19 RESULTS
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COMMENT We checked to what extent the 85 γ-secretase substrates described in figure 2b of this paper were associated with distinct Alzheimer’s disease molecular subtypes we identified (Tijms et al., 202 3). These AD subtypes were defined based on untargeted CSF p
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 In this work, Glasauer and colleagues investigated RNA expression differences of pyramidal neurons and astrocytes from organoids with a MAPT mutation compared to their isogenic controls. Most differences were found in neurons, where MAPT also has the high
COMMENT Even though APOE ε4 genotype is the strongest genetic risk factor for Alzheimer’s disease, the processes through which risk is increased remain largely unclear. In this study, Julia TCW and colleagues scrutinize effects of APOE e4 on transcriptomics in hu
COMMENT We read this new study with a lot of pleasure. Johnson and colleagues thrust ahead and show that, for proteomic analyses, more really is more. By using tandem-mass-tag (TMT) mass spectrometry, they were able to measure five times more proteins in tissue t
COMMENT This study is a massive undertaking, relating genetic variants to protein levels in plasma. Proteomics measured in biofluids provides impelling opportunities to study in great detail how genetic risk factors impact on disease pathogenesis in patients. Fer
COMMENT AD pathology can now be assessed in plasma with assays for Aβ42/40, total-tau, and p-tau. Jiang et al. studied a broader panel of plasma proteins, not including these key AD markers, as a predictor for a clinical diagnosis of AD relative to cognitively no
COMMENT How AD genetic risk variants eventually lead to dementia is a difficult but important topic of research. Wingo and colleagues took a PWAS approach to study relationships between AD genetic risk variants and abundances of 1,475 proteins quantified in the d
COMMENT Biological heterogeneity of Alzheimer’s disease is a relatively unexplored territory, even though there is ample evidence based on clinical and imaging studies that heterogeneity does exist. Here, Neff and colleagues explored heterogeneity in gene express
COMMENT Johnson et al. provide fascinating findings on mass spectroscopy proteomics in brain tissue from over 2,000 pathologically defined individuals with AD, other dementias, and controls as part of the multicenter Accelerating Medicine Partnership for AD (AMP-
COMMENT In general the data confirm previous findings, and highlights that intervening in APOE-related mechanisms is still a useful therapeutic avenue for AD. The neuropathological confirmation in a subset of 5,000 participants is a strong asset. It is of interes
COMMENT Cross-sectional neuropathological studies suggested that amyloid accumulation follows a distinct pattern with 3 to 5 stages (Braak and Braak, 1991; Thal et al., 2002). With the availability of amyloid PET tracers, these patterns can now also be assessed i
COMMENT The NIA-AA 2018 framework for Alzheimer’s disease changed scope and now has the ambition to provide a research-only framework, with the explicit disclaimer that it should not be seen as criteria for clinical use. The authors did a great job in reviewing a
COMMENT The U.K. Biobank will be a tremendous resource for studies on neurodegeneration, both for data discovery and for replication. In addition, it will be a useful reference set for single-subject imaging markers. We have not used the data set ourselves, but m
COMMENT One remarkable finding of this interesting study is the observation that the CSF Aβ1-42 abnormality index only increases to 30 percent at the late AD stage. However, amyloid PET binding (which correlates around 0.8 with CSF Aβ1-42 in ADNI [Toledo et al.,
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