Research Models

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33 Models

Name Other Names Strain Name Genetic Background Gene Mutation Modification Info Modification Disease Neuropathology Behavior/Cognition Other Phenotype Availability Primary Paper Visualization
Mouse Models (33)
B6.Cg-Apoetm1.1(APOE*4)Adiuj Abca7em#2Adiuj Trem2em1Adiuj/J C57BL/6J Abca7, APOE, Trem2 TREM2 R47H CRISPR/Cas9 was used to introduce the rs3752246 SNP mutation (p.A1527G) into the Abca7 gene of double mutant mice with a humanized APOE4 gene and the R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, The Jackson Laboratory Stock# 028709). Abca7: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030283. Cryopreserved. The Jackson Laboratory Yes
B6.Cg-Apoetm1.1(APOE*4)Adiuj Abca7em#1Adiuj Trem2em1Adiuj/J C57BL/6J Abca7, APOE, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a knock-out mutation of the Abca7 gene of double mutant mice with a humanized APOE4 gene and the p.R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, The Jackson Laboratory Stock# 028709). Abca7: Knock-Out; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030320. Cryopreserved. The Jackson Laboratory Yes
APOE2 KI C57BL/6; 129P2, backcrossed to C57BL/6J APOE The human APOE2 cDNA sequence was knocked-in at the endogenous mouse APOE locus; inserted in frame with non-coding sequences, exon 1, intron 1 and the first 18 bp of exon 2 such that expression is regulated by endogenous regulatory elements and the mouse APOE gene inactivated. APOE: Knock-In Alzheimer's Disease, Traumatic Brain Injury Unknown. Unknown. 2-fold higher level of steady state APOE in brain and higher APOE in serum compared with APOE3 and APOE4 KI animals. Highest levels of serum cholesterol and triglycerides after a 6hr fast. No longer available through Bruce Lamb Mann et al., 2004 No
<p>-</p>, <p>E2F</p> C57BL/6J APOE The coding region of the mouse Apoe gene, from the translation initiation codon in exon 2 to the termination codon in exon 4, was replaced with the corresponding human APOE (ε2 allele) sequence, flanked by loxP sites. APOE: Knock-In Alzheimer's Disease Unknown. Unknown. Available through a material transfer agreement with the Cure Alzheimer’s Fund. Huynh et al., 2019 Yes
<p>-</p>, <p>APOE2 KI</p>, <p>APOE*2 KI</p> B6.Cg-Apoeem3(APOE*)Adiuj/J C57BL/6J APOE APOE2 KI mice were generated by using CRISPR/Cas9 to introduce two point mutations (leading to arginine to cysteine substitutions at amino acids 130 and 176) in an existing humanized APOE4 knock-in allele (The Jackson Laboratory Stock# 027894). APOE: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 029017. Live. The Jackson Laboratory Yes
<p>-</p>, <p>APOE2 Humanized Knock-in</p> B6.129P2-Apoetm1(APOE*2)Mae N9 129 x C57BL/6; back-crossed to C57BL/6 APOE APOE R176C (ApoE2) Targeted gene replacement of the endogenous murine APOE gene with the human APOE2 allele. Targeting construct included exons 2-4 of APOE2. APOE: Knock-In Alzheimer's Disease, Multiple Conditions None reported. White-matter integrity, as assessed by fractional anisotropy, was reported to be higher in the hippocampus and caudate putamen of year-old female APOE2 mice, compared with APOE3 females; these genotype differences were not seen in males. Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. Characteristics of type III hyperlipoproteinemia. Plasma cholesterol and triglyceride levels 2-3x higher than APOE3 mice. Impaired clearance of very-low-density lipoprotein (VLDL) particles. Atherosclerotic plaques. Compared with APOE3 mice, APOE2 mice exhibited higher levels of glucose uptake in the cortex and hippocampus and up-regulation of genes involved in glucose utilization. Taconic: Stock# 1547-F and 1547-M Sullivan et al., 1998 No
<p>-</p>, <p>E3F</p> C57BL/6J APOE The coding region of the mouse Apoe gene, from the translation initiation codon in exon 2 to the termination codon in exon 4, was replaced with the corresponding human APOE (ε3 allele) sequence, flanked by loxP sites. APOE: Knock-In Alzheimer's Disease Unknown. Unknown. Available through a material transfer agreement with the Cure Alzheimer’s Fund. Huynh et al., 2019 Yes
<p>-</p>, <p>APOE3 KI</p>, <p>APOE*3 KI</p> B6(SJL)-ApoEem2(APOE*)Adiuj/J C57BL/6J APOE CRISPR/Cas9 used to introduce a point mutation (leading to an arginine-to-cysteine substitution at amino acid 130) into an existing humanized APOE4 knock-in allele. APOE: Knock-In Alzheimer's Disease No data. No data. The Jackson Laboratory, Stock # 029018; Live The Jackson Laboratory Yes
