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22 Models
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Mouse Models (21)
	Name	Other Names	Strain Name	Genetic Background	Gene	Mutation	Modification Info	Modification	Disease	Neuropathology	Behavior/Cognition	Other Phenotype	Availability	Primary Paper	Visualization
	5xFAD (B6SJL)	<p>-</p>, <p>5XFAD</p>, <p>APP/PS1</p>, <p>Tg6799</p>, <p>Tg-5xFAD</p>	B6SJL-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmjax	C57BL/6 x SJL	APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Two transgenes: mutant human APP with the APP Swedish, Florida, and London mutations and containing the 5' untranslated region driven by the mouse Thy1 promoter; and mutant human PSEN1 including the M146L and L286V mutations driven by the mouse Thy1 promoter.	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid pathology starting at 2 months, including amyloid plaques. Accumulation of intraneuronal Aβ before amyloid deposition. Gliosis and synapse degeneration. Neuron loss in cortical layer 5 and subiculum. No neurofibrillary tangles.	Age-dependent memory deficits including spatial memory, stress-related memory, and memory stablization. Motor phenotype.		The Jackson Lab; available through the JAX MMRRC Stock# 034840; Live.	Oakley et al., 2006	Yes
	5xFAD (C57BL6)	<p>-</p>, <p>5XFAD</p>, <p>APP/PS1</p>, <p>Tg6799</p>, <p>Tg-5xFAD</p>	B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmjax	C57BL6	APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Two transgenes: mutant human APP with the APP Swedish, Florida, and London mutations and containing the 5' untranslated region driven by the mouse Thy1 promoter; and mutant human PSEN1 including the M146L and L286V mutations driven by the mouse Thy1 promoter.	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid pathology starting at 2 months, including amyloid plaques. Accumulation of intraneuronal Aβ before amyloid deposition. Gliosis and synapse degeneration. Neuron loss in cortical layer V.	Age-dependent memory deficits, motor phenotype, and reduced anxiety.	The parental origin of the transgenes has been shown to influence plaque burdens in 5xFAD mice on a C57BL6 background—with plaque burdens higher in mice who inherited the APP and PSEN1 transgenes from their fathers, compared with those who inherited the transgenes from their mothers.	Available from The Jackson Laboratory, JAX MMRRC Stock# 034848. Research with this model is available from Scantox Neuro.	Jawhar et al., 2012, Richard et al., 2015	Yes
	AAV-sTREM2 5xFAD	<p>-</p>, <p>5xFAD-sTREM2</p>		5xFAD (C57BL6)	TREM2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Adeno-associated viruses (AAV2/8) expressing EGFP- and FLAG-tagged human TREM2 (amino acids 1-171) under the control of the CAG promoter were injected bilaterally into the lateral ventricles of neonatal 5xFAD mice.	TREM2: Virus; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	AAV-mediated over expression of sTREM2 decreased amyloid plaque burdens and increased numbers of plaque-associated microglia in the brains of 5xFAD mice.	5xFAD mice show impaired learning and memory in the Morris water maze, but AAV-sTREM2 5xFAD mice performed as well as non-transgenic controls.	Long-term potentiation at Shaeffer collateral-CA1 synapses is impaired in 5xFAD mice. AAV-mediated over expression of sTREM2 rescued LTP in AAV-sTREM2 5xFAD mice.	5xFAD mice are available from The Jackson Laboratory, JAX MMRRC Stock# 034848. Research with 5xFAD is available from Scantox Neuro.	Zhong et al., 2019	Yes
	AD-BXD	<p>-</p>, <p>5xFAD BxD</p>	(B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmjax x BXD[strain number]	C57BL/6J X BXD[strain number]	APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	“AD-BXD” refers to a panel of transgenic mouse strains, created by crossing 5XFAD mice to members of the BXD genetic reference panel. 5XFAD mice carry APP (with the Swedish, Florida, and London mutations) and PSEN1 (with M146L and L286V mutations) transgenes. The BXD genetic reference panel is a set of recombinant inbred mouse strains derived from crossing the C57BL/6J and DBA/2J inbred strains.	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Transgenic AD-BXD mice develop amyloid plaques by 6 months of age, although the extent of plaque deposition is strain-dependent.	Transgenic AD-BXD mice exhibit cognitive deficits, assessed using contextual fear conditioning. The age of onset and severity of impairment are strain-dependent.		Individual AD-BXD strains are available as F1 hybrids from The Jackson Laboratory (each strain has its own stock number).	Neuner et al., 2019	Yes
	APP23	<p>-</p>, <p>B6-Tg/Thy1APP23Sdz</p>	B6.Cg-Tg(Thy1-APP)3Somm/J	C57BL/6	APP	APP K670_M671delinsNL (Swedish)	Transgene containing human APP (isoform 751) containing the Swedish (KM670/671NL) mutation under the murine Thy1 promoter.	APP: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Aβ deposits first observed at 6 months. Congophilic plaques increase in size and number with age and are surrounded by activated microglia, astrocytes, and dystrophic neurites containing hyperphosphorylated tau (although no neurofibrillary tangles). Neuronal loss in the CA1 region of the hippocampus. Mice also develop CAA, and microhemorrages occur at later ages.	Spatial memory defects in Morris Water maze at 3 months and progresses with age. Memory deficits in passive avoidance were observed in 25 month-old mice, but not at younger ages.	Hyperactivity observed between the ages of 6 weeks to 6 months. It is not known whether this persists or resolves in older animals. Abnormalities in open field test and impaired performance on rotorod observed from 3 months.	Available through The Jackson Laboratory Stock# 030504, Live	Sturchler-Pierrat et al., 1997	Yes
