Calcium sensor Yellow Cameleon 3.6 as a tool to support the calcium hypothesis of Alzheimer's disease

被引：3
作者：
Miller, Morgan R. [1 ,2 ]
Lee, Yee Fun [1 ,2 ,3 ]
Kastanenka, Ksenia V. [1 ,2 ]
机构：
[1] Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Neurol, Charlestown, MA 02129 USA
[2] Harvard Med Sch, Charlestown, MA 02129 USA
[3] Boston Univ, Dept Anat & Neurobiol, Sch Med, Boston, MA USA
来源：
ALZHEIMERS & DEMENTIA | 2023年 / 19卷 / 09期
基金：
美国国家卫生研究院;
关键词：
Alzheimer's disease; Calcium Hypothesis; GECI; genetically encoded calcium indicators; GREEN FLUORESCENT PROTEINS; A-BETA-PLAQUES; AMYLOID HYPOTHESIS; NEURAL ACTIVITY; IN-VIVO; CA2+; INDICATOR; HOMEOSTASIS; EMISSION; TAU;
D O I：
10.1002/alz.13111
中图分类号：
R74 [神经病学与精神病学];
学科分类号：
摘要：
INTRODUCTION: Alzheimer's disease (AD) is a neurodegenerative disease with increasing relevance as dementia cases rise. The etiology of AD is widely debated. The Calcium Hypothesisof Alzheimer's disease and brain aging states that the dysfunction of calcium signaling is the final common pathway leading to neurodegeneration. When the Calcium Hypothesis was originally coined, the technology did not exist to test it, but with the advent of Yellow Cameleon 3.6 (YC3.6) we are able to test its validity. METHODS: Here we review use of YC3.6 in studying Alzheimer's disease using mouse models and discuss whether these studies support or refute the Calcium Hypothesis. RESULTS: YC3.6 studies showed that amyloidosis preceded dysfunction in neuronal calcium signaling and changes in synapse structure. This evidence supports the Calcium Hypothesis. DISCUSSION: In vivo YC3.6 studies point to calcium signaling as a promising therapeutic target; however, additional work is necessary to translate these findings to humans.
引用
收藏
页码：4196 / 4203
页数：8
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