57 RESULTS
COMMENT The AD therapeutic problem has become a diagnostic one: How to define and detect prodromal AD? Even more important: How to stratify the different types of AD early in the disease process? A daunting task we must recognize and attack. fred.vanleuven 0 ...
COMMENT Very good to learn that protein tau is making more headlines in the AD field and that ardent baptists see the "tau-light." We just added our contribution to tau diagnostics, see below. The data is in mouse models for the time being. There can ...
COMMENT This study by Gregory Antonios and the group of Thomas Bayer—and their previous study in 2013—pertains to actions of their antibody, NT4X, in a broad array of assays and models in vitro, ex vivo, and in vivo. The data mainly confirm the seminal work of ...
COMMENT This study examined the effects of chronic administration of two different anti-amyloid antibodies, 3D6 and β1, in two cohorts of two different mouse strains, PDAPP and Tg2576, which both stand as models for the amyloid component of Alzheimer’s disease. ...
COMMENT Interesting findings. They illustrate perfectly the major problem that troubles fundamental research into protein tau, in the first instance in AD but evidently in all tauopathies. As opposed to APP and amyloid, we do know the major physiological function ...
COMMENT The reported work is encouraging but I, for one, propose a caveat: please separate tauopathy and protein tau in terms of spreading. While it has been clear for a long time that tauopathy is spreading from early- to later-affected brain regions, this does ...
COMMENT The issues surrounding protein tau remain among the toughest nuts to crack in normal brain physiology, and even more in brain pathology of AD and FTDP-17, as well as in the 55 or so known tauopathies. It takes the best hands and minds and most ...
COMMENT This paper reports a long-overdue in vitro approach to a long-standing problem. Nevertheless, it is important to keep in mind that neurons in culture are in a permanently stressed situation that does not reflect normal neurons in the brain but could be ...
COMMENT We will miss his generosity in sharing information and antibodies, his stuborness and his willingness to discuss, his big mind in his big body ... fred.vanleuven 0 ...
COMMENT This is excellent work allowing me to pitch two points: 1. Is there no need to target phosphorylated or conformational tau epitopes, as linear "naked" ones appear to work fine, at least in mice? 2. This is confirmation of what we thought all ...
COMMENT I daresay, "most intriguing" (referring to the famous Belgian Janssen twins). This could add weight to the Tomm40 implication in AD—but also to "cognitive ageing"? fred.vanleuven 0 A genome-wide association study implicates the APOE ...
COMMENT It is still amazing how many scientists in this field want to believe instead of look at facts and interpret them: Plenty of evidence says amyloid is "bad" and involved in pathology (AD); not enough evidence says it is "good," i.e., ...
COMMENT I agree with Lennart Mucke, Akihiko Takashima, and Michel Goedert that this is a major opus by Ittner and Goetz and coworkers, and will become seminal in the long-standing question of how amyloid and tau are related to each other in the pathogenic ...
COMMENT I agree with the three previous commentators that the levels of Aβ used in these experiments are high. Then again, we have no idea what the Aβ content is in and around our neurons, or rather our synapses—the active ones that is—where Aβ is claimed to be ...
COMMENT Agreed and supported by our AAV-tau models; see reference below. fred.vanleuven 0 AAV-tau mediates pyramidal neurodegeneration by cell-cycle re-entry without neurofibrillary tangle formation in wild-type mice. ...