	APP751SL/PS1 KI	<p>-</p>, <p>APP(SL)PS1KI</p>, <p>APPxPS1-Ki</p>, <p>APPSL/PS1KI</p>, <p>APP(SL)/PS1(KI)</p>, <p>APP/PS1KI</p>		The PS1KI line was established in 129SV and backcrossed >7 times to C57BL/6 background. The PS1KI were bred with APPSL mice on a C57BL background (two rounds) to obtain a homozygote PS1KI and heterozygote APP.	APP, PSEN1	APP K670_M671delinsNL (Swedish), APP V717I (London), PSEN1 M233T, PSEN1 L235P	This animal is a cross between a PSEN1 knock-in line and an APP over-expressing line. The PS1 knock-in line was generated by introducing two point mutations in the wild-type mouse PSEN1, corresponding to the mutations M233T and L235P. APP751SL overexpresses human APP751 carrying the London (V717I) and Swedish (K670N/M671L) mutations under the control of the Thy1 promoter.	APP: Transgenic; PSEN1: Knock-In	Alzheimer's Disease	Acceleration of extracellular Aβ deposition compared to the single transgenics. Age-dependent neuronal loss in the hippocampus with extensive neuronal loss in the CA1/2 at 10 months with detection as early as 6 months in female mice. Intraneuronal Aβ and thioflavin-S-positive deposits before neuronal loss. Astrogliosis in proximity of Aβ-positive neurons.	Age-dependent impairments in working memory as measured by the Y maze and T-maze continuous alternation task. No deficit at 2 months, but deficits at 6 and 12 months compared to PS1KI littermates.	Viable and fertile. 6 month-old animals develop decreases in body weight, and a spinal deformity (kyphosis) is common. Impaired neurogenesis.	Available through Thomas Bayer or Benoit Delatour	Casas et al., 2004	Yes
	APP Knock-in	<p>-</p>, <p>APP KI</p>, <p>line ADF</p>	App^tm1Sud/J	Strain of origin: (129X1/SvJ x 129S1/Sv)F1-Kitl<+>; C57BL/6 and maintained on a mixed background	APP	APP K670_M671delinsNL (Swedish), APP V717I (London), APP E693Q (Dutch)	Knock-in of wild-type mouse APP exon 16 (truncated after residue KM), FLAG tag (2 repeats), a stop codon, a poly A signal region from the human growth hormone gene and an additional copy of exon 16 carrying the Swedish mutation and a modified exon 17 with the London and Dutch mutations.	APP: Knock-In	Alzheimer's Disease	Unknown.	Unknown.		The Jackson Lab: Stock# 008390; Cryopreserved	The Jackson Laboratory	No
	APPSweLon	<p>-</p>, <p>APP YAC Swe/Lon (line J1.96)</p>, <p>B6-J1-96</p>	B6.129S4-Tg(APPSwLon)96Btla/Mmjax	129S4/SvJae-derived J1 ES cells; backcrossed to C57BL/6	APP	APP K670_M671delinsNL (Swedish), APP V717I (London)	A 650 kb YAC transgene containing the entire human APP gene carrying the Swedish and London mutations with ~ 250 kb of flanking sequence; founder animals (line J1.96) have a single copy of the transgene.	APP: Transgenic	Alzheimer's Disease	No amyloid plaques observed at 2 years.	Unknown.		The Jackson Lab; available through the JAX MMRRC Stock# 034837; Cryopreserved	Lamb et al., 1997	No
	APP(V717I)	<p>-</p>, <p>APPlon</p>, <p>APP-london</p>, <p>APPLd</p>, <p>APP-ld</p>, <p>APP(V717I)</p>, <p>APP[V717I]</p>, <p>APP.V717I</p>, <p>APP(London) (line 2)</p>, <p>APP/LD/2</p>	Tg(Thy1-APPLon)2Vln/0	Originally generated on FVB/N background; available at reMYND as C57BL/6xFVB/N	APP	APP V717I (London)	Transgene containing human APP (isoform 695) with the London mutation driven by the Thy1 promoter.	APP: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Plaques start in the subiculum, spreading to the frontal cortex as dense and diffuse aggregates. Prominent amyloid deposits in brain vessels after 15 months. Microbleeds. Amyloid-associated inflammation. CSF Aβ42/Aβ40 ratio decreases from 15 months. Dystrophic neurites containing hyperphosphorylated tau, but no tangle pathology.	From the age of 6 months, spatial and non-spatial orientation and memory deficits by Morris water maze. Impaired associative learning. Increased agitation/anxiety from 8 weeks. Reduced ambulation, especially with age. Hyperactivity and aggression.	Increased mortality (72% by day 180). Increased incidence of seizures.	Available through the KU Leuven Research and Development Office; the CRO InnoSer offers research services with this line.	Moechars et al., 1999	Yes
	APP(V717I) x PS1(A246E)	<p>-</p>, <p>APPxPS1</p>, <p>APP(V717I)x PS1(A246E)</p>, <p>APP[V717I]x PS1[A246E]</p>, <p>APP.V717I x PS1.A246E</p>	Tg(Thy1-APPLon)2Vln/0; Tg(Thy1-PSEN1*A246E)2Vln/0	Originally generated on FVB/N background; available at reMYND as C57BL/6xFVB/N	APP, PSEN1	APP V717I (London), PSEN1 A246E	The transgene overexpresses the mutant human amyloid protein precursor APP (isoform 695), which bears the London (V717I) mutation, and human presenilin-1 with the A246E mutation, both under the control of the neuron-specific murine Thy1 promoter.	APP: Multi-transgene; PSEN1: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Soluble, oligomeric Aβ at 2 months and increases with age. Amyloid plaques at 6-9 months, earlier than APP(V717I) single transgenics. Plaques start in the subiculum and spread to the frontal cortex. Amyloid-associated inflammation. CAA pathology at 8 months; microbleeds at 12-15 months. Dystropic neurites containing hyperphosphorylated tau, but no tangle pathology.	From the age of 5 months, spatial and non-spatial orientation and memory deficits by Morris Water Maze. Impaired associative learning, hyperactivity, anxiety, and aggression.		The CRO InnoSer offers research services with this line.	Dewachter et al., 2000	Yes
	E2FAD	<p>-</p>, <p>APOE2-FAD</p>, <p>APOE2 Targeted Replacement x 5xFAD</p>		C57BL/6	APOE, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APOE2 Targeted Replacement mice were crossed with the 5xFAD line.	APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques starting at 4 months and increasing with age. Gliosis and loss of synaptic proteins.	In the Y maze and Morris water maze, E2FAD mice performed better than E4FAD mice, and were comparabile to E3FAD mice.		5xFAD mice are available through The Jackson Lab, Stock# 034840; Live. APOE2 Targeted Replacement mice are available through Taconic, Stock# 1547-F or 1547-M.	Youmans et al., 2012	Yes
