WebInflammatory processes in the brain of a patient with Alzheimer's disease were first described by Alois Alzheimer. Yet, only in the past decade has it been appreciated that neuroinflammation is not just a bystander reaction in response to neuronal death and accumulation of cellular debris and misfolded and aggregated proteins, but actively drives … WebOur new preprint, "TREM2-dependent senescent microglia conserved in aging and Alzheimer’s disease", is out! #alzheimersdisease #senescence…
Francesca Cignarella, PhD - United States - LinkedIn
WebSep 13, 2024 · The brain resident myeloid cells, microglia, are key in regulating AD pathology and controlling amyloid pathology. A Triggering Receptor Expressed on Myeloid cells (TREM2) has been discovered as a key regulator of microglia by controlling microglia activation and metabolic activities in brain tissues. WebTrem2 R47H KI mice (4 months old) showed significant down-regulation of Trem2 expression, and decreased microglia density and CD68 levels in the hippocampus. (A) Gene expression in hippocampal homogenates from homozygous (HO) and heterozygous (HE) Trem2 R47H KI mice relative to Rps28 and then expressed relative to WT within the … ruthies bk
TREM2: Modulator of Lipid Metabolism in Microglia - Neuron
WebApr 9, 2024 · Previously, we reported that H157Y, a rare coding variant on exon 3 of the triggering receptor expressed on myeloid cells 2 gene (TREM2), was associated with Alzheimer’s disease (AD) risk in a Han Chinese population. To date, how this variant increases AD risk has remained unclear. In this study, using CRISPR-Cas9-engineered BV2 … WebOct 3, 2024 · Microglia are the macrophages of the brain and play an important role in Alzheimer’s disease (AD). In Cell, Ulland et al. (2024) recently reported that mutations in TREM2, a protein implicated in AD, disrupt microglial energy state and function, thus sabotaging the microglia’s ability to defend the brain against amyloid plaques. WebAndrés Cruz-Herranz, Sharon A. Sagan, Raymond A. Sobel, Ari J. Green, and Scott S. Zamvil. Aquaporin-4 (AQP4)-specific antibodies are instrumental in promoting central nervous system (CNS) tissue injury in neuromyelitis optica (NMO), yet evidence indicates that AQP4-specific T cells also have a pivotal role in NMO pathogenesis. ruthies cabanas