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29625 RESULTS

AAV-AD

RESEARCH MODELS Summary Adeno-associated viral (AAV) 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. AAV-AD rats develop am

BACE1 conditional knock-out (Hu, Yan)

RESEARCH MODELS Summary These transgenic mice were designed to mimic BACE1 inhibition, while avoiding the developmental effects of Bace1 deficiency that are seen in germline knock-outs. They were generated by crossing mice with a floxed Bace1 gene (Bace1 fl/fl) to mice c

BACE1 cKO (Hu, Yan) X 5xFAD

RESEARCH MODELS Summary These transgenic mice were designed to mimic BACE1 inhibition in the context of amyloid pathology, while avoiding the developmental effects of Bace1 deficiency that are seen in germline knockouts. Mice are hemizygous for human APP and PSEN1 transg

Snx1*D465N/APOE4/Trem2*R47H

RESEARCH MODELS Summary The epsilon-4 allele of Apolipoprotein E and the R47H variant of TREM2  have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. The SNX1 (sorting nexin 1) gene enco

Kif21b*T82T/APOE4/Trem2*R47H

RESEARCH MODELS Summary The epsilon-4 allele of Apolipoprotein E and the R47H variant of TREM2  have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. The motor protein KIF21B (Kinesin Fa

Clasp2*L163P/APOE4/Trem2*R47H

RESEARCH MODELS Summary The epsilon-4 allele of Apolipoprotein E and the R47H variant of TREM2  have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. CLASP2 (CLIP-associating protein 2)

Sorl1*A528T/APOE4/Trem2*R47H

RESEARCH MODELS Summary The epsilon-4 allele of Apolipoprotein E and the R47H variant of TREM2 have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. A528T is a common variant of SORL1 th

hCR1 KI on APOE4/Trem2

RESEARCH MODELS Summary The epsilon-4 allele of Apolipoprotein E and the R47H variant of TREM2  have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. Variations in complement receptor 1

Mthfr*C677T/APOE4/Trem2*R47H

RESEARCH MODELS Summary The epsilon-4 allele of Apoliporotein E and the R47H variant of TREM2  have each been found to confer an approximately threefold increased risk for Alzheimer’s disease in humans heterozygous for either allele. The C677T variant of MTHFR (methylene

TDP-43 (Wt-TAR6/6)

RESEARCH MODELS Summary This mouse model of ALS expresses wild-type human TDP-43 in postnatal neurons. Mice homozygous for the human TARDP transgene are referred to as TAR6/6, while mice hemizygous for the transgene are called TAR6. This description refers to homozygous,

AAV-GFP–(GR)100

RESEARCH MODELS Summary The six-nucleotide (GGGGCC) repeat expansion in C9ORF72 encodes five dipeptide repeat proteins that accumulate in ALS/FTD: glycine-arginine (GR), proline-arginine (PR), glycine-alanine (GA), proline-alanine (PA), and glycine-proline (GP). The GFP–

AAV-GFP-(GA)50

RESEARCH MODELS Summary The six-nucleotide (GGGGCC) repeat expansion in C9ORF72 encodes five dipeptide-repeat proteins that accumulate in ALS/FTD: glycine-arginine (GR), proline-arginine (PR), glycine-alanine (GA), proline-alanine (PA), and glycine-proline (GP). The GFP-

Trem2 R47H KI (Haass)

RESEARCH MODELS R47H is a rare variant in TREM2 that triples the risk of Alzheimer’s disease in heterozygous carriers. To create a mouse model carrying a single copy of R47H Trem2 under the control of its natural regulatory elements, CRISPR/Cas9 was used to introduce the

APP+PS1

RESEARCH MODELS Summary APP+PS1 transgenic rats express human APP with the Swedish and Indiana mutations and human PSEN1 with the L166P mutation. Both transgenes are driven by the ubiquitin-