	E3FAD	<p>-</p>, <p>APOE3-FAD</p>, <p>APOE3 Targeted Replacement x 5xFAD</p>		C57BL/6	APOE, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APOE3 Targeted Replacement mice were crossed with the 5xFAD line.	APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques starting at 4 months and increasing with age. Gliosis and loss of synaptic proteins.	In the Y maze and Morris water maze E3FAD mice performed better than E4FAD mice, and were comparabile to E2FAD mice.		5xFAD mice are available through The Jackson Lab, Stock# 034840; Live. APOE3 Targeted Replacement mice are available through Taconic, Stock# 1548-F or 1548-M.	Youmans et al., 2012	Yes
	mThy1-hAPP751 (TASD41)	<p>TASD41</p>, <p>Line 41</p>, <p>hAPPSL</p>, <p>hAPP-SL</p>, <p>AβPP751</p>, <p>mThy1-hAβPP751 Swe Lon (line 41)</p>, <p>APP751SL</p>, <p>hAPPlon/swe line 41</p>, <p>APP41</p>	mThy1-hAβPP751 Swe Lon	C57BL/6 x DBA	APP	APP K670_M671delinsNL (Swedish), APP V717I (London)	The transgene over-expresses the mutant human amyloid protein precursor (751 isoform), which bears both the Swedish (K670N/M671L) and the London (V717I) mutations, under the control of the murine Thy1 promoter.	APP: Transgenic	Alzheimer's Disease	Age-dependent increases in Aβ40 and Aβ42, with Aβ42 > Aβ40. Plaques at an early age, starting at 3-6 months in the frontal cortex. At 5-7 months, size and number of plaques increased in the frontal cortex, and dense amyloid deposits appear in hippocampous, thalamus, and olfactory region.	Age-associated impairment in spatial memory and learning in the water maze task and habituation in the hole-board task, with significant deficits at 6 months of age. Some gender-specific differences in open field exploration.		Available through Eliezer Masliah. The CRO PsychoGenics offers research services with this line.	Rockenstein et al., 2001	Yes
	PLB1-triple (hAPP/hTau/hPS1)	<p>hAPP/hTau/hPS1</p>, <p>PLB1(Triple)</p>		C57BL6	APP, MAPT, PSEN1	APP V717I (London), APP K670_M671delinsNL (Swedish), PSEN1 A246E, MAPT P301L, MAPT R406W	Targeted insertion of human APP and tau sequences at the HPRT site on the X chromosome, driven by mouse CaMKII-α. Human APP (isoform 770) with the Swedish and London mutations. Human tau (isoform 2N/4R, 441 amino acids) with P301L and R406W. APP/tau-expressing animals (PLB1-double) were crossed with hPS1 (A246E) transgenic mice (Borchelt et al., 1997) to generate the triple transgenic.	APP: Multi-transgene; MAPT: Multi-transgene; PSEN1: Multi-transgene	Alzheimer's Disease	Age-related neuropathology including intraneuronal and oligomeric Aβ accumulation and hyperphosphorylated tau in the hippocampus and cortex from six months. Minimal amyloid plaques up to 21 months. Subtle tau pathology, but no overt tangles. Cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain by FDG-PET/CT.	Cognitive deficits in recognition memory and spatial learning emerging between five and 12 months. Impairments in hippocampal plasticity.	Litter size and overall health were normal. Mice spent more time awake at six months and had fragmented sleep. Quantitative EEG showed heightened delta power during wakefulness and REM sleep.	Available through Bettina Platt	Platt et al., 2011	Yes
	Plcg2*M28L x 5xFAD	<p>-</p>, <p>5xFAD<sup>M28L</sup></p>		C57BL/6J	Plcg2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Plcg2M28L/APOE4/Trem2R47H mice (JAX 030674) were backcrossed to C57BL/6J mice to remove the APOE4 sequence and Trem2 R47H mutation. The resulting Plcg2^M28L mice were then intercrossed with 5xFAD (JAX 034848) to create mice homozygous for the Plcg2 M28L mutation and hemizygous for the 5xFAD APP and PSEN1 transgenes.	Plcg2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Plaque burdens in the cortex and subiculum were elevated in 5xFAD^M28L mice but microglia showed less interaction with plaques, compared with 5xFAD.	Six-month-old 5xFAD^M28L and 5xFAD mice showed similar deficits in working memory, assessed in the Y-maze.	Impaired synaptic function—including deficits in basal synaptic transmission and long-term potentiation—similar to 5xFAD. Differences in microglial gene expression, compared with 5xFAD.	For Plcg2^M28Lmice, contact Andy Tsai. 5xFAD available from The Jackson Laboratory, JAX MMRRC Stock# 034848.	Tsai et al., 2023	Yes
	Plcg2*P522R x 5xFAD	<p>-</p>, <p>5xFAD<sup>P522R</sup></p>		C57BL/6J	Plcg2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	CRISPR/Cas9 gene editing was used to introduce the P522R mutation into the mouse Plcg2 gene in APOE4 Knock-In mice (JAX 027894). Correctly targeted mice were then backcrossed to C57BL/6J mice to remove the APOE4 sequence. The resulting Plcg2R522 mice (JAX 029598) were then intercrossed with 5xFAD (JAX 034848) to create mice homozygous for the Plcg2 P522R mutation and hemizygous for the 5xFAD APP and PSEN1 transgenes.	Plcg2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Plaque burdens in the cortex and subiculum were lower in 5xFAD^P522R mice and microglia showed increased interaction with plaques, compared with 5xFAD.	The PLCγ2 P522R variant protected against deficits in the Y-maze test of working memory in 5xFAD mice.	The PLCγ2 P522R variant protected against synaptic deficits in 5xFAD mice. Differences in microglial gene expression, compared with 5xFAD.	Plcg2^R522 available from The Jackson Laboratory, JAX Stock# 029598; 5xFAD available from The Jackson Laboratory, JAX MMRRC Stock# 034848.	Tsai et al., 2023	Yes
