Role of presynaptic calcium stores for neural network dysfunction in Alzheimer's disease
Chommanad Lerdkrai
Olga Garaschuk
摘要：Alzheimer's disease (AD) is the most common form of dementia representing a major problem for public health.In 2017 there were an estimated 50 million patients worldwide and this number is expected to almost double every 20 years,reaching 75 million in 2030 and 131.5 million in 2050 ( there are two forms of the disease:the sporadic form (also called late onset AD,LOAD) and the familial form (FAD).LOAD is the most common form.Its prevalence increases with advancing age from 1％ in the 65-70 years old cohort to more that 30％ after the age of 85.It is characterized by moderate to extreme severity with the advancing age being the main risk factor for LOAD.Familiar AD represents some 5-10％ of all AD cases.FAD is linked to mutations in a specific set of genes,most often in the genes encoding amyloid precursor protein (APP) and the presenilins (PS) 1 and 2.Interestingly,the vast majority of AD related mutations are located on PS1 (Steiner et al.,2008;Mattson,2010) thus identifying this protein as one of the main targets for FAD-modifying therapies.Here we address the role of AD-related presenilin mutations for Ca2+ dyshomeostasis and in vivo neural network dysfunction in AD.
机标关键词：
资助基金：the VolkswagenStiftung (grant No.90233)
论文发表日期：2018-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 977-978 )