疾病
神经退行性变
神经科学
阿尔茨海默病
生物
遗传学
医学
病理
作者
Yun Chen,Jason D. Ulrich
出处
期刊:Neuron
[Elsevier]
日期:2024-06-01
卷期号:112 (11): 1723-1724
标识
DOI:10.1016/j.neuron.2024.04.030
摘要
Sporadic Alzheimer's disease (AD) and autosomal dominant Alzheimer's disease (ADAD) share pathological features, but differing mechanisms, leading to disease. In this issue of Neuron, Almeida, Eger, et al. 1 Almeida M.C. Eger S.J. He C. Audouard M. Nikitina A. Glasauer S.M.K. et al. Single-nucleus RNA sequencing demonstrates an autosomal dominant Alzheimer's disease profile and possible mechanisms of disease protection. Neuron. 2024; 112: 1778-1794.e7 Google Scholar uncovered molecular processes that may distinguish sporadic AD from ADAD and how the APOE-Christchurch variant may be protective. Sporadic Alzheimer's disease (AD) and autosomal dominant Alzheimer's disease (ADAD) share pathological features, but differing mechanisms, leading to disease. In this issue of Neuron, Almeida, Eger, et al. 1 Almeida M.C. Eger S.J. He C. Audouard M. Nikitina A. Glasauer S.M.K. et al. Single-nucleus RNA sequencing demonstrates an autosomal dominant Alzheimer's disease profile and possible mechanisms of disease protection. Neuron. 2024; 112: 1778-1794.e7 Google Scholar uncovered molecular processes that may distinguish sporadic AD from ADAD and how the APOE-Christchurch variant may be protective. Single-nucleus RNA sequencing demonstrates an autosomal dominant Alzheimer's disease profile and possible mechanisms of disease protectionAlmeida et al.NeuronFebruary 27, 2024In BriefAlmeida, Eger, and colleagues find specific autophagy and chaperone gene signatures that distinguish autosomal dominant Alzheimer's disease (ADAD) from sporadic cases. Protection from dementia due to the APOE3-Christchurch variant may arise from increased LRP1 expression in astrocytes and, consequently, their increased TAU uptake. Full-Text PDF
科研通智能强力驱动
Strongly Powered by AbleSci AI