	rTg9191	<p>-</p>, <p>APP<sub>NLI</sub></p>		129S6FVB F1	APP	APP K670_M671delinsNL (Swedish), APP V717I (London)	These are bigenic mice with the CAMKII-α promoter driving expression of tetracycline transactivator (tTa) in excitatory neurons in the forebrain, and a responder transgene consisting of mutant human APP (isoform 695) carrying the Swedish and London mutations. The expression of the transgene is constitutive until suppressed by doxycycline.	APP: Transgenic	Alzheimer's Disease	Age-associated pathology in the cerebral cortex and hippocampus starting at 8 and 10½-12½ months of age, respectively. Gliosis and hyperphosphorylated tau in the vicinity of dense-core plaques. Fibrillar oligomeric species, e.g., Aβ dimers.	No transgene-related deficits seen in Morris water maze (4, 12, 21, 24, months of age) or fixed consecutive-number (23 months of age) tests.	Reduced body weight at 24-27 months relative to non-Tg littermates and those expressing only tTA.	Available through Karen Ashe	Liu et al., 2015	Yes
	TREM2-BAC X 5xFAD	<p>-</p>, <p>BAC-TREM2 X 5xFAD</p>		TREM2-BAC: FVB/NJ; 5xFAD: C57BL/6 X SJL	TREM2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	TREM2-BAC mice were crossed with 5xFAD mice.	TREM2: Transgenic; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques with plaque-associated microgliosis. Reduced plaque burden, altered microglial and plaque morphology, and less severe plaque-associated neuritic dystrophy, compared with 5xFAD.	5xFAD/TREM2 mice perform comparably to wild-type mice in a contextual fear conditioning test, while 5xFAD mice are impaired.		TREM2-BAC: Available through X. William Yang. 5xFAD: The Jackson Lab; available through the JAX MMRRC Stock# 034840; Live	Lee et al., 2018	Yes
	Trem2-H157Y x 5xFAD			C57Bl/6J	Trem2, APP, PSEN1	TREM2 H157Y, APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	CRISPR/Cas9 gene editing was used to introduce the H157Y mutation into the mouse Trem2 gene. The resulting Trem2-H157Y knock-in mice were then intercrossed with 5xFAD mice.	Trem2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Age-dependent effects on amyloid-β pathology and gliosis. At 4 months, plaque burdens, microgliosis, and astrogliosis were similar among genotypes. By 8.5 months, amyloid burdens, microgliosis, and astrogliosis were reduced in homozygous carriers of the H157Y variant, compared with 5xFAD mice homozygous for wild-type Trem2.	Unknown.	Increased TREM2 shedding, decreased TREM2 signaling, and accelerated Aβ42 clearance from the interstitial fluid in 5xFAD homozygous for Trem2 H157Y, compared with 5xFAD homozygous for wild-type Trem2. Downregulation of disease-associated microglia (DAM) genes, microglial immune-related genes, genes encoding inflammatory cytokines, and genes expressed by astrocytes in H157Y homozygotes.	Trem2-H157Y knock-in mice are available through Na Zhao (zhao.na@mayo.edu). 5xFAD mice are available from The Jackson Laboratory, JAX MMRRC Stock# 034848.	Qiao et al., 2023	Yes
	TREM2, humanized (R47H) X 5XFAD	<p>-</p>, <p>R47H<sup>+</sup>mTrem2<sup>−/−</sup>5XFAD</p>		C57BL/6 X CBA, back-crossed for at least 4 generations to C57BL/6	Trem2, TREM2, APP, PSEN1	TREM2 R47H, APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	BAC-transgenic mice carrying the human TREM2 (R47H variant), TREML1, and TREML2 were back-crossed to Trem2 KO mice (Colonna) to yield mice that express the R47H variant of human TREM2 in the absence of mouse Trem2. These mice were then crossed with 5XFAD mice.	Trem2: Knock-Out; TREM2: Transgenic; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Lower density of activated microglia surrounding amyloid plaques in 5XFAD mice expressing the R47H variant of human TREM2 compared with those expressing the common variant.	No data.		TREM2 mice: available through Marco Colonna; 5XFAD: The Jackson Lab; available through the JAX MMRRC Stock# 034848; Live	Song et al., 2018	Yes
	Trem2 KO (Colonna) x 5XFAD	<p>-</p>, <p>Trem2<sup>-/-</sup>5XFAD</p>, <p>mTrem2<sup>-/-</sup>5XFAD</p><p> </p>	C57BL/6 -TREM2^tm1cln; B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmja	C57BL/6	Trem2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	5XFAD mice were crossed with Trem2 KO mice. TREM2 KO: Targeted deletion of exons 3 and 4 of mouse Trem2. 5XFAD express two transgenes: 1) human APP with the Swedish, Florida and London mutations, containing the 5' untranslated region and driven by the mouse Thy1 promoter and 2) human PSEN1 with the M146L and L286V mutations driven by the mouse Thy1 promoter.	Trem2: Knock-Out; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Compared with 5XFAD, mice deficient in TREM2 show an age- dependent increase in amyloid accumulation in the hippocampus, more severe plaque-associated neuritic dystrophy, and exaggerated neuron loss in the cortex. Microglial containment of plaques is compromised in TREM2-deficient animals. Microglia accumulate autophagosomes.	No data.		Trem2 KO: available through Marco Colonna. 5XFAD: The Jackson Lab; available through the JAX MMRRC Stock# 034848; Live	Wang et al., 2015	Yes
Rat Models (1)
	AAV-AD	<p>-</p>, <p>AgenT</p>		Wistar	APP, PSEN1	APP K670_M671delinsNL (Swedish), APP V717I (London), PSEN1 M146L (A>C)	Adeno-associated viral vectors separately encoding human APP with the Swedish and London mutations and human PSEN1 with the M146L mutation were injected bilaterally into the hippocampi of young adult (8-week-old) rats.	APP: Virus; PSEN1: Virus	Alzheimer's Disease	Amyloid plaques and cerebral amyloid angiopathy observed 30 months post-injection. Anti-phospho-tau immunostaining suggests the presence of (pre)tangle-like structures. No astrogliosis seen up to 30 months post-injection.	Compared with control rats at 8 months post-injection, AAV-AD spent less time in the target quadrant of the Morris water maze in probe tests administered 3 and 5 days after training and less time in the center of the open field.	At 8 months post-injection, long-term potentiation was impaired in hippocampal slices obtained from AAV-AD rats, compared with controls, but the groups did not differ with regards to long-term depression.	Viral vectors are available through AgenT SAS under collaboration or partnership agreements.	Audrain et al., 2017	Yes

