11505 RESULTS
COMMENT Over the past decade, there have been significant technological advancements in single-cell transcriptome and epigenome profiling, as well as in spatial transcriptomics and proteomics. These methods have been crucial in understanding altered gene regulati
COMMENT anonymous comments saying that numbers and error bars were missing from a standard curve. I don't think
COMMENT Makarava and her colleagues reveal an interesting insight into the neuropathological features within the brain during prion disease. They describe how, as the disease progresses, a proportion of the microglia in prion disease-affected brain appear to engu
COMMENT This quite interesting manuscript describes the partial enveloping of reactive microglia around viable neurons, which are positive for Pr PSc and negative for apoptotic markers and decreased neural activity. It is plausible that chronic proteotoxic stress
COMMENT Engulfment of live neurons and “stressed but viable” neurons has been known for some time (Hugh Perry and Guy Brown come to mind for their papers, reviews and commentary). However, the authors are to be commended for providing critical details of events a
COMMENT This paper finds something unexpected during the development of prion disease in mice that may be relevant to Alzheimer’s disease. Microglia are found to partially enwrap neuronal cell bodies, such that up to 40 percent of cortical neurons are covered by
COMMENT It’s great to see additional studies investigating genetic and molecular associations with tau pathology. Particularly with how closely tau burden and topography may impact clinical presentations, a better understanding of underlying drivers could influen
COMMENT The observation that microglia partially envelop non-apoptotic, viable neurons in prion diseases is quite intriguing. The finding that these enveloped neurons show functional decline might imply that microglia, which amassed high levels of the lysosomal p
COMMENT Jerome Badaut and colleagues suggest using the term “blood-brain border” rather than “blood-brain barrier,” being kind in that the acronym BBB need not be abandoned. I must agree that I welcome this change in terminology. With our own work in using low-in
COMMENT Research groups at Denali and Roche have demonstrated encouraging preliminary results in amyloid reduction with lower ARIA rates using plaque-targeting antibodies bound to an antibody transport vehicle targeting the transferrin receptor. Both groups propo
COMMENT This study is very exciting and opens new ways to assess cell heterogeneity in the brain that were not possible before. We have, and are, learning a lot from single-cell transcriptomes, and these new technologies would allow us to dive more deeply into th
COMMENT In recent years, scientists have started to be investigate the role of m 6 A-RNA regulation in brain aging and Alzheimer’s disease. Where, and how, m 6 A changes in the transcriptome are critical questions that have primarily been approached using bulk ti
COMMENT Both these studies are outstanding and provide excellent in vivo evidence for a role of oligodendrocytes in plaque formation and neuronal hyperactivity in AD. Moreover, both studies highlight that BACE1 is not only active in neurons—the cell type most pre
COMMENT The study from Lam et al. focuses on assessing the relationship between epileptiform activity found in Alzheimer’s disease (AD) patients and the pathophysiological changes characterizing the disease (i.e., Aβ, tau and cortical atrophy). They focus on a ve
COMMENT This pair of studies from the Busche and Nave groups nicely replicate each other’s key finding: that oligodendrocytes, not just excitatory neurons, contribute to amyloid plaque formation in an APP knock-in mouse model. In my opinion, the most striking con