<p>-</p>, <p>APOE3 KI</p> C57BL/6; 129P2, backcrossed to C57BL/6J APOE The human APOE3 cDNA sequence was knocked-in at the endogenous mouse APOE locus; inserted in frame with non-coding sequences, exon 1, intron 1 and the first 18bp of exon 2 such that expression is regulated by endogenous regulatory elements and the mouse APOE gene inactivated. APOE: Knock-In Alzheimer's Disease, Traumatic Brain Injury Unknown. Unknown. Intermediate brain APOE and serum cholesterol levels compared with mice with knock-in of APOE4 or APOE2. No longer available through Bruce Lamb Mann et al., 2004 Yes
<p>-</p>, <p>APOE3 Humanized Knock-in</p> B6.129P2-Apoetm2(APOE*3)Mae N8 129 x C57BL/6; back-crossed to C57BL/6 APOE Targeted replacement of the endogenous mouse APOE gene with the human APOE3 allele. Targeting vector contained exons 2-4 of human APOE3. APOE: Knock-In Alzheimer's Disease, Multiple Conditions None reported. APOE3 was considered the neutral allele against which the other human APOE genotypes were compared in most studies of neurological phenotypes in Targeted Replacement mice. Data comparing Targeted Replacement mice to wild-type mice are limited. Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. On a standard diet, homozygous mice have normal cholesterol and triglyceride levels, but are more susceptible than wild-type animals to diet-induced atherosclerosis. Data comparing neurological phenotypes in Targeted Replacement mice to wild-type mice are sparse, but APOE3 mice resemble wild-type mice with respect to aspects of hippocampal anatomy and physiology, including LTP and neurogenesis. Taconic: Stock# 1548-F and 1548-M Sullivan et al., 1997 No
<p>-</p>, <p>E4F</p> C57BL/6J APOE The coding region of the mouse Apoe gene, from the translation initiation codon in exon 2 to the termination codon in exon 4, was replaced with the corresponding human APOE (ε4 allele) sequence, flanked by loxP sites. APOE: Knock-In Alzheimer's Disease Unknown. Unknown. Available through a material transfer agreement with the Cure Alzheimer’s Fund. Huynh et al., 2019 Yes
<p>-</p>, <p>APOE4 KI</p>, <p>APOE*4 KI</p> B6(SJL)-ApoEtm1.1(APOE*4)Adiuj/J C57BL/6J APOE Mouse ApoE exons 2, 3, and most of exon 4 replaced with human APOE sequence including exons 2, 3, 4 and a portion of the 3' UTR sequence. APOE: Knock-In Alzheimer's Disease No data. No data. The Jackson Laboratory, Stock # 027894; Live The Jackson Laboratory Yes
APOE4 KI C57BL/6; 129P2, backcrossed to C57BL/6J APOE The human APOE4 cDNA sequence was knocked-in at the endogenous mouse APOE locus; inserted in frame with non-coding sequences, exon 1, intron 1 and the first 18 bp of exon 2 such that expression is regulated by endogenous regulatory elements and the mouse APOE gene inactivated. APOE: Knock-In Alzheimer's Disease, Traumatic Brain Injury Unknown. Unknown. Human ApoE is detectable in serum and astrocytes. Compared to mice with knock-in of APOE2 or APOE3, APOE4 mice had the lowest serum cholesterol after a 6 hour fast. No longer available through Bruce Lamb Mann et al., 2004 No
<p>-</p>, <p>APOE4 Humanized Knock-in</p> B6.129P2-Apoetm3(APOE*4)Mae N8 129 x C57BL/6, back-crossed to C57BL/6 APOE APOE C130R (ApoE4) Targeted replacement of the endogenous murine APOE gene with the human APOE4 allele; targeting construct contained exons 2–4 of APOE4. APOE: Knock-In Alzheimer's Disease, Multiple Conditions Mice do not develop amyloid plaques or neurofibrillary tangles. Genotype-dependent differences in brain structure have been reported, but findings are mixed. While some groups have found smaller hippocampal volumes, enlarged ventricles, and compromised white matter in APOE4 mice compared with APOE3, others did not observe these differences. Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. Increased risk of atherosclerosis. Elevated cholesterol, APOE, and APOB-48 on a high fat diet. Transcriptomic and functional evidence for increased aerobic glycolysis and decreased mitochondrial respiration in APOE4 compared with APOE3 mice. Electrophysiological and imaging studies suggest that aged APOE4 mice exhibit neural hyperactivity compared with APOE3 mice in some brain regions. Taconic: Stock# 1549-F or 1549-M Knouff et al., 1999 No