AD-related Research Models

When visualized, these phenotypes will distributed over a 18 month timeline demarcated at the following intervals: 3mo, 6mo, 9mo, 1yr, 15mo, 18mo+.

5xFAD (B6SJL)

Observed

X
Plaques at 8

Extracellular amyloid deposition begins around 2 months, first in the subiculum and layer V of the cortex. Aβ42 also accumulates intraneuronally in an aggregated form within the soma and neurites starting at 1.5 months.
X
Neuronal Loss at 23

Neuron loss in cortical layer V and subiculum.
X
Gliosis at 9

Gliosis begins at 2 months.
X
Synaptic Loss at 16

Levels of the presynaptic marker synaptophysin begin to decline by 4 months; levels of syntaxin, another presynaptic marker, and PSD-95, a postsynaptic marker, decline by 9 months
X
Changes in LTP/LTD at 25

Basal synaptic transmission and LTP in hippocampal area CA1 begin to deteriorate between 4 and 6 months
X
Cognitive Impairment at 18

Impaired spatial working memory in the Y-maze test and impaired remote memory stabilization in a contextual-fear-conditioning test by 4 to 5 months of age.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid pathology starting at 2 months, including amyloid plaques. Accumulation of intraneuronal Aβ before amyloid deposition. Gliosis and synapse degeneration. Neuron loss in cortical layer 5 and subiculum. No neurofibrillary tangles.	Age-dependent memory deficits including spatial memory, stress-related memory, and memory stablization. Motor phenotype.

expand

5xFAD (C57BL6)

Observed

X
Plaques at 8

Amyloid plaques observed in hippocampus, cortex, thalamus, and spinal cord. Amyloidosis more severe in females than males.
X
Neuronal Loss at 52

Approximate 40 percent loss of layer V pyramidal neurons at one year.
X
Gliosis at 8

Microgliosis and astrogliosis are associated with amyloid plaques; microgliosis is associated with vascular damage.
X
Synaptic Loss at 24

Spine density was reduced in pyramidal neurons in somatosensory and prefrontal cortices, but not in the hippocampi, of 5xFAD mice crossed with mice expressing yellow fluorescent protein (YFP mice), compared with mice expressing YFP alone.
X
Changes in LTP/LTD at 8

LTD was induced in layer V cortical neurons of 8- to 10-week-old 5xFAD mice using the same protocol that induced spike-timing-dependent LTP in neurons of non-transgenic mice. LTP at Schaffer collateral-CA1 synapses was decreased in 5xFAD by 4 months of age.
X
Cognitive Impairment at 24

Impairments of spatial working memory and reduced anxiety emerge between 3 and 6 months and worsen with age.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid pathology starting at 2 months, including amyloid plaques. Accumulation of intraneuronal Aβ before amyloid deposition. Gliosis and synapse degeneration. Neuron loss in cortical layer V.	Age-dependent memory deficits, motor phenotype, and reduced anxiety.

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AAV-AD

Observed

X
Plaques at 128

Amyloid plaques and cerebral amyloid angiopathy observed 30 months post-injection.
X
Changes in LTP/LTD at 40

Deficits in LTP as Schaffer collateral-CA1 synapse at 10 months (8 months post-injection). LTD similar to controls.
X
Cognitive Impairment at 40

AAV-AD spent less time in the target quadrant of the Morris water maze in probe tests administered 3 and 5 days after training.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP K670_M671delinsNL (Swedish), APP V717I (London), PSEN1 M146L (A>C)	APP: Virus; PSEN1: Virus	Alzheimer's Disease	Amyloid plaques and cerebral amyloid angiopathy observed 30 months post-injection. Anti-phospho-tau immunostaining suggests the presence of (pre)tangle-like structures. No astrogliosis seen up to 30 months post-injection.	Compared with control rats at 8 months post-injection, AAV-AD spent less time in the target quadrant of the Morris water maze in probe tests administered 3 and 5 days after training and less time in the center of the open field.

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AAV-sTREM2 5xFAD

Observed

X
Plaques at 28

When examined at 7 months of age, amyloid plaque burdens in the hippocampus and cortex of AAV-sTREM2 5xFAD mice were about half those of 5xFAD mice injected with control vector.
X
Gliosis at 28

The number of plaque-associated microglia was increased in AAV-sTREM2 5xFAD mice examined at 7 months of age.
X
Changes in LTP/LTD at 24

Long-term potentiation at Shaeffer collateral-CA1 synapses is impaired in 5xFAD mice. AAV-mediated over expression of sTREM2 rescued LTP in AAV-sTREM2 5xFAD mice.
X
Cognitive Impairment at 24

5xFAD mice show impaired learning and memory in the Morris water maze, but AAV-sTREM2 5xFAD mice performed as well as non-transgenic controls.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
TREM2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	TREM2: Virus; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	AAV-mediated over expression of sTREM2 decreased amyloid plaque burdens and increased numbers of plaque-associated microglia in the brains of 5xFAD mice.	5xFAD mice show impaired learning and memory in the Morris water maze, but AAV-sTREM2 5xFAD mice performed as well as non-transgenic controls.

