Cheng Feixiong, Feng Yayan, Flanagan Margaret, Bonakdarpour Borna, Jamshidi Pouya, Castellani Rudolph, Mao Qinwen, Chu Xiaona, Gao Hongyu, Liu Yunlong, Xu Jielin, Hou Yuan, Martin William, Nelson Peter, Leverenz James, Pieper Andrew, Cummings Jeffrey
Res Sq. 2024 Aug 16:rs.3.rs-4871032. doi: 10.21203/rs.3.rs-4871032/v1.
Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. Here, we report single-nucleus multiome (snRNA-seq and snATAC-seq) analysis of 103,861 nuclei isolated from cerebellum from 9 human cases of AD/ADRD and 8 controls, and with frontal cortex of 6 AD donors for additional comparison. Using peak-to-gene linkage analysis, we identified 431,834 significant linkages between gene expression and cell subtype-specific chromatin accessibility regions enriched for candidate cis-regulatory elements (cCREs). These cCREs were associated with AD/ADRD-specific transcriptomic changes and disease-related gene regulatory networks, especially for RAR Related Orphan Receptor A (RORA) and E74 Like ETS Transcription Factor 1 (ELF1) in cerebellar Purkinje cells and granule cells, respectively. Trajectory analysis of granule cell populations further identified disease-relevant transcription factors, such as RORA, and their regulatory targets. Finally, we prioritized two likely causal genes, including Seizure Related 6 Homolog Like 2 (SEZ6L2) in Purkinje cells and KAT8 Regulatory NSL Complex Subunit 1 (KANSL1) in granule cells, through integrative analysis of cCREs derived from snATAC-seq, genome-wide AD/ADRD loci, and Hi-C looping data. This first cell subtype-specific regulatory landscape in the human cerebellum identified here offer novel genomic and epigenomic insights into the neuropathology and pathobiology of AD/ADRD and other neurological disorders if broadly applied.
虽然已知人类小脑在阿尔茨海默病(AD)和AD相关痴呆(ADRD)中存在神经病理学损伤,但导致这种病理变化的细胞类型特异性转录和表观基因组变化尚不清楚。在这里,我们报告了对从9例AD/ADRD患者和8例对照的小脑中分离出的103,861个细胞核进行的单核多组学(snRNA-seq和snATAC-seq)分析,并对6例AD供体的额叶皮质进行了额外比较。通过峰-基因连锁分析,我们在基因表达与富含候选顺式调控元件(cCRE)的细胞亚型特异性染色质可及性区域之间鉴定出431,834个显著的连锁关系。这些cCRE与AD/ADRD特异性转录组变化和疾病相关基因调控网络相关,特别是分别与小脑浦肯野细胞和颗粒细胞中的视黄酸相关孤儿受体A(RORA)和E74样ETS转录因子1(ELF1)相关。颗粒细胞群体的轨迹分析进一步确定了与疾病相关的转录因子,如RORA及其调控靶点。最后,通过对snATAC-seq衍生的cCRE、全基因组AD/ADRD位点和Hi-C环化数据的综合分析,我们确定了两个可能的因果基因,包括浦肯野细胞中的癫痫相关6同源物样2(SEZ6L2)和颗粒细胞中的KAT8调节性NSL复合物亚基1(KANSL1)。这里确定的人类小脑中首个细胞亚型特异性调控图谱,如果广泛应用,将为AD/ADRD和其他神经系统疾病的神经病理学和病理生物学提供新的基因组和表观基因组见解。