<p>-</p>, <p>APOE KO</p>, <p>APOE -/-</p>, <p>APOE TM1</p> B6.129P2-Apoetm1Unc N11 129 x C57BL/6, back-crossed to C57BL/6 APOE Inactivation of the endogenous mouse APOE by homologous recombination and insertion of a neomycin cassette. APOE: Knock-Out Alzheimer's Disease Unknown. Unknown. Viable; healthy. Undetectable ApoE protein in plasma. Plasma cholesterol 5x higher than wild-type. Artherosclerotic lesions which progress to occlusions of coronary artery by 8 months. Taconic: Stock# APOE-M and APOE-F Piedrahita et al., 1992 No
B6.Cg-Apoetm1.1(APOE*4)Adiuj Appem2Adiuj Trem2em1Adiuj/J C57BL/6J APOE, App, Trem2 TREM2 R47H CRISPR/Cas9 was used to introduce a 94-bp deletion in exon 14 (APP695 numbering) of  the App gene of double mutant mice with a humanized APOE4 gene and the p.R47H point mutation knocked into the mouse Trem2 gene (The Jackson Laboratory Stock# 028709). APOE: Knock-In; App: Knock-Out; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031722. Cryopreserved. The Jackson Laboratory Yes
<p>-</p>, <p>APOE4/Trem2*R47H/Ceacam1 knock-out</p> B6.Cg-Apoetm1.1(APOE*4)Adiuj Ceacam1em#1Adiuj Trem2em1Adiuj/J C57BL/6J APOE, Ceacam1, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a knock-out mutation of the Ceacam1 gene of double mutant mice with a humanized APOE4 gene and the p.R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, The Jackson Labortory Stock# 028709). APOE: Knock-In; Ceacam1: Knock-Out; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030673. Cryopreserved. The Jackson Laboratory Yes
B6(SJL)-Apoetm1.1(APOE*4)Adiuj Clasp2em1Adiuj Trem2em1Adiuj/J C57BL/6J Clasp2, APOE, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a knock-in L163P mutation of the Clasp2 gene of APOE4/Trem2*R47H mice—double-mutant mice with a humanized Apoe (ε4 allele) gene and the R47H point mutation knocked into the mouse Trem2 gene. Clasp2: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031944. Cryopreserved. The Jackson Laboratory Yes
<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
<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
<p>-</p>, <p>APOE4-FAD</p>, <p>APOE4 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 APOE4 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.  Age-dependent learning and memory deficits in the Y maze and Morris water maze. 5xFAD mice are available through The Jackson Lab, Stock# 034840; Live. APOE4 Targeted Replacement mice are available through Taconic, Stock# 1549-F or 1549-M. Youmans et al., 2012 Yes
<p>-</p>, <p>APOE4 (line1)/APOE KO</p>, <p>Tg(GFAP-APOE*4)1Hol</p> B6.Cg-Apoetm1Unc Cdh18Tg(GFAP-APOE_i4)1Hol/J. Formerly: B6.Cg-Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/J B6/CBA; back-crossed onto C57BL6 background APOE Transgene of human APOE4 driven by the GFAP promoter; crossed to APOE knock-out mice. APOE: Transgenic; APOE: Knock-Out Alzheimer's Disease Developing and adult mice express human APOE4 in glia and neuropil. Unknown. Mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The Jackson Lab: Stock# 004631; Cryopreserved Sun et al., 1998 No
<p>LOAD2</p> B6.Cg-Apoetm1.1(APOE*4)Adiuj Appem#1Adiuj Trem2em1Adiuj/J C57BL/6J APOE, APP, Trem2 TREM2 R47H CRISPR/Cas9 was used to introduce the G601R, F606Y, and R609H (APP695 numbering) point mutations into the App gene of double mutant mice with a humanized APOE4 gene and the p.R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, Jackson Lab Stock# 028709). APOE: Knock-In; APP: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030670. Live. The Jackson Laboratory Yes
B6(SJL)-Cr2tm1(CR2,CR1)How Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J C57BL/6J Cr2, CR1, CR2, APOE, Trem2 TREM2 R47H This mutant line was generated by crossing APOE4/Trem2*R47H mice to mice in which the endogenous Cr2 gene was replaced with human CR1 and CR2 (The Jackson Laboratory Stock# 027713). Cr2: Knock-Out; CR1: Knock-In; CR2: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031668. Cryopreserved. The Jackson Laboratory Yes
B6.Cg-Apoetm1.1(APOE*4)Adiuj Il1rapem#1Adiuj Trem2em1Adiuj/J C57BL/6J APOE, Il1rap, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a knock-out mutation of the Il1rap gene of double mutant mice with a humanized APOE4 gene and the R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, The Jackson Laboratory Stock# 028709). APOE: Knock-In; Il1rap: Knock-Out; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030304. Cryopreserved. The Jackson Laboratory Yes