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AD-BXD

Observed

X
Plaques at 24

Transgenic AD-BXD mice develop amyloid plaques by 6 months of age, the earliest age examined. The extent of plaque deposition is strain-dependent.
X
Gliosis at 25

Strain-dependent gliosis by 6 months.
X
Cognitive Impairment at 60

In the AD-BXD population as a whole, transgenic mice performed similarly to non-transgenic littermates in a contextual fear-conditioning test at 6 months, but were impaired at 14 months. The age of onset and severity of impairment are strain-dependent.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Transgenic AD-BXD mice develop amyloid plaques by 6 months of age, although the extent of plaque deposition is strain-dependent.	Transgenic AD-BXD mice exhibit cognitive deficits, assessed using contextual fear conditioning. The age of onset and severity of impairment are strain-dependent.

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APP23

Observed

X
Plaques at 26

Congophillic, dense-core amyloid plaques first appear at 6 months, and increase in size and number with age. Amyloid plaques can occupy more than 25% of the neocortex and hippocampus in 24 month-old mice (Sturchler-Pierrat et al., 1997; Calhoun et al., 1998).
X
Neuronal Loss at 61

Neuronal loss (14-28%) has been reported in the CA1 region of the hippocampus in 14-18 month old mice (Calhoun et al., 1998).
X
Gliosis at 26

Activated microglia in close proximity to dense amyloid plaques (Stalder et al., 1999). Upregulation of neuroinflammatory markers and activation of astrocytes and macrophages. Age-associated increase in components of the complement system, namely C1q and C3, at later ages (9 and 18 months, respectively) (Reichwald et al., 2009).
X
Cognitive Impairment at 13

Spatial memory defects in Morris Water maze at 3 months and progresses with age (Van dam et al., 2003; Kelly et al., 2003).

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP	APP K670_M671delinsNL (Swedish)	APP: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Aβ deposits first observed at 6 months. Congophilic plaques increase in size and number with age and are surrounded by activated microglia, astrocytes, and dystrophic neurites containing hyperphosphorylated tau (although no neurofibrillary tangles). Neuronal loss in the CA1 region of the hippocampus. Mice also develop CAA, and microhemorrages occur at later ages.	Spatial memory defects in Morris Water maze at 3 months and progresses with age. Memory deficits in passive avoidance were observed in 25 month-old mice, but not at younger ages.

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APP751SL/PS1 KI

Observed

X
Plaques at 11

Aβ deposition at 2.5 months compared to 6 months in APPSL mice. At 6 months, numerous compact Aβ deposits in the cortex, hippocampus, and thalamus, whereas in age-matched APPSL mice only very few deposits restricted mainly to the subiculum and deeper cortical layers. At 10 months, deposits increased in distribution, density, and size in both models (Casas et al., 2004).
X
Neuronal Loss at 23

Some cell loss detectable as early as 6 months in female mice. At 10 months extensive neuronal loss (>50%) is present in the CA1/2 hippocampal pyramidal cell layer. SNeuronal loss also occurs in the frontal cortex and cholinergic system (Casas et al., 2004; Christensen et al., 2008; Christensen et al., 2010).
X
Gliosis at 11

Astrogliosis occurs in parallel with Aβ deposition, starting around 2.5 months, and in proximity to Aβ-positive neurons (Wirths et al., 2010).
X
Synaptic Loss at 24

At 6 months, levels of pre- and post-synaptic markers are reduced (Breyhan et al., 2009).
X
Changes in LTP/LTD at 28

At 6 months there is a large reduction of long-term potentiation and disrupted paired pulse facilitation. No deficit at 4 months (Breyhan et al., 2009).
X
Cognitive Impairment at 27

Age-dependent impairments in working memory as measured by the Y maze and T-maze continuous alternation task. No deficit at 2 months, but deficits at 6 and 12 months compared to PS1KI littermates (Wirths et al., 2008).

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP K670_M671delinsNL (Swedish), APP V717I (London), PSEN1 M233T, PSEN1 L235P	APP: Transgenic; PSEN1: Knock-In	Alzheimer's Disease	Acceleration of extracellular Aβ deposition compared to the single transgenics. Age-dependent neuronal loss in the hippocampus with extensive neuronal loss in the CA1/2 at 10 months with detection as early as 6 months in female mice. Intraneuronal Aβ and thioflavin-S-positive deposits before neuronal loss. Astrogliosis in proximity of Aβ-positive neurons.	Age-dependent impairments in working memory as measured by the Y maze and T-maze continuous alternation task. No deficit at 2 months, but deficits at 6 and 12 months compared to PS1KI littermates.

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APP(V717I)

Observed

X
Plaques at 43

Plaques start in the cortex and subiculum at ~10 months. Diffuse amyloid deposits and compact neuritic plaques at 13-18 months especially in the hippocampus and cortex, with occasional deposits in the thalamus and fimbria, external capsule, pontine nuclei, and white matter (Moechars et al., 1999). Prominent amyloid deposits in brain vessels after 15 months (Van Dorpe et al, 2000).
X
Gliosis at 43

GFAP, microglial activation, and other markers of brain inflammation are elevated by 10 months.
X
Changes in LTP/LTD at 26

Significant deficit in LTP in CA1 region of the hippocampus at 6 months.
X
Cognitive Impairment at 26

From the age of 6 months, spatial and non-spatial orientation and memory deficits by Morris water maze and other tests. Also deficits in associative learning.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP	APP V717I (London)	APP: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Plaques start in the subiculum, spreading to the frontal cortex as dense and diffuse aggregates. Prominent amyloid deposits in brain vessels after 15 months. Microbleeds. Amyloid-associated inflammation. CSF Aβ42/Aβ40 ratio decreases from 15 months. Dystrophic neurites containing hyperphosphorylated tau, but no tangle pathology.	From the age of 6 months, spatial and non-spatial orientation and memory deficits by Morris water maze. Impaired associative learning. Increased agitation/anxiety from 8 weeks. Reduced ambulation, especially with age. Hyperactivity and aggression.

