Kinetics of Human Mutant Tau Prion Formation in the Brains of 2 Transgenic Mouse Lines

Abstract

We are pleased to announce that in early , The JAMA Network will launch a new journal-JAMA Network Open. Our editorial goal is to publish the very best clinical research across all disciplines, serving the worldwide community of investigators and clinicians and meeting the evolving needs and requirements of authors and funders. With the launch of JAMA Network Open, we simultaneously assert our editorial commitment to excellence and to the authorship community regardless of requirements of funders. This will be a fully open access journal and follows the launch of JAMA Oncology in and JAMA Cardiology in , which are hybrid journals offering open access options for research articles. , Frederick P. Rivara, MD, MPH, current editor in chief of JAMA Pediatrics, will be the editor in chief of JAMA Network Open.Medical journals and publishing have changed substantially during the past decades following the emergence and ascendance of the internet and the mobilization of journal content. Journals have gone "digital"-virtually all journals release content online ahead of or instead of print, and connect with their readers via electronic table of contents and through social media. Open access publishing has risen to prominence concurrent with these changes, with a primary goal to make research findings more accessible to potential users around the world. In addition, many funders now require that authors publish their results in open access journals, and this requirement will almost assuredly expand in the future.Our decision to launch an open access journal was based on careful thought and planning and represents our response to the rapidly evolving landscape of scientific discovery and medical journals and publishing. Between and , the number of major articles indexed annually in Web of Science increased from to (Figure , A). During the same time, at JAMA and The JAMA Network specialty journals the number of research manuscripts submitted increased from to , but the number of research manuscripts published declined from to (Figure, B). In , following the launches of

Hepatitis B core VLP-based mis-disordered tau vaccine elicits strong immune response and alleviates cognitive deficits and neuropathology progression in Tau.P301S mouse model of Alzheimer’s disease and frontotemporal dementia

“…To explore the effects of T294-HBc VLP vaccine on the animal models of FTD and AD, we applied the vaccine to the Tau.P301S transgenic mouse model, which is widely used to mimic the incidence and progression of FTD and AD and recapitulates the essential molecular and cellular features of the human tauopathies, including truncated tau generation, hyperphosphorylation, tau filament formation, and neurodegeneration [ 31 , 39 ]. Woerman et al’s report showed that the PS19 mouse model exhibited great variability in pathology onset at ages over 31 weeks, but it was relatively uniform before age 30 weeks [ 40 ]; the mice at 22 weeks of age that we used conformed the latter age range. Our results showed that T294-HBc vaccine improved cognition and memory of Tau.P301S mice and reduced the levels of truncated tau monomer, oligomer, and hyperphosphorylated tau.…”

New Insights Into the Pathogenesis of Alzheimer's Disease

“…Brain-derived Aβ and synthetic Aβ from AD patients injected into the brain of transgenic mice showed prion-like appearances (93), which induced plaque formation and extensive deposition of Aβ. Brain extracts from age-matched patients without AD showed minimal accumulation of Aβ (94). An autopsy in a few studies also revealed that some patients had a large amount of Aβ deposition in the brain after death, after receiving dura mater transplantation and cadaveric growth hormone, which may mean that Aβ can be transmitted interpersonally through iatrogenic methods.…”

Longitudinal Microglial Activation in Tau Transgenic P301S Mice Predicts Increased Tau Accumulation and Deteriorated Spatial Learning

“…1B). We selected these target VOIs based on our immunohistochemical findings of tau accumulation in our earlier studies of the P301S mouse model [9][10][11][12].…”

“…The transgenic P301S mouse model accumulates tau in the brainstem [9][10][11], hippocampus [10,12] and cerebral cortex [10], and this accumulation is accompanied by a decline in spatial learning [12].…”