the swedish, iberian, and arctic mutations n/a aβ plaques (2 mo), gliosis (2 mo), synaptic loss (4 mo), cognitive impairment (6 mo) tau models jnpl3 mapt express 4 repeat human tau carrying the p301l mutation murine prp neurofibrillary tangles (4.5 mo), neuronal loss (10 mo), gliosis (10 mo) pr5 mapt over-express 4 repeat human tau carrying the p301l mutation murine thy1 cognitive impairment (5 mo), ltp deficits (6 mo), gliosis (7 mo), neurofibrillary tangles (8 mo) tau p301s mapt over-express human tau carrying the p301s mutation murine prp gliosis (3 mo), synaptic loss (3 mo), neurofibrillary tangles (6 mo), ltp defects (6 mo), cognitive impairment (6 mo), neuronal loss (9-12 mo) psen models ps1 m146v psen1 over-express psen1 with the m146v mutation rat pdgfβ neuropathology is absent in these mice. cognitive ability has not been observed. other models tapp app, mapt over-expression of human app carrying the swedish mutation and 4 repeat human tau with the p301l mutation. hamster prp, murine prp neurofibrillary tangles (3 mo), gliosis (3 mo), aβ plaques (9 mo) 3xtg-ad app, psen1, mapt express human app with the swedish mutation, mapt with the p301l mutation, and psen1 with the m146v mutation murine thy1 (ps1 knockin) cognitive impairment (4 mo), aβ plaques (6 mo), ltp deficits (6 mo), gliosis (7 mo), neurofibrillary tangles (12 mo) psapp app, psen1 over-express human app with the swedish mutation and psen1 with the m146l mutation hamster prp, pdgfβ cognitive impairment (3 mo), aβ plaques (6 mo), gliosis (6 mo), neuronal loss (22 mo) 5xfad (b6sjl) app, psen1 over-express human app with the swedish, florida, and london mutations and psen1 with the m146l and l286v mutations murine thy1 aβ plaques (2 mo), gliosis (2 mo), synaptic loss (4 mo), cognitive impairment (4-5 mo), ltp deficit (4-6 mo), neuronal loss (4-6 mo) 5xfad (c57bl6) app, psen1 over-express human app with the swedish, florida, and london mutations and psen1 with the m146l and l286v mutations murine thy1 ltp defecits (2 mo), aβ plaques (2 mo), gliosis (2 mo), cognitive impairment (3-6 mo), synaptic loss (3-6 mo), neuronal loss (12 mo) huapoe ki apoe2, apoe3, apoe4 express humanized apoe2, apoe3, or apoe4 n/a no data rat models name genes modification information promoter known pathology (age of onset in months) mcgill-r-thy1-app app express human app with the swedish and indiana mutations murine thy1.2 cognitive impairment (3 mo), ltp deficits (3 mo), aβ plaques (6 mo), gliosis (6 mo), neuronal loss (18 mo), synaptic loss (20 mo) appnl-g-fki app express humanized aβ with the swedish, arctic, and iberian mutations n/a aβ plaques (1 mo), cognitive impairment (5-7 mo), gliosis (6 mo), synaptic loss (6 mo), neuronal loss (12 mo) app+ps1 app, psen1 express human app with the swedish and indiana mutations and human psen1 with the l166p mutation ubc cognitive impairment (10 mo); aβ plaques (19 mo), neuronal loss (19 mo) tgf344-ad app, psen1 express human app with the swedish mutation and human psen1 with the δexon9 mutation murine prp gliosis (6 mo), cognitive impairment (6 mo), aβ plaques (6 mo), neurofibrillary tangles (16 mo), neuronal loss (16 mo) non-human primates non-human primates can be used by researchers to study mechanisms of alzheimer's disease as well as develop therapeutics. non-human primates are useful as they have a more similar aging pattern to humans compared to rodent models. during non-human primate aging, they can display neuropathy, cognitive changes, and amyloid-β deposits, similar to that of alzheimer's disease. while these models are useful in studying the process of aging, they are not always exact models of alzheimer's disease. common non-human primates used in ad research include: rhesus monkeys (macaca mulattas), stump-tailed macaques (macaca arctoides), mouse lemurs (microcebus murinus), the common marmoset (callithrix jacchus), and crab-eating macaques (macaca fascicularis). these models can be studied both spontaneously or through artificial induction of alzheimer's disease responses. common techniques used to induce these models include: cholinergic nervous system injury, amyloid-β injection, intrinsic formaldehyde, and streptozotocin (a methyl nitrosourea sugar compound which induces diabetes). alternative organisms zebrafish drosophila caenorhabditis elegans