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APP(V717I) x PS1(A246E)

Observed

X
Plaques at 17

Plaques start in cortex, hippocampus and subiculum at 4-6 months.
X
Gliosis at 20

Elevated GFAP, microglial activation, and other markers of brain inflammation increase as of 4.5 months.
X
Changes in LTP/LTD at 26

Significant deficit in LTP in CA1 region of the hippocampus at 6 months.
X
Cognitive Impairment at 22

From the age of 5 months, spatial and non-spatial orientation and memory deficits by Morris water maze and other tests. Also deficits in associative learning.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, PSEN1	APP V717I (London), PSEN1 A246E	APP: Multi-transgene; PSEN1: Transgenic	Alzheimer's Disease, Cerebral Amyloid Angiopathy	Soluble, oligomeric Aβ at 2 months and increases with age. Amyloid plaques at 6-9 months, earlier than APP(V717I) single transgenics. Plaques start in the subiculum and spread to the frontal cortex. Amyloid-associated inflammation. CAA pathology at 8 months; microbleeds at 12-15 months. Dystropic neurites containing hyperphosphorylated tau, but no tangle pathology.	From the age of 5 months, spatial and non-spatial orientation and memory deficits by Morris Water Maze. Impaired associative learning, hyperactivity, anxiety, and aggression.

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E2FAD

Observed

X
Plaques at 17

Plaques develop in the subiculum and deep cortical layers by 4 months.
X
Gliosis at 26

Microgliosis and astrocytosis in the subiculum and cortex at 6 months.
X
Synaptic Loss at 17

Protein levels of NMDA receptor subunits decreased from 2 to 6 months.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APOE, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques starting at 4 months and increasing with age. Gliosis and loss of synaptic proteins.	In the Y maze and Morris water maze, E2FAD mice performed better than E4FAD mice, and were comparabile to E3FAD mice.

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E3FAD

Observed

X
Plaques at 17

Plaques develop in the subiculum and deep cortical layers by 4 months.
X
Gliosis at 26

Microgliosis and astrocytosis in the subiculum and cortex at 6 months.
X
Synaptic Loss at 17

Protein levels of NMDA receptor subunits decreased from 2 to 6 months.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APOE, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques starting at 4 months and increasing with age. Gliosis and loss of synaptic proteins.	In the Y maze and Morris water maze E3FAD mice performed better than E4FAD mice, and were comparabile to E2FAD mice.

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mThy1-hAPP751 (TASD41)

Observed

X
Plaques at 13

Plaques start at 3-6 months in the frontal cortex and become widespread with age, affecting the piriform and olfactory cortices, hippocampus, and thalamus (Rockenstein et al., 2001; Havas et al., 2011).
X
Gliosis at 27

Inflammation related to activated microglia (increased CD11) and reactive astrocytes (increased GFAP) is significant by 6 months and increases with age.
X
Synaptic Loss at 52

Dystrophic neurites and synaptic loss starting at 12 months.
X
Cognitive Impairment at 26

Cognitive impairment observed by 6 months by Morris Water Maze (Rockenstein et al., 2005).

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP	APP K670_M671delinsNL (Swedish), APP V717I (London)	APP: Transgenic	Alzheimer's Disease	Age-dependent increases in Aβ40 and Aβ42, with Aβ42 > Aβ40. Plaques at an early age, starting at 3-6 months in the frontal cortex. At 5-7 months, size and number of plaques increased in the frontal cortex, and dense amyloid deposits appear in hippocampous, thalamus, and olfactory region.	Age-associated impairment in spatial memory and learning in the water maze task and habituation in the hole-board task, with significant deficits at 6 months of age. Some gender-specific differences in open field exploration.

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PLB1-triple (hAPP/hTau/hPS1)

Observed

X
Gliosis at 52

Increased inflammation (GFAP labelling) detected at 12 months in cortex and hippocampus (Platt, unpublished observation).
X
Changes in LTP/LTD at 26

Impairments in long-term and short-term hippocampal plasticity. LTP following theta-burst stimulation decayed faster and paired-pulse facilitation was reduced relative to wild-type mice at both six and 12 months of age. Synaptic transmission impacted at 12 months.
X
Cognitive Impairment at 22

Social recognition memory was impaired by five months and further impaired by 12 months. Similarly, object recognition memory was impaired by eight months. Spatial learning impairments were seen later; at 12 months deficits in spatial acquisition learning were seen in the open field water maze that were not apparent at 5 months.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP, MAPT, PSEN1	APP V717I (London), APP K670_M671delinsNL (Swedish), PSEN1 A246E, MAPT P301L, MAPT R406W	APP: Multi-transgene; MAPT: Multi-transgene; PSEN1: Multi-transgene	Alzheimer's Disease	Age-related neuropathology including intraneuronal and oligomeric Aβ accumulation and hyperphosphorylated tau in the hippocampus and cortex from six months. Minimal amyloid plaques up to 21 months. Subtle tau pathology, but no overt tangles. Cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain by FDG-PET/CT.	Cognitive deficits in recognition memory and spatial learning emerging between five and 12 months. Impairments in hippocampal plasticity.

