavili progresiju bolesti u njemu bi se u velikoj mjeri pomoglo osobama oboljelima od demencije, te im omogućilo normalniji i kvalitetniji život. 66
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