11572 RESULTS
COMMENT In the age of big data, it has become an almost impossible task to genuinely assess papers reporting on thousands of samples, short of repeating the analyses. Although with resource manuscripts like this, the long-term impact can be difficult to gauge ini
COMMENT Johnson et al. show beautiful analyses of CSF proteomic alterations in relation to estimated year of disease onset (EYO), providing, for the first time, in-depth insight into when, and which, molecular processes are dysregulated in autosomal-dominant AD.
COMMENT This is even more evidence that the key step in anti-amyloid therapy is removal of the existing deposits. Immunotherapy is one of the few anti-amyloid approaches that remove existing deposits in animal models, instead of preventing additional deposits (as
COMMENT The DS and cerebrovascular disease sessions at AAIC showed that both DSAD and ADAD have more CAA than sporadic AD, and it has been suggested that individuals with DSAD have fewer hemorrhages than individuals with APP duplication. In this sense the studies
COMMENT This research of the Ablasser lab nicely explores the role of the cGAS-STING signaling pathway in age-related inflammation with subsequent neuronal damage and memory loss. Interestingly, there is a striking accordance with our recently published paper: Va
COMMENT It was great to hear the talks from Lance Johnson and graduate student Lesley Golden on the APOE4-to-APOE2 “switch mouse” (APOE4s2) model at AAIC in Amsterdam. Although isogenic APOE iPSCs have been established in vitro using the CRISPR gene editing techn
COMMENT Neuroscience in 2022 and 2016, respectively, showed absence of TDP-43 filaments. I saw comments that this may
COMMENT The interest in research on CAA has grown exponentially since the results of multiple clinical trials with anti-Aβ immunotherapy showed that these novel therapies are associated with the development of ARIA. In a sizeable percentage of patients, immunothe
COMMENT This new model is intriguing for its potential to swing the pathogenic activities of ApoE in such dramatic extremes. This should create a strong contrast between the downstream consequences, such as profiles of gene expression. But one could achieve that
COMMENT Aging is associated with loss of cellular resilience and damage to molecules, both of which accumulate over time. This leads to activation of the innate immune system to generate detrimental inflammatory responses that are now considered as critical deter
COMMENT This report fits really well with our findings that activation of cGAS-STING, accelerated by tau pathology, represents a converging pathway and a promising therapeutic target for aging-associated neurodegeneration beyond AD (Udeochu et al., 2023). Besides
COMMENT This work from the Ablasser team reveals how cGAS–STING, a ubiquitous senescence pathway sensing exogenous insults, can be activated in the liver by irradiation, in the brain by physiological aging, and in microglia by exposure to mtDNA. Thereby, it contr
COMMENT This is a rigorous exploration into the cGAS-STING pathway as a source of neuroinflammation in the aging brain. The findings are likely relevant to age-related neurodegenerative disorders since they complement work from Li Gan’s group, who recently report
COMMENT In this important analysis, Arseni et al. build on their previous work. They demonstrate that the fibrils underpinning the two most common TDP-43 subtypes are composed of distinct folds of the same LCD region—chevron-like in type A and spiral-like in type
COMMENT This manuscript by the Ryskeldi-Falcon lab clarifies several important issues. It is clear now that TDP-43 forms amyloid fibers in FTLD Type A and Type B—and, as in other neurodegenerative diseases, these fibers show distinct structures and are therefore