B6(SJL)-Kif21bem1Adiuj Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J C57BL/6J Kif21b, APOE, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a knock-in T82T mutation of the Kif21b gene of APOE4/Trem2*R47H mice—double-mutant mice with a humanized Apoe (ε4 allele) gene and the R47H point mutation knocked into the mouse Trem2 gene. Kif21b: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031938. Cryopreserved. The Jackson Laboratory Yes
B6(SJL)-Mthfrem1Adiuj Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J C57BL/6J Mthfr, APOE, Trem2 TREM2 R47H CRISPR/Cas9 was used to introduce the A262V mutation into the Mthfr gene of APOE4/Trem2*R47H mice—double mutant mice with a humanized APOE4 gene and the R47H point mutation knocked into the mouse Trem2 gene. Mthfr: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030922. Cryopreserved. The Jackson Laboratory Yes
Origin: C57BL/6J; backcrossed with murine APOE-null mice APOE ApoE3 minigene driven by the rat neuron-specific enolase promoter. APOE: Transgenic Alzheimer's Disease Human ApoE3 protected against the age-dependent neurodegeneration seen in APOE -/- mice. Unknown. Widespread neuronal expression of ApoE in the brain. Expression of ApoE3 protected against kainic acid-induced neuronal damage (loss of synaptophysin-positive presynaptic terminals and MAP2-positive neuronal dendrites in the neocortex and hippocampus, and a disruption of neurofilament-positive axons in the hippocampus). Available through Robert Mahley Raber et al., 1998 No
Origin: C57BL/6J; backcrossed with murine ApoE-null mice APOE The ApoE4 minigene driven by the rat neuron-specific enolase promoter. APOE: Transgenic Alzheimer's Disease Not observed. NSE-ApoE4 mice showed impairments in learning a water maze task and in vertical exploratory behavior that increased with age and seen primarily in females. Neuronal ApoE expression was widespread in the brain. Expression of ApoE4 did not protect against kainic acid-induced neuronal damage. Available through Robert Mahley Raber et al., 1998 No
B6.Cg-Apoetm1.1(APOE*4)Adiuj Plcg2em2Adiuj Trem2em1Adiuj/J C57BL/6J APOE, Plcg2, Trem2 TREM2 R47H CRISPR/Cas9 was used to introduce the p.M28L mutation (methionine to leucine at position 28) into the Plcg2 gene of double mutant mice with a humanized APOE4 gene and the p.R47H point mutation knocked into the mouse Trem2 gene (B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J, The Jackson Laboratory Stock# 028709). APOE: Knock-In; Plcg2: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 030674. Cryopreserved. The Jackson Laboratory Yes
B6(SJL)-Apoetm1.1(APOE*4)Adiuj Snx1em1Adiuj Trem2em1Adiuj/J C57BL/6J Snx1, APOE, Trem2 TREM2 R47H CRISPR/cas9 was used to generate a D465N mutation in the Snx1 gene of APOE4/Trem2*R47H mice—double-mutant mice with a humanized Apoe (ε4 allele) gene and the R47H point mutation knocked into the mouse Trem2 gene. Snx1: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031942. Cryopreserved. The Jackson Laboratory Yes
B6(SJL)-Apoetm1.1(APOE*4)Adiuj Sorl1em1Adiuj Trem2em1Adiuj/J C57BL/6J Sorl1, APOE, Trem2 TREM2 R47H, SORL1 A528T (SNP 13), APOE C130R (ApoE4) CRISPR/cas9 was used to generate a knock-in A528T mutation of the Sorl1 gene of APOE4/Trem2*R47H mice—double-mutant mice with a humanized Apoe (ε4 allele) gene and the R47H point mutation knocked into the mouse Trem2 gene. Sorl1: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. Unknown. The Jackson Laboratory, Stock# 031940. Cryopreserved. The Jackson Laboratory Yes
<p>LOAD1</p>, <p>APOE4/Trem2*R47H</p>, <p>APOE*4/Trem2*R47H</p>, <p>APOE4.Trem2*R47H</p> B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J C57BL/6J APOE, Trem2 TREM2 R47H, APOE C130R (ApoE4) This double-mutant line was generated by crossing APOE4 KI mice (Jackson Lab Stock# 027894), which carry a humanized APOE4 gene, to Trem2 R47H KI mice (Jackson Lab Stock # 027918), which have an R47H missense mutation knocked into the mouse Trem2 gene. APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease No neuron loss, amyloid plaques, neurofibrillary tangles, vascular leakage, myelin loss, or reactive microglia in mice up to 24 months of age. Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice. Age-, sex-, and region-dependent differences in glucose uptake and cerebral blood flow, compared with wild-type mice. Increased mortality at 24 months of age. Down-regulation of genes related to immune function and degradation of biological material in aged mice. The Jackson Lab:Stock# 028709; Live Kotredes et al., 2021 Yes

