Publications by authors named "Nicholas Sweeney"

Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer's disease (AD). To find cross-talk dysregulations involved in AD, we reconstructed cross-talk networks from single-nucleus transcriptional profiles of 67 clinically and neuropathologically well-characterized controls and AD brain donors from the Knight Alzheimer Disease Research Center and the Dominantly Inherited Alzheimer Network cohorts. We predicted a role for TREM2 and additional AD risk genes mediating neuron-microglia cross-talk in AD.

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Lipid dyshomeostasis and tau pathology are present in frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD). However, the relationship between lipid dyshomeostasis and tau pathology remains unclear. We report that GRAM Domain Containing 1B (GRAMD1B), a nonvesicular cholesterol transporter, is increased in excitatory neurons of human neural organoids (HNOs) with the MAPT R406W mutation.

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The communities of viruses studied in rabbits and hares (family Leporidae) have largely been those with clinical significance. Consequently, less is known broadly about other leporid viruses. Anelloviruses (family ) are likely commensal members of the single-stranded DNA virome in mammals.

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Article Synopsis
  • This study compares the costs of two strategies for delivering an online HIV prevention program: centralized direct-to-consumer marketing and decentralized distribution through community-based organizations.
  • In the direct-to-consumer approach, the total costs were significantly lower, averaging $501 per participant, compared to $4,239 per participant in the community-based organization approach.
  • The findings highlight the importance of understanding these cost dynamics to make informed decisions about program sustainability and funding for future implementations.
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Article Synopsis
  • Early to mid-life traumatic brain injury (TBI) has been identified as a potential risk factor for developing Alzheimer's disease (AD) and related dementia.
  • The study indicates that TBI reduces the expression of BCL2-associated athanogene 3 (BAG3), leading to a chain reaction of cognitive deficits and pathological changes in mice, including hyperphosphorylated tau accumulation and synaptic dysfunction.
  • Overexpressing BAG3 specifically in neurons mitigated these AD-like symptoms, suggesting that targeting BAG3 could be a promising therapeutic approach to address TBI-induced cognitive decline.
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