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Plcg2*M28L x 5xFAD

Observed

X
Plaques at 30

Diffuse and compact amyloid plaques observed in mice studied at 7.5 months of age. Higher plaque burdens than 5xFAD.
X
Gliosis at 31

Microgliosis observed in mice studied at 7.5 months of age.
X
Synaptic Loss at 32

Decreased basal synaptic transmission, lower frequencies and amplitudes of spontaneous excitatory postsynaptic currents and spontaneous inhibitory postsynaptic currents recorded in hippocampal CA1 region, compared with wild-type mice.
X
Changes in LTP/LTD at 33

Impaired LTP at Schaffer collateral-CA1 synapses, compared with wild-type.
X
Cognitive Impairment at 24

Deficits in working memory (decreased spontaneous alternation in the Y-maze), compared with wild-type.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
Plcg2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Plcg2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Plaque burdens in the cortex and subiculum were elevated in 5xFAD^M28L mice but microglia showed less interaction with plaques, compared with 5xFAD.	Six-month-old 5xFAD^M28L and 5xFAD mice showed similar deficits in working memory, assessed in the Y-maze.

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Plcg2*P522R x 5xFAD

Observed

X
Plaques at 30

Diffuse and compact amyloid plaques observed in mice studied at 7.5 months of age. Lower plaque burdens than 5xFAD.
X
Gliosis at 31

Microgliosis observed in mice studied at 7.5 months of age.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
Plcg2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Plcg2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Plaque burdens in the cortex and subiculum were lower in 5xFAD^P522R mice and microglia showed increased interaction with plaques, compared with 5xFAD.	The PLCγ2 P522R variant protected against deficits in the Y-maze test of working memory in 5xFAD mice.

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rTg9191

Observed

X
Plaques at 35

Plaques emerge first in the cerebral cortex, starting around 8 months of age. This is followed by plaques in the hippocampus at 10.5 to 12.5 months of age. Some dense core plaques develop.
X
Neuronal Loss at 9

Expression of the tetracycline transactivator (tTA) resulted in reduced forebrain weight and smaller dentate gyri in rTg9191 mice compared to non-Tg littermates. This effect was also observed in mice expressing tTA alone, and is thought to be a developmental effect, as it was observed even in young mice (e.g., 2-6 months of age).
X
Gliosis at 104

rTg9191 mice develop reactive gliosis (astrocytosis and microgliosis) in the vicinity of dense-core plaques by 24 months of age.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
APP	APP K670_M671delinsNL (Swedish), APP V717I (London)	APP: Transgenic	Alzheimer's Disease	Age-associated pathology in the cerebral cortex and hippocampus starting at 8 and 10½-12½ months of age, respectively. Gliosis and hyperphosphorylated tau in the vicinity of dense-core plaques. Fibrillar oligomeric species, e.g., Aβ dimers.	No transgene-related deficits seen in Morris water maze (4, 12, 21, 24, months of age) or fixed consecutive-number (23 months of age) tests.

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TREM2-BAC X 5xFAD

Observed

X
Plaques at 28

Observed at 7 months, the youngest age examined.
X
Gliosis at 28

Microgliosis observed; however, fewer plaque-associated microglia and altered microglial morphology (more ramified processes) compared with 5xFAD at 7 months, the only age examined.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
TREM2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	TREM2: Transgenic; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Amyloid plaques with plaque-associated microgliosis. Reduced plaque burden, altered microglial and plaque morphology, and less severe plaque-associated neuritic dystrophy, compared with 5xFAD.	5xFAD/TREM2 mice perform comparably to wild-type mice in a contextual fear conditioning test, while 5xFAD mice are impaired.

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Trem2-H157Y x 5xFAD

Observed

X
Plaques at 16

Decreased plaque burdens and densities in 5xFAD;Trem2^H157Y/H157Y compared with 5xFAD;Trem2^+/+ at 8.5 months, but genotypes similar at 4 months.
X
Gliosis at 16

Decreased microgliosis and astrogliosis in 5xFAD;Trem2^H157Y/H157Y compared with 5xFAD;Trem2^+/+ at 8.5 months, but genotypes similar at 4 months.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
Trem2, APP, PSEN1	TREM2 H157Y, APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Trem2: Knock-In; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Age-dependent effects on amyloid-β pathology and gliosis. At 4 months, plaque burdens, microgliosis, and astrogliosis were similar among genotypes. By 8.5 months, amyloid burdens, microgliosis, and astrogliosis were reduced in homozygous carriers of the H157Y variant, compared with 5xFAD mice homozygous for wild-type Trem2.	Unknown.

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TREM2, humanized (R47H) X 5XFAD

Observed

X
Plaques at 34

Plaques observed in 8.5-month-old mice, the only age reported thus far.
X
Gliosis at 34

Microgliosis observed in 8.5-month-old mice, the only age reported thus far. Fewer plaque-associated microglia in mice expressing the R47H variant, compared with the common variant of human TREM2.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
Trem2, TREM2, APP, PSEN1	TREM2 R47H, APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Trem2: Knock-Out; TREM2: Transgenic; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Lower density of activated microglia surrounding amyloid plaques in 5XFAD mice expressing the R47H variant of human TREM2 compared with those expressing the common variant.	No data.

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Trem2 KO (Colonna) x 5XFAD

Observed

X
Plaques at 16

Plaques present by 4 months, the earliest age studied.
X
Neuronal Loss at 32

Loss of cortical layer V neurons by 8 months, the earliest age studied.
X
Gliosis at 16

MIcrogliosis by 4 months, the earliest age studied.

Absent

No Data

Genes	Mutations	Modification	Disease	Neuropathology	Behavior/Cognition
Trem2, APP, PSEN1	APP K670_M671delinsNL (Swedish), APP I716V (Florida), APP V717I (London), PSEN1 M146L (A>C), PSEN1 L286V	Trem2: Knock-Out; APP: Transgenic; PSEN1: Transgenic	Alzheimer's Disease	Compared with 5XFAD, mice deficient in TREM2 show an age- dependent increase in amyloid accumulation in the hippocampus, more severe plaque-associated neuritic dystrophy, and exaggerated neuron loss in the cortex. Microglial containment of plaques is compromised in TREM2-deficient animals. Microglia accumulate autophagosomes.	No data.

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