Publications by authors named "J B Leverenz"

Article Synopsis
  • High microglial diversity complicates the creation of targeted treatments for Alzheimer's disease (AD).
  • A comprehensive analysis of RNA-sequencing data revealed specific microglial subtypes associated with AD and identified potential drug targets, including microglial transition networks.
  • The study highlights ketorolac as a promising anti-inflammatory treatment for AD, showing its association with lower AD incidence in patient databases.
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Article Synopsis
  • A study was conducted to investigate the X-chromosome's role in Alzheimer's Disease (AD), which had been overlooked in previous genome-wide association studies.
  • The research included 115,841 AD cases and 613,671 controls, considering different X-chromosome inactivation (XCI) states in females.
  • While no strong genetic risk factors for AD were found on the X-chromosome, seven significant loci were identified, suggesting areas for future research.
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Background: Rapidly progressive Alzheimer's disease (rpAD) is a clinical subtype distinguished by its rapid cognitive decline and shorter disease duration. rpAD, like typical AD (tAD), is characterized by underlying neuropathology of amyloid plaques and neurofibrillary tangles. There is early evidence that the composition of amyloid plaques could vary between the rpAD and tAD.

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Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. However, current treatments are directed at symptoms and lack ability to slow or prevent disease progression. Large-scale genome-wide association studies (GWAS) have identified numerous genomic loci associated with PD, which may guide the development of disease-modifying treatments.

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Article Synopsis
  • Transposable element (TE) dysregulation is linked to neuroinflammation in Alzheimer's disease (AD) and this study aims to identify TE quantitative trait loci (teQTLs) in the brains of aged individuals with AD.
  • Utilizing large-scale RNA sequencing and whole-genome sequencing data from three human AD brain biobanks, researchers discovered 26,188 significant teQTLs and demonstrated an association between these elements and AD-related genetic factors.
  • Experimental CRISPR interference assays indicated that an upregulated TE affects neuroinflammation by suppressing the expression of the anti-inflammatory gene C1QTNF4 in neurons derived from human induced pluripotent stem cells.
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