9681 RESULTS
COMMENT This thorough study pinpoints a mechanism describing lysosomal dysfunction in AD. In both DS and FAD mouse models, the Nixon group show that a phosphorylated form of β-CTF of APP directly interacts with and inhibits a v-ATPase subunit that is involved in
COMMENT This very interesting resource defines a common RNA aging signature or “common aging score.” Strikingly, the score maps to regions rich in myelin and, on a cellular level, to glia, particularly microglia and myelinating oligodendrocytes. Together, these d
COMMENT In recent years, several studies have been conducted to investigate the changes in gene expression associated with aging in both human and mouse brains (Colantuoni et al., 2011; Ham et al., 2020; Lee et al., 2000; Zahn et al., 2007). This new work by Hahn
COMMENT This study explores the mechanisms of tau propagation through brain networks, using whole-brain staining methods with anti-p-tau nanobodies in 3D-imaged, P301S tau-mutated mice from 3 to 12 months old. The authors applied network propagation modeling to a
COMMENT I think this is an interesting paper. It shows the power of the screening method to pick out genes with even subtle effects on cell biology. I would need a little more data to convince me that they have truly found modifiers of tau oligomer formation/clea
COMMENT This is another example of a missense variant affecting shedding and maturation of SORL1 in a family, segregating incompletely with AD, and with large diversity of ages of onset. Such diversity, and putative inheritance from the father with dementia at th
COMMENT I think this variant is definitely a strong contributor to AD. However, the pedigrees also show that the patients with DNA available and carrying the variant also carry one APOE4 allele. Actually, APOE4 segregates as well as does SORL1 in these pedigrees.
COMMENT In this article, the authors conducted spatiotemporal RNA-Seq of the mouse brain, profiling 1,076 samples from 15 regions across seven ages and two rejuvenation interventions. This is a very thorough study using the most advanced techniques available toda
COMMENT Here, Pesämaa et al. used two different models—GRN KO mice with TREM2 KO mice, and hiMGL with GRN mutations—to identify a panel of six biomarkers for microglia activation. They then validated the upregulation of some of these biomarkers in both FTD and AD
COMMENT There is an urgent need to identify biomarkers associated with microglial activation in order to increase its protective mechanisms against pathology. In this study, the authors observed that GRN KO mice, which show microglial hyperactivation, present upr
COMMENT Amid development of disease-modifying treatments for Alzheimer's disease, including emerging microglia-modulating therapies, we need to develop reliable biomarkers for evaluating microglial dynamics in humans. CSF sTREM2 has been extensively studied
COMMENT As we enter the age of plausible microglia-targeted therapeutics, it is essential that relevant biomarkers, applicable across neurodegenerative diseases, be identified. Positron emission tomography (PET) studies with tracers targeting the TSPO protein hav
COMMENT is a co-author of this comment. aft25 0
COMMENT This is a lovely article that complements so much of the work on tau. G3BP is the classic initiator for stress granules and is commonly studied in this context. It works great in studies of dividing cells. Indeed, G3BP is known to bind TDP-43, and associ
COMMENT scastillo_317286 Follow comments on this article: 0 References: Individualized prognosis of cognitive decline and
