Publications by authors named "Yuhao Min"

Alzheimer's disease (AD) brains are characterized by neuropathologic and biochemical changes that are highly variable across individuals. Capturing epigenetic factors that associate with this variability can reveal novel biological insights into AD pathophysiology. We conducted an epigenome-wide association study of DNA methylation (DNAm) in 472 AD brains with neuropathologic measures (Braak stage, Thal phase, and cerebral amyloid angiopathy score) and brain biochemical levels of five proteins (APOE, amyloid-β (Aβ)40, Aβ42, tau, and p-tau) core to AD pathogenesis.

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Alzheimer's disease (AD) is the most common neurodegenerative dementia with multi-layered complexity in its molecular etiology. Multiple omics-based approaches, such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, and lipidomics are enabling researchers to dissect this molecular complexity, and to uncover a plethora of alterations yielding insights into the pathophysiology of this disease. These approaches reveal multi-omics alterations essentially in all cell types of the brain, including glia.

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Article Synopsis
  • Genetic variants in the ABCA7 gene are linked to a higher risk of Alzheimer's disease (AD), but the exact function of ABCA7 in AD development remains uncertain.* -
  • Researchers created a zebrafish model lacking the abca7 gene, revealing that ABCA7 is essential for the expression of neuropeptide Y (NPY) and other neurotrophic factors vital for brain health.* -
  • Findings suggest that decreased NPY due to impaired ABCA7 function contributes to synaptic issues and a higher risk of AD, with clinical data showing a correlation between NPY levels and disease progression.*
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To uncover molecular changes underlying blood-brain-barrier dysfunction in Alzheimer's disease, we performed single nucleus RNA sequencing in 24 Alzheimer's disease and control brains and focused on vascular and astrocyte clusters as main cell types of blood-brain-barrier gliovascular-unit. The majority of the vascular transcriptional changes were in pericytes. Of the vascular molecular targets predicted to interact with astrocytic ligands, SMAD3, upregulated in Alzheimer's disease pericytes, has the highest number of ligands including VEGFA, downregulated in Alzheimer's disease astrocytes.

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Article Synopsis
  • Alzheimer's disease (AD) is a complicated condition linked to cognitive decline and memory loss, with genetic variations playing a significant role in its development, although the exact mechanisms are still unclear.
  • Researchers developed a knockout zebrafish model of an established AD-risk gene using CRISPR/Cas9, which exhibited decreased astroglial growth, synaptic density, and microglial levels when exposed to amyloid beta 42 (Aβ42).
  • Findings from single-cell transcriptomics indicated that neuropeptide Y (NPY) signaling is crucial for neuronal and glial interaction, while clinical data in humans showed a correlation between reduced gene expression and advanced AD stages, along with genetic variations linked to the disease.
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Progressive supranuclear palsy (PSP) is a neurodegenerative parkinsonian disorder characterized by cell-type-specific tau lesions in neurons and glia. Prior work uncovered transcriptome changes in human PSP brains, although their cell-specificity is unknown. Further, systematic data integration and experimental validation platforms to prioritize brain transcriptional perturbations as therapeutic targets in PSP are currently lacking.

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Article Synopsis
  • Neurogenesis, which helps the brain stay resilient, decreases in Alzheimer's disease (AD), leading to reactive astrocytes that hinder neurogenesis; restoring neurogenesis could potentially counteract neurodegenerative effects.
  • Researchers used a mouse model to explore the role of Nerve growth factor receptor (Ngfr) in promoting neurogenesis in astrocytes during AD, finding that Ngfr reduces a marker (Lcn2) associated with reactive astrocytes, thereby enhancing neurogenic outcomes.
  • The study indicates that by boosting Ngfr expression, it's possible to decrease amyloid plaques and improve neurogenesis, suggesting that targeting astrocytes to promote their neurogenic potential could offer new therapeutic strategies for Alzheimer's disease.
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d-alanine (d-Ala) and several other d-amino acids (d-AAs) act as hormones and neuromodulators in nervous and endocrine systems. Unlike the endogenously synthesized d-serine in animals, d-Ala may be from exogenous sources, e.g.

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Microglia have fundamental roles in health and disease; however, effects of age, sex, and genetic factors on human microglia have not been fully explored. We applied bulk and single-cell approaches to comprehensively characterize human microglia transcriptomes and their associations with age, sex, and APOE. We identified a novel microglial signature, characterized its expression in bulk tissue and single-cell microglia transcriptomes.

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Article Synopsis
  • The study identified many differentially expressed genes in Alzheimer's disease (AD) and progressive supranuclear palsy (PSP), showing similar gene expression changes between these two neurodegenerative diseases.
  • Researchers used RNA-Seq data from brain samples to discover that these changes are conserved across different brain regions, indicating a broader impact on related areas.
  • The findings suggest that both AD and PSP share common biological pathways, which could help in developing comprehensive therapies and biomarkers for neurodegenerative diseases.
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Most native producers of ribosomally synthesized and post-translationally modified peptides (RiPPs) utilize N-terminal leader peptides to avoid potential cytotoxicity of mature products to the hosts. Unfortunately, the native machinery of leader peptide removal is often difficult to reconstitute in heterologous hosts. Here we devised a general method to produce bioactive lanthipeptides, a major class of RiPP molecules, in Escherichia coli colonies using synthetic biology principles, where leader peptide removal is programmed temporally by protease compartmentalization and inducible cell autolysis.

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Matrix-assisted laser desorption/ionization time-of-flight (MALDI-ToF) mass spectrometry (MS) imaging has been used for rapid phenotyping of enzymatic activities, but is mainly limited to single-step conversions. Herein we report a label-free method for high-throughput engineering of multistep biochemical reactions based on optically guided MALDI-ToF MS analysis of bacterial colonies. The bacterial cells provide containment of multiple enzymes and access to substrates and cofactors via metabolism.

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Genome-scale engineering is indispensable in understanding and engineering microorganisms, but the current tools are mainly limited to bacterial systems. Here we report an automated platform for multiplex genome-scale engineering in Saccharomyces cerevisiae, an important eukaryotic model and widely used microbial cell factory. Standardized genetic parts encoding overexpression and knockdown mutations of >90% yeast genes are created in a single step from a full-length cDNA library.

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