7 RESULTS
COMMENT This is an interesting, in-vitro study with recombinant tau (297–391), analyzing structures of intermediate amyloid species that form during the assembly into filaments containing the Alzheimer or CTE fold, leading to a model in which prefibrillar, oligom
COMMENT On the choice of epitope for Tau therapeutic antibodies: For bepranemab, we have published on the antibody and the choice of epitope (Courade et al., 2018). We had raised a broad spectrum of antibodies, run them through our functional assay using human AD
COMMENT We applaud this new research framework, as it reflects the improved molecular understanding of AD. Therapies targeting disease modification, and potentially disease interception, will have to be based on the molecular biology, and such experimental therap
COMMENT I was deeply saddened by the loss of Dale Schenk, a great pioneer of modern AD research and drug discovery in neurodegeneration. Dennis’ In Memoriam captures Dale and his extraordinary contributions perfectly. Since the early '90s, I had the chance t
COMMENT In this Scientific Reports publication, Steve Paul and colleagues demonstrate microglial degradation of pathological tau in a number of in vitro and ex vivo paradigms, including incubation of human brain sections with primary mouse microglia. They also sh
COMMENT Over the last years a number of studies have addressed potential on-target liabilities of therapeutic BACE1 inhibition. Many of these studies were based on knockout data alone, or addressed developmental myelination. In contrast, the new study by Herms an
COMMENT Over the last two years, several studies have suggested that levels of BACE1 protein are elevated in sporadic Alzheimer’s disease brains (1-4). It is not completely clear if the elevation of BACE1 protein is accompanied by an elevation in BACE1 message (a
