219 RESULTS
COMMENT Norambuena and colleagues used an APP SAA / App NL-G-I knock-in mouse model of AD to demonstrate mitochondrial dysfunction in the very early stage of AD development. It is hard to understand why the authors used a copy model of our App NL-G-F and other kn
COMMENT Until a century ago, most people used to die before the age of 50 with few exceptions, suggesting our creator did not expect us to live long enough to suffer from late-onset Alzheimer’s disease (LOAD). Kotredes and colleagues have tried to generate a mous
COMMENT Nobuhisa Iwata, a former member of my laboratory and currently professor of Nagasaki University, quantified plasma Aβ40 and 42 in wild-type and neprilysin knockout mice. Aβ40 and 42 were 1.6 and 1.7 times higher in the knockout mice, respectively, and the
COMMENT In Yasuo Ihara, I lost my lifetime mentor. I kept thinking that I would like to talk to him just one more time, but that dream did not come true. In the 1990s, I got into Alzheimer's from basic research on proteolysis. The motivation for this was my
COMMENT Laboratory. I have some comments that may help the students and postdocs who may be using the LOAD models. As
COMMENT Just a note to add. Some scientists want to transfer the mutant mice from another laboratory, rather than RIKEN BRC. This is fine, but I ask them to obtain permission from RIKEN BRC to do so. I also ask them to maintain the genetic background as described
COMMENT RIKEN has now made the App (Saito et al., 2014; Watamura et al., 2022), MAPT crosses (Hashimoto et al., 2019), and Psen1 (Sasaguri et al., 2018) knock-in mice available to nonprofit researchers worldwide as fully open resources with minimal requirements.
COMMENT It must have been difficult for the FDA to make the decision because they can be simultaneously praised and criticized, as seen in Alzforum. One factor that has affected the decision appears to be the extraordinary resources that have been spent for the R
COMMENT Just a note. The double mutants are heterozygous for the PSEN1 mutation, making it easy to breed them. We expect homozygous mutants to show even more aggressive pathology. saido 0
COMMENT The new knock-in mice described by Xia and colleagues carry Swedish (NL), Arctic (G) and Austrian (I) mutations (NL-G-I mice) are conceptually identical to our mice that carry Swedish, Arctic, and Beyreuther/Iberian (F) mutations (NL-G-F mice) (Saito et a
COMMENT My colleagues and I express sincere condolences to the family of the late Peter Davies. His passing is such a big loss to the research community. I have had several opportunities to communicate with Peter via telephone and email, although I did not have a
COMMENT We have developed mouse models that accumulate Aβ without overexpressing APP or APP/PS1 (Saito et al., 2014). They are being used by more than 400 laboratories world-wide, so overexpression artifacts are not always a problem with AD models. Still, in our
COMMENT As Sam Gandy pointed out, the APP fragment termed APP 113, or others, are presumptive CTF-βs (Nordstedt et al., 1991). It would be more informative to identify which protein fragments exactly correspond to CTF-β and CTF-α. saido 0 Alzheimer beta/A4 amyloi
COMMENT A simple question: Does CTF-β accumulate in preclinical and clinical AD patients? I believe that the findings must be confirmed in human brains. saido 0
COMMENT The overexpression paradigm is less problematic for modeling tauopathy than for Aβ amyloidosis because limited proteolysis is not a prerequisite for physiological and pathological processing of tau protein. Overexpression of APP results in overproduction
