11522 RESULTS
COMMENT Using sophisticated SRS (stimulated Raman scattering) imaging analyses combined with mouse and fly tauopathy in vivo models, or in vitro in human neurons carrying a V337M Tau mutation, the authors show that tauopathy is associated with an accumulation of
COMMENT Accumulation of lipids in glia was first noted as a hallmark of Alzheimer’s disease when it was first described over 100 years ago, but only recently has there been a number of studies characterizing this phenomenon at a molecular and mechanistic level (M
COMMENT The work from Li et al. beautifully demonstrates how upregulated lipid synthesis and downregulated lipid turnover leads to pathological lipid accumulation in both neurons and glia in multiple tauopathy model systems—iPSC-derived cells as well as transgeni
COMMENT The blood biomarker p-tau217 is currently being studied for improving the mild cognitive impairment (MCI) differential AD diagnosis. This recent study offers new insights into its benefits and limitations. Below is a brief summary of the major findings fr
COMMENT The lixipark study is great news for PD patients as it shows halt of disease progression and confirms earlier clinical trials testing exenatide (Athauda et al., 2017; Aviles-Olmos et al., 2014) as well as a small Phase 2 trial testing the GLP-1 analogue l
COMMENT In this article, Schwartz’s group elegantly demonstrated the presence of senescent microglia in aged mice and in the 5xFAD Alzheimer’s disease (AD) mouse model by using CyTOF. While expressing senescent proteins, such as CD38, senescent microglia surprisi
COMMENT In this elegant study by Bretou et al., new mechanistic evidence is provided for APP-mediated endolysosomal dysfunction in AD. Altered lysosomal Ca2+ levels due to APP-CTF accumulation at the lysosome side of lysosome-ER contact sites appear to be the dri
COMMENT autophagy revisited: normal acidification of lysosomes in cells lacking PSEN1 and PSEN2. Comments on
COMMENT I think this is a beautiful paper with a lot of high-quality cell biology on the role of APP and γ-secretase on endolysosomal function. The authors convincingly show that the inhibition, or loss, of γ-secretase activity results in endolysosomal dysfunctio
COMMENT Previous studies in human neurons have established that mutations in APP and PSEN1 causal for AD result in endolysosomal and autophagy dysfunction as a consequence of reduced turnover of C-terminal fragments of APP (APP-CTFs), and that this is probably a
COMMENT This study provides exciting mechanistic insights into how APP CTFs, and not Aβ, may contribute to the lysosomal dysfunction in Alzheimer’s disease. This cell biological study is comprehensive, carefully conducted, convincing, and in good agreement with p
COMMENT I really enjoy reading papers from the Annaert lab because of their high level of cell biology, which is so needed for our field to better understand the cellular mechanisms underlying AD. This paper by Bretou et al. is a tour de force with diverse and el
COMMENT This article serves to validate and confirm a series of findings from previous papers, highlighting the presence of senescent microglia in AD-like pathology and their DAM-like identity. Previous studies from our group, using the APP/PS1 model (Hu et al.,
COMMENT This insightful paper by the Schwartz lab delves into the analysis of microglia in Alzheimer’s disease (AD) and aging models, shedding light on intriguing findings. The key discovery revolves around identifying two distinct subsets of microglia within the
COMMENT This is an exciting study by Juan Bonifacino’s group where they explored the regulation and importance of the BORC adaptor complex in axonal transport of lysosomes using new BORC-deficient iPSC-derived human neurons. Whereas the role of lysosomes has been