24 Visualizations

AD-related Research Models

Phenotypes Examined

  • Plaques
  • Tangles
  • Neuronal Loss
  • Gliosis
  • Synaptic Loss
  • Changes in LTP/LTD
  • Cognitive Impairment

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

Abca7*A1527G/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Abca7, APOE, Trem2 TREM2 R47H Abca7: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

expand

Abca7 KO/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Abca7, APOE, Trem2 TREM2 R47H Abca7: Knock-Out; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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APOE2 Knock-In, floxed (CureAlz)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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APOE2 Knock-In (JAX)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

Unknown.

Unknown.

expand

APOE3 Knock-In, floxed (CureAlz)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

Unknown.

Unknown.

expand

APOE3 Knock-In (JAX)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

No data.

No data.

expand

APOE3 Knock-In (Lamb)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease, Traumatic Brain Injury

Unknown.

Unknown.

expand

APOE4 Knock-In, floxed (CureAlz)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

Unknown.

Unknown.

expand

APOE4 Knock-In (JAX)

Observed
Absent
  • Cognitive Impairment at

    At 2 and 12 months of age, APOE4 KI mice perform similarly to wild-type mice in tests of locomotor activity, motor coordination, and working memory.

No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE APOE: Knock-In Alzheimer's Disease

No data.

No data.

