11699 RESULTS
COMMENT Defects in proteostasis and the accumulation of toxic misfolded proteins, as well as mitochondrial dysfunction and a neuroenergetic crisis are intimately linked to each other in the pathogenesis of neurodegenerative diseases. This preprint tries to shed l
COMMENT The increased level of LRP1 in astrocytes observed in this study is quite interesting. It could be a contributing mechanism of protection by the APOE Christchurch variant. Other mechanisms could include reduced binding to HSPG and other apoE receptors suc
COMMENT The characterization of tau in CSF and blood has marked a milestone in the field of biomarkers for AD, and we now have a range of assays targeting different tau forms. However, most tau biomarkers are highly correlated among each other and this prompts th
COMMENT As most phosphorylated-tau biomarkers available in blood or CSF reflect mainly Aβ-related pathology, there is an urgent need for the identification of cost-effective and scalable fluid biomarkers specific for tau aggregate pathology in Alzheimer’s disease
COMMENT This study tests the performance of another blood test from the UGOT team in the well-characterized Biofinder cohort. The authors showed convincing results that support that the variance of their new NTA-tau assay is much better explained by tau PET than
COMMENT Lantero-Rodriguez and colleagues have conducted a comprehensive characterization of the NTA-tau assay, which employs anti-tau mAb (HT7) for capture and anti-tau (Tau12) for detection. This assay was developed and validated by the Clinical Neurochemistry L
COMMENT This impressive study characterizes the longitudinal biomarker changes in sporadic AD. The pattern of changes in other forms of AD, such as autosomal-dominant AD (Bateman et al., 2012) or Down Syndrome AD (Fortea et al., 2020) have previously been reporte
COMMENT These two papers describing the timeline of the trajectory from amyloid positivity to symptom onset are extremely important, with very practical implications for clinical trials and patient care. What is so remarkable is how similar the results are in the
COMMENT comments already posted in Alzforum. We have long maintained that there is an important role for epigenetic
COMMENT This is a beautiful study with compelling results. That the authors discovered a role for glia in protecting neurons from wake-related oxidative stress is quite unexpected and eye-opening. The next step will be to test the extent to which this mechanism a
COMMENT This is an exciting finding. It builds on work from Hugo Bellen’s lab, which showed that astrocytes can take up lipid droplets from stressed/injured neurons as a neuroprotective mechanism. This new paper provides a novel connection to sleep deprivation, w
COMMENT This exciting new paper from the Seghal lab makes an unexpected connection between reactive oxygen species (ROS), lipid metabolism, and sleep. Previous work had shown that neurons release ROS-damaged peroxidated lipids when overexcited or stressed; these
COMMENT This is a fantastic study. It addresses fundamental issues of brain bioenergetic metabolism that relate and link to several AD-relevant phenomena, including neuron-glia interplay, apolipoprotein E biology, lipid metabolism, oxidative stress, circadian rhy
COMMENT One great drawback when studying proteins like TDP-43 is the incredible number of genes whose expression is controlled by this protein, and which become misregulated following TDP-43 aggregation in pathological conditions. From a therapeutic point of view
COMMENT Adapted from a LinkedIn post. In order to fully understand the biology of Alzheimer’s disease, to create new predictive models, and to identify novel causal and druggable targets, we need large-scale, unbiased omic analyses. For the last three years, my l
