Cutar Alzheimer
Cutar Alzheimer (AD), kuma ana kiranta da kawai Alzheimer's, cuta ce ta neurodegenerative na yau da kullun wacce yawanci ke farawa sannu a hankali kuma a hankali yana ta'azzara akan lokaci.[1][2] Shi ne sanadin kashi 60-70% na lamurra na hauka.[1][2] Alamar farko ta gama gari ita ce wahala wajen tunawa da abubuwan da suka faru kwanan nan.[1] Yayin da cutar ke ci gaba, alamun na iya haɗawa da matsaloli tare da harshe, rashin tunani (ciki har da samun sauƙi a ɓace), sauye-sauyen yanayi, asarar dalili, rashin kula da kai, da kuma al'amurran halayya.[1][2] Yayin da yanayin mutum ya ragu, sau da yawa yakan janye daga iyali da kuma al'umma.[1] A hankali, ayyukan jiki suna ɓacewa, a ƙarshe yana haifar da mutuwa.[3] Ko da yake saurin ci gaba na iya bambanta, yanayin rayuwa na yau da kullun bayan ganewar asali shine shekaru uku zuwa tara.[4][5]
| Cutar Alzheimer | |
|---|---|
 | |
Description (en)  | |
| Iri | tauopathy (en) , aging-associated disease (en) cuta |
| Specialty (en) | neurology (en) |
| Sanadi | unknown (en) |
| Symptoms and signs (en) | memory loss that disrupts daily life (en) , confusion with time and space (en) , challenges in planning or solving problems (en) , difficulty completing familiar tasks at home, at work or at leisure (en) , trouble understanding visual images and spatial relationships (en) , decreased or poor judgment (en) , withdrawal from work or social activities (en) , problems with words in speaking or writing (en) , changes in mood and personality (en) , misplacing things and losing the ability to retrace steps (en) Dementia |
| Physical examination (en) | neurological diagnostic techniques (en) , medical history (en) , magnetic resonance imaging (en) psychological test (en) |
| Genetic association (en) | APOE (en) , NKAIN2 (en) , BMPER (en) , SLC8A1-AS1 (en) , MS4A3 (en) , CR1 (en) , CD2AP (en) , ABCA7 (en) , INPP5D (en) , ZCWPW1 (en) , CELF1 (en) , FERMT2 (en) , CASS4 (en) , PTK2B (en) , SORL1 (en) , SQSTM1 (en) , NDUFAF6 (en) , AP2A2 (en) , IGH (en) , SPPL2A (en) , TRIP4 (en) , CD33 (en) , GLIS3 (en) , PRRC2C (en) , FMN2 (en) , CTNNA2 (en) , LIMS2 (en) , MOBP (en) , STK32B (en) , AFF1 (en) , ANKRD55 (en) , CAMK4 (en) , DMXL1 (en) , MEGF10 (en) , SAP30L (en) , PLEKHG1 (en) , CYCS (en) , ELMO1 (en) , HECW1 (en) , EXOC4 (en) , CSMD1 (en) , ST18 (en) , NCS1 (en) , PLPP4 (en) , ARHGAP20 (en) , SLC4A8 (en) , CRADD (en) , ANO4 (en) , GPC6 (en) , MYO16 (en) , CLMN (en) , GABRG3 (en) , VAT1L (en) , CACNA1G (en) , BCAS3 (en) , PPIAP59 (en) , TGM6 (en) , PARVB (en) , APOC1 (en) , NECTIN2 (en) , TOMM40 (en) , TREM2 (en) , MPZL1 (en) , ATXN7L1 (en) , LUZP2 (en) , CDON (en) , PCNX1 (en) , PICALM (en) , PPP1R3B (en) , SLC4A1AP (en) , POLN (en) , CNTNAP2 (en) , STK24 (en) , VSNL1 (en) , BIN1 (en) , MPP7 (en) , ZNF320 (en) , STK11 (en) , DIP2C (en) , DCHS2 (en) , CLU (en) , CCDC134 (en) , MTHFD1L (en) , RELN (en) , PCDH11X (en) , GAB2 (en) , APP (en) da PLD3 (en) |
| Suna saboda | Alois Alzheimer (en) |
| Medical treatment (en) | |
| Magani | quetiapine (en) , aripiprazole (en) , galantamine (en) , donepezil (en) , risperidone (en) , memantine (en) , rivastigmine (en) , rivastigmine (en) , memantine (en) da pyritinol (en) |
| Identifier (en) | |
| ICD-10-CM | G30.9 da G30 |
| ICD-9-CM | 331.0 da 290.1 |
| OMIM | 104300 |
| DiseasesDB | 490 |
| MedlinePlus | 000760 |
| eMedicine | 000760 |
| MeSH | D000544 |
| GeneReviews | NBK1161 |
| Disease Ontology ID | DOID:10652 |
Ba a fahimci dalilin cutar Alzheimer ba.[1] Kusan kashi 70 cikin 100 na haxarin an yi imanin gadon su ne daga iyayen mutum, tare da yawancin kwayoyin halitta.[6] Sauran abubuwan haɗari sun haɗa da tarihin raunin kai, damuwa, da hauhawar jini.[1] Tsarin cutar yana hade da plaques da neurofibrillary tangles a cikin kwakwalwa.[6] Mahimmin ganewar asali yana dogara ne akan tarihin rashin lafiya da gwajin tunani tare da hoton likita da gwajin jini don kawar da wasu dalilai masu yiwuwa.[7] Alamun farko galibi ana kuskure da tsufa na al'ada.[1] Ana buƙatar gwajin ƙwayar ƙwayar ƙwayar cuta don takamaiman ganewar asali.[6] motsa jiki na tunani da na jiki, da nisantar kiba na iya rage haɗarin AD; duk da haka, shaidun da ke goyan bayan waɗannan shawarwarin suna da rauni.[6][8] Babu magunguna ko kari waɗanda aka nuna don rage haɗari.[9]
Babu wani magani da zai dakatar ko mai da ci gabansa, kodayake wasu na iya inganta alamun na ɗan lokaci.[2] Mutanen da abin ya shafa suna ƙara dogara ga wasu don taimako, galibi suna dora nauyi kan mai kulawa.[10] Matsanancin na iya haɗawa da zamantakewa, tunani, jiki, da abubuwan tattalin arziki.[10] Shirye-shiryen motsa jiki na iya zama masu fa'ida game da ayyukan rayuwar yau da kullun kuma suna iya haɓaka sakamako.[11] Matsalolin ɗabi'a ko ciwon hauka saboda ciwon hauka galibi ana bi da su tare da magungunan kashe qwari, amma wannan ba yawanci ana ba da shawarar ba, saboda ƙarancin fa'ida da haɗarin mutuwa da wuri.[12][13]
A cikin 2015, akwai kusan mutane miliyan 29.8 a duk duniya tare da AD.[2][14] Yawancin lokaci yana farawa a cikin mutane sama da shekaru 65, kodayake kashi 4-5% na lokuta ne farkon farkon cutar Alzheimer.[15] Yana shafar kusan kashi 6% na mutane masu shekaru 65 da haihuwa.[1] A cikin 2015, ciwon hauka ya haifar da mutuwar kusan miliyan 1.9.[16] An fara bayyana ta ne daga baya, daga baya, masanin ilimin halin dan Adam na kasar Jamus Alois Alzheimer a shekarar 1906.[17] A kasashen da suka ci gaba, AD na daya daga cikin cututtuka masu tsadar kudi.[18][19]