44 RESULTS
COMMENT It is well known that the cortex swells slightly as Alzheimer’s disease develops (see for example recent work from Phan et al., 2024), probably due to reactive changes (gliosis, not inflammation) as the Aβ amyloid aggregates and deposits in the parenchyma
COMMENT Generally, increased oversight and improved Quality Assurance/Quality Control (QA/QC) is a good thing for the field, particularly as we move into routine clinical practice with significant public health implications. Blood screens for AD need to be shown
COMMENT Is late-onset, “sporadic” Alzheimer’s disease genetic? Is this a trick question? Ever since Strittmatter and Roses published the first evidence of the association between ApoE and Aβ-amyloid in 1993 (Strittmatter et al., 1993), and as long as he lived, Al
COMMENT Iatrogenic Alzheimer’s disease: a medical misadventure? Premised on our current understanding of the continuum of pathogenic changes in AD evolution, the U.K. National Prion Monitoring Cohort (NPMC) now reports eight cases of likely young-onset (38-55 yea
COMMENT This study of more than a million transfusion recipients sends us a warning signal of what might be in store. Several years ago we (Alnakhli et al., 2020) published a similar finding on 184 persons with death certificates from the 2,940-person cohort of A
COMMENT Some of us are old enough to remember the 1986 useful proteomic discovery of a 14-3-3 spot on a two-dimensional gel, which proved to be of diagnostic value for Creutzfeldt-Jakob disease (Harrington et al., 1986). Since then, proteomic approaches on bioflu
COMMENT The twists and turns of TDP The argument regarding whether the presence of specific fibrils in particular cases stems from different extraction procedures or case-specific neuropathological conditions seems to find support from both sides. This study led
COMMENT Yasuo Ihara (1945-2023): Pioneer Alzheimer’s disease researcher. We first met and got to know Yasuo Ihara, and realized his deep insight into Alzheimer’s disease, at the 11th meeting of the International Society for Neurochemistry (ISN) held at the Maputo
COMMENT Fresh eyes reveal diversity of Aβ fibrillar structures in amyloid plaques. It’s always good to see fresh eyes looking at the major AD unsolved questions: What constitutes an Aβ plaque, its central core, peripheral halo, and surrounding tau-positive reacti
COMMENT Where and when do Aβ and tau interact? One of the most important questions left to answer in the puzzle of Alzheimer’s disease is when and where do aggregating forms of Aβ and tau interact to give rise to extracellular Aβ amyloid and intracellular tau-rea
COMMENT The authors are on the right track, with some success in lowering the Aβ amyloid load after three months treatment, starting at three months of age. The pharmacokinetics of verubecestat ad libitum in mouse chow proved difficult, with sex differences compl
COMMENT Aβ, also known as “the peptide from hell,” is very difficult to work with, because of its high degree of hydrophobicity and aggregability. We first described oligomers of Aβ in 1985 (A-8 dimers, A-16 tetramers, etc.; Masters et al., 1985). There have been
COMMENT We thank Drs. Colonna, Wang, and Pluvinage for their comments. Our study found that plasma sCD22
COMMENT It’s surprising to see three very similar papers on TMEM106B appear at the same time. First impressions on these findings from the sarkosyl pellets from a diverse series of postmortem brain specimens raise questions about whether this is a new type of int
COMMENT There’s very little I can add to the comments already posted. John was a good friend to all of us,
