Journal of Literature Pharmacy Sciences

Alzheimer Hastalığı ve Demans
Alzheimer Disease and Dementia
Arda Can AYDINa
aMarmara Üniversitesi Eczacılık Fakültesi, Farmakoloji ABD, Istanbul, TÜRKIYE
Lit Pharm Sci. 2020;9(2):125-36
doi: 10.5336/pharmsci.2019-71813
Article Language: TR
Full Text
ÖZET
 Demans, akut bilinç bozukluğu ya da deliryum olmaksızın santral sinir sisteminin hasarına bağlı gelişen, hastanın günlük yaşamını etkileyen, ilerleyici, en az iki kognitif alanda yıkım ile seyreden semptomların klinik bütünlüğü durumunda konulan bir tanıdır. Alzheimer hastalığı (AH) ise orta ve geç yaş popülasyonda ortaya çıkan, hafızayı ve düşünme becerileri gibi en basit işleri yapma yeteneğini yavaşça yok eden, geri dönüşü olmayan, ilerleyen bir beyin hastalığıdır. Türkiye'de 65 yaş öncesi AH 30.000-40.000 kişide görülürken, 65 yaş üstünde toplumun %5'ini etkilemekte, 85 yaş üstü popülasyonun ise %30-50'sinde görülmektedir. Hastalık, klinik olarak bellek, konuşma, yüksek serebral işlevler ve görsel-uzaysal beceriler gibi birden çok sistemi etkileyen, bilişsel işlevlerde ilerleyici kayıp ile seyreden, nörolojik açıdan sinaps ve nöron kaybı, gliozis, amiloid plak ve nörofibriler yumak oluşumları ile karakterizedir. Genetik, biyokimyasal ve nöropatolojik veriler, Aβ agregasyonunun AH patogenezinde önemli rol oynadığını göstermektedir. Normal bir nöronal membran proteini olan APP'nin kesilmesi sonucu amiloid beta (Aβ) 40/42 olarak adlandırılan ekstraselüler fragman oluşur. Bu nörotoksik fragmanlar sıklıkla bir araya toplanır; Aβ 40/42 oligomerizasyonu plak oluşumu ile sonuçlanır. Normal fizyolojik koşullar altında glutamat N-metil D-aspartat (NMDA) reseptörlerini uyararak kalsiyum iyonlarının postsinaptik aralıktan nöronun içine akmasını sağlar. Nörona iletilen kalsiyum iyonları beyinde öğrenme, hafıza gibi yüksek düzey işlerin devamını sağlamaktadır. AH'li bireylerde biriken Aβ 40/42 plaklar, glutamat NMDA reseptörleri ile aşırı Ca+2 üretimini tetikler. Aşırı üretilen Ca+2 nitrik oksit seviyesini artırır, mitakondriyal etkinliği engeller ve hücre içi ATP seviyesinin tükenmesine neden olarak nöronda enerji kaybına, nöronal disfonksiyona ve hücre ölümüne neden olur.

Anahtar Kelimeler: Demans; Alzheimer hastalığı; bellek; bilişsel bozukluklar
ABSTRACT
 Dementia is a diagnosis of clinical integrity of symptoms associated with destruction of at least two progressive cognitive areas that affect the daily life of the patient, resulting from damage to the central nervous system without acute impairment or delirium. Alzheimer's disease (AD) is an irreversible, progressive brain disease that slowly eradicates the ability to perform simple tasks such as memory and thinking skills in the middle and late age population. AH 30,000-40,000 before the age of 65 in Turkey affects 5% of the population over the age of 65 seen in person, while the population over age 85 is seen in 30-50%. Disease clinically memory, speech, higher cerebral functions and visual. It is characterized by neurological synapse and loss of neurons, gliosis, amyloid plaque and neurofibrillary tangles, affecting multiple systems such as spatial skills, progressive loss of cognitive functions. Genetic, biochemical and neuropathological data suggest that Aβ aggregation plays an important role in the pathogenesis of AD. The cutting of APP, a normal neuronal membrane protein, results in an extracellular fragment called amyloid beta (Aβ) 40/42. These neurotoxic fragments are often pooled together; oligomerization of Aβ 40/42 results in plaque formation. Under normal physiological conditions, glutamate N-methyl D-aspartate (NMDA) stimulates its receptors to allow calcium ions to flow through the postsynaptic space into the neuron. Calcium ions transmitted to the neuron provide the continuation of high level tasks such as learning and memory in the brain. Accumulated Aβ 40/42 plaques in patients with Alzheimer's disease trigger excess Ca+2 production by glutamate NMDA receptors. Over-produced Ca+2 increases nitric oxide levels, inhibits mitochondrial activity, and leads to depletion of intracellular ATP levels, leading to energy loss, neuronal dysfunction, and cell death.

Keywords: Dementia; Alzheime's disease; memory; cognitive disorders
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Ortadoğu Advertisement Presentation Publishing Tourism Education Architecture Industry and Trade Inc. may block the website to users in the following events:

-Information with wrong, incomplete, deceiving or immoral expressions is recorded to the website,

-Proclamation, advertisement, announcement, libelous expressions are used against natural person or legal identity,

-During various attacks to the website,

-Disruption of the website because of a virus.

Written, visual and audible materials of the website, including the code and the software are under protection by legal legislation.

Without the written consent of Ortadoğu Advertisement Presentation Publishing Tourism Education Architecture Industry and Trade Inc. the information on the website cannot be downloaded, changed, reproduced, copied, republished, posted or distributed.

All rights of the software and the design of the website belong to Ortadoğu Advertisement Presentation Publishing Tourism Education Architecture Industry and Trade Inc.

Ortadoğu Advertisement Presentation Publishing Tourism Education Architecture Industry and Trade Inc. will be pleased to hear your comments about our terms of use. Please share the subjects you think may enrich our website or if there is any problem regarding our website.

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