{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T05:19:35Z","timestamp":1794028775648,"version":"4.8.0"},"reference-count":64,"publisher":"Society for Neuroscience","issue":"15","license":[{"start":{"date-parts":[[2013,10,10]],"date-time":"2013-10-10T00:00:00Z","timestamp":1381363200000},"content-version":"vor","delay-in-days":183,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2013,4,10]]},"abstract":"<jats:p>\n                    Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001). The \u201camyloid cascade hypothesis\u201d posits that cerebral amyloid sets neurotoxic events into motion that precipitate Alzheimer dementia (Hardy and Allsop, 1991). Yet, faithful recapitulation of all AD features in widely used transgenic (Tg) mice engineered to overproduce A\u03b2 peptides has been elusive. We have developed a Tg rat model (line TgF344-AD) expressing mutant human amyloid precursor protein (\n                    <jats:italic>\n                      APP\n                      <jats:sub>sw<\/jats:sub>\n                    <\/jats:italic>\n                    ) and presenilin 1 (\n                    <jats:italic>PS1<\/jats:italic>\n                    \u0394\n                    <jats:italic>E9<\/jats:italic>\n                    ) genes, each independent causes of early-onset familial AD. TgF344-AD rats manifest age-dependent cerebral amyloidosis that precedes tauopathy, gliosis, apoptotic loss of neurons in the cerebral cortex and hippocampus, and cognitive disturbance. These results demonstrate progressive neurodegeneration of the Alzheimer type in these animals. The TgF344-AD rat fills a critical need for a next-generation animal model to enable basic and translational AD research.\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.3672-12.2013","type":"journal-article","created":{"date-parts":[[2013,4,10]],"date-time":"2013-04-10T12:34:32Z","timestamp":1365597272000},"page":"6245-6256","source":"Crossref","is-referenced-by-count":509,"title":["A Transgenic Alzheimer Rat with Plaques, Tau Pathology, Behavioral Impairment, Oligomeric A\u03b2, and Frank Neuronal Loss"],"prefix":"10.1523","volume":"33","author":[{"given":"Robert M.","family":"Cohen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kavon","family":"Rezai-Zadeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tara 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