11549 RESULTS
COMMENT The concept of using biomarkers to monitor disease is so appealing that it sometimes leads us to forget essential scientific critical thinking. This move follows a long process that increasingly equates dementia of the Alzheimer's type to the presenc
COMMENT It is strange to read this article and the two positive comments from Drs. Salloway and Knopman.
COMMENT Amyloid PET imaging offers advantages over CSF analysis for establishing the presence of elevated brain amyloid, and this has implications for routine diagnosis but especially for therapeutics. As we enter the new therapeutic era with lecanemab, the CMS d
COMMENT I welcome the CMS decision to end the CED for PET amyloid imaging and the removal of the limit on amyloid PET to a single lifetime scan. Assuming that local MACs follow suit, this should provide wider access for amyloid PET in clinical practice, opening t
COMMENT This manuscript is enormously important for understanding disease mechanisms in PSP and FTD. In Alzheimer’s, the identification of many genetic risk variants over the last decade had shown us the crucial involvement of lipid metabolism, immune dysfunction
COMMENT Tau pathology is a common feature of several neurodegenerative diseases, but there are intriguing disease-specific differences: Each tauopathy is associated with a different spectrum of genetic risk factors, distinct cell types are affected, and recent cr
COMMENT It is exciting to start seeing results of the worldwide push to understand and map the complexity of the brain in order to both better understand what makes us human and to pave the way for treatments for neurological and psychiatric diseases. As a neuros
COMMENT It is fantastic to see confirmation of our study, published earlier this year, that human microglia and astrocytes engulf synapses in Alzheimer’s disease (Tzioras et al., 2023). Both of our studies found more synapses inside astrocytes than inside microgl
COMMENT The authors performed incredibly thorough analyses of synaptic structure in postmortem human brain which enabled, for the first time, a very detailed look into the interactions among synapses, astrocytes, and microglia as they relate to cognitive decline.
COMMENT This research by Maniv et al. provides further insights into the molecular connection between UBB+1 and the pathology of Alzheimer's disease (AD). UBB+1, a ubiquitin RNA frameshift mutation identified by van Leeuwen and colleagues more than two decad
COMMENT These findings are very intriguing. Given the importance of 3R and 4R ratios in neurodegeneration, the potential differential effects of acetylation on 3R and 4R could have important implications and warrant further exploration in cell-based studies and i
COMMENT I think it is quite intriguing that UBB+1 specifically targets AD pathologies (Aβ and p-tau), but not other pathologies, such as α-synuclein. It would be important to know how UBB+1 selectively modulates APP degradation, but not the degradation of other p
COMMENT Together with a recent study that solved the structure of GTP1 in complex with tau PHFs from an AD brain sample (Merz et al., 2023), now we have the CryoEM structure for the AD tau PHF:MK6240 complex, which is also obtained with a 1:1 stoichiometry. We ca
COMMENT Sun et al. provide a comprehensive assessment of human microglia phenotypes in the aged and Alzheimer’s disease brain. Utilizing the data-rich ROS/MAP cohort the authors established the presence of 12 different microglia transcriptional states, identifyin
COMMENT The paper by Xiong et al. represents a seminal contribution to our understanding of Alzheimer's disease from a functional genomics perspective, elucidating previously unrecognized aspects of the disease's molecular etiology. One of the most sign
