Publications by authors named "L W Bonham"
Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk. However, most prior analyses have not utilized longitudinal analyses or whole-brain neuroimaging biomarkers of AD. Herein, we employed longitudinal modeling and structural neuroimaging analyses to test the hypothesis that accelerated epigenetic aging would predict AD progression.
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- Recent transcriptomics studies show increased interferon (IFN) responses in various neurodegenerative diseases such as Alzheimer's and Parkinson's, highlighting these responses in both microglia and T cells.
- The literature indicates that abnormal IFN signaling is also linked to neuropsychiatric disorders like major depression and PTSD.
- This review aims to summarize findings about IFN responses in neurodegeneration, discuss how sex and ancestry influence these responses, and explore potential reasons for elevated antiviral IFN signaling in neurological and psychiatric conditions without viral involvement.
Article Synopsis
- In frontotemporal lobar degeneration (FTLD), abnormal protein buildup in the brain correlates with declines in social-emotional and language skills, primarily involving TDP-43 or tau proteins.
- The study investigates how degeneration patterns in FTLD relate to gene expression of recently evolved genetic regions, using neuroimaging and transcriptomic data to examine targeted brain areas.
- Results indicate that FTLD subtypes uniquely or overlappingly affect brain regions tied to genes evolved in humans, with a notable relationship between TDP-43 function impairment and cryptic splicing in affected genes.
Introduction: Altered immune signatures are emerging as a central theme in neurodegenerative disease, yet little is known about immune responses in early-onset Alzheimer's disease (EOAD).
Methods: We examined single-cell RNA-sequencing (scRNA-seq) data from peripheral blood mononuclear cells (PBMCs) and droplet digital polymerase chain reaction (ddPCR) data from CD4 T cells from participants with EOAD and clinically normal controls.
Results: We analyzed PBMCs from 16 individuals by scRNA-seq and discovered increased interferon signaling-associated gene (ISAG) expression and striking expansion of antiviral-like ISAG T cells in EOAD.
Introduction: A hexanucleotide repeat expansion (HRE) intronic to chromosome 9 open reading frame 72 () is recognized as the most common genetic cause of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and ALS-FTD. Identifying genes that show similar regional co-expression patterns to may help identify novel gene targets and biological mechanisms that mediate selective vulnerability to ALS and FTD pathogenesis.
Methods: We leveraged mRNA expression data in healthy brain from the Allen Human Brain Atlas to evaluate co-expression patterns.