Russell H. Swerdlow

Jan 8, 2025 | nature.com | Mohammad Haeri |Xiang Zhou |Lindong Jiang |Yi-Ping Phoebe Chen |Xiaoxin Yan |Russell H. Swerdlow | +1 more

AbstractAging increases the risk for Alzheimer’s disease (AD), driving pathological changes like amyloid-β (Aβ) buildup, inflammation, and oxidative stress, especially in the prefrontal cortex (PFC). We present the first subcellular-resolution spatial transcriptome atlas of the human prefrontal cortex (PFC), generated with Stereo-seq from six male AD cases at varying neuropathological stages and six age-matched male controls.

Jun 9, 2024 | nature.com | Russell H. Swerdlow

AbstractThe etiopathogenesis of late-onset Alzheimer’s disease (AD) is increasingly recognized as the result of the combination of the aging process, toxic proteins, brain dysmetabolism, and genetic risks. Although the role of mitochondrial dysfunction in the pathogenesis of AD has been well-appreciated, the interaction between mitochondrial function and genetic variability in promoting dementia is still poorly understood.

Dec 12, 2023 | biorxiv.org | Xiaoyu Zhang |Mohammad Haeri |Russell H. Swerdlow |Ning WANG

AbstractBackground: DNA breaks are accumulated in Alzheimer's disease (AD) brains as genomic lesion. However, DNA breaks are also required for normal cognitive function by facilitating the expression of genes related to nervous system function, and this process involves TOP2B, a DNA topoisomerase that catalyzes the formation of DNA double-strand breaks (DSBs). Objective: To characterize how AD impacts DNA breaks at genes related to nervous system function.