11522 RESULTS
COMMENT I thoroughly enjoyed reading this manuscript, especially its elucidation of a groundbreaking mechanism crucial for maintaining axonal homeostasis. The study sheds light on the key role of lysosome-related vesicles in transporting and localizing specific m
COMMENT This is an important publication, given it essentially replicates the findings of Athauda et al., who reported positive Phase 2 data of a very similar GLP-1 receptor agonist drug, exenatide, when given to patients with Parkinson’s disease (Athauda et al.,
COMMENT It is wonderful to see a treatment strategy, proposed by my collaborators and me in 2002 in publications describing the neuroprotective/neurotrophic actions of GLP-1 receptor agonists, demonstrating efficacy in Parkinson’s disease (Perry et al., 2002; Per
COMMENT commentators take exception to the difference in outcomes between participants receiving HMTM as monotherapy
COMMENT Agree that it is no longer correct to assume that white matter rarefaction is equivalent to or completely accounted for by small vessel disease. Our comprehensive postmortem study suggests that neuofibrillary tangles are statistically a much greater predi
COMMENT The publication of Gibbons et al., like most clinical biomarker studies, suffers first and foremost from the use of an inadequate gold standard. The clinical diagnoses of Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy are all
COMMENT Kac and colleagues validated an immunoassay for plasma p-Tau212 in multiple clinical and autopsy cohorts. They demonstrated that their p-Tau212 antibody does not cross-react with p-Tau217. However, the results for their plasma p-Tau212 and p-Tau217 assays
COMMENT This highly interesting study supports an important role of sumoylation as a post-translational modification that solubilizes aggregation prone proteins. The study focuses on SUMO2, and it will be interesting to see how modification by SUMO2 compares to m
COMMENT It’s been almost a decade since the exciting initial discovery of tau SUMOylation by SUMO1, which inhibits degradation of tau and promotes its accumulation. However, it is unknown whether other SUMO isoforms have a similar role. Perhaps surprisingly, thes
COMMENT This is an exciting study by Hou and colleagues showing that modulating LILRB4 using an antibody likely inhibits LILRB4 binding to APOE, activating microglia and attenuating Aβ-related measures, such as plaque load and neuronal dystrophy. This study follo
COMMENT Microglia with unique transcriptional signatures have been identified in Alzheimer’s disease patients and animal models (Keren-Shaul et al., 2017). Understanding the regulation and impact of these states is essential if we want to know how to modulate mic
COMMENT This is very interesting work, as it dives into the plethora of receptors that control microglial function. For very good reasons, the field has focused extensively on some specific molecules, such as TREM2 or CD33, but microglia express a vast diversity
COMMENT Lecanemab did not work for women, which is bad news because there are twice as many women as men with AD. Lecanemab did not work for APOE4 carriers, which is bad news for AD patients, 60–75 percent of whom have one or two APOE4 genes. Remarkably, for some
COMMENT The original paper on the App-SAA knock-in mouse model of Alzheimer’s disease (JAX: 034711) reported that FDG-PET uptake, a surrogate for glucose utilization in brain, revealed cortical hypermetabolism across the studied lifespan of 5-20 months in homozyg
COMMENT A word of caution for those who are trying to extract biological meaning from tau RD biosensor cell lines: Nuclear tau aggregates are an artifact of the truncation used in the model. Disease-relevant full-length tau aggregates never localize to the nucleu