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App KO/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, App, Trem2 TREM2 R47H APOE: Knock-In; App: Knock-Out; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Ceacam1 KO/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, Ceacam1, Trem2 TREM2 R47H APOE: Knock-In; Ceacam1: Knock-Out; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Clasp2*L163P/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Clasp2, APOE, Trem2 TREM2 R47H Clasp2: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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E2FAD

Observed
  1. X
    Plaques at 17

    Plaques develop in the subiculum and deep cortical layers by 4 months.

  2. X
    Gliosis at 26

    Microgliosis and astrocytosis in the subiculum and cortex at 6 months.

  3. X
    Synaptic Loss at 17

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

Absent
No Data
  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    E2FAD mice had performance in learning and memory tasks comparable to E3FAD animals and better than E4FAD mice.

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
  1. X
    Plaques at 17

    Plaques develop in the subiculum and deep cortical layers by 4 months.

  2. X
    Gliosis at 26

    Microgliosis and astrocytosis in the subiculum and cortex at 6 months.

  3. X
    Synaptic Loss at 17

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

Absent
No Data
  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    E3FAD mice had performance in learning and memory tasks comparable to E4FAD and E2FAD animals.

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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E4FAD

Observed
  1. X
    Plaques at 17

    Plaques develop in the subiculum and deep cortical layers by 4 months.

  2. X
    Gliosis at 26

    Microgliosis and astrocytosis in the subiculum and cortex at 6 months.

  3. X
    Synaptic Loss at 17

    Decreased protein levels of PSD95 and NMDA receptor subunits by 4 months.

  4. X
    Cognitive Impairment at 8

    Modest learning deficits in the Morris water maze by 2 months. Progressive decrease in performance on learning and memory tasks. 

Absent
No Data
  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Changes in LTP/LTD at

    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. 

Age-dependent learning and memory deficits in the Y maze and Morris water maze.

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hAbeta/APOE4/Trem2*R47H (LOAD2)

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, APP, Trem2 TREM2 R47H APOE: Knock-In; APP: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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hCR1 KI on APOE4/Trem2

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Cr2, CR1, CR2, APOE, Trem2 TREM2 R47H Cr2: Knock-Out; CR1: Knock-In; CR2: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Il1rap KO/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, Il1rap, Trem2 TREM2 R47H APOE: Knock-In; Il1rap: Knock-Out; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Kif21b*T82T/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Kif21b, APOE, Trem2 TREM2 R47H Kif21b: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Mthfr*C677T/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Mthfr, APOE, Trem2 TREM2 R47H Mthfr: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Plcg2*M28L/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, Plcg2, Trem2 TREM2 R47H APOE: Knock-In; Plcg2: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Snx1*D465N/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Neuronal Loss at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Snx1, APOE, Trem2 TREM2 R47H Snx1: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Sorl1*A528T/APOE4/Trem2*R47H

Observed
Absent
No Data
  • Plaques at

    No data.

  • Tangles at

    No data.

  • Neuronal Loss at

    No data.

  • Gliosis at

    No data.

  • Synaptic Loss at

    No data.

  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

  • Cognitive Impairment at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
Sorl1, APOE, Trem2 TREM2 R47H, SORL1 A528T (SNP 13), APOE C130R (ApoE4) Sorl1: Knock-In; APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

Unknown.

Unknown.

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Trem2 R47H KI x APOE4 (LOAD1)

Observed
Absent
  • Plaques at

    Not observed in cortex or hippocampus up to 24 months of age.

  • Tangles at

    Not observed in cortex or hippocampus up to 24 months of age.

  • Neuronal Loss at

    Not observed in cortex or hippocampus up to 24 months of age.

  • Gliosis at

    Microgliosis not observed in cortex or hippocampus up to 24 months of age.

  • Cognitive Impairment at

    Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice.

No Data
  • Synaptic Loss at

    No data.

  • Changes in LTP/LTD at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
APOE, Trem2 TREM2 R47H, APOE C130R (ApoE4) APOE: Knock-In; Trem2: Knock-In Alzheimer's Disease

No neuron loss, amyloid plaques, neurofibrillary tangles, vascular leakage, myelin loss, or reactive microglia in mice up to 24 months of age.

Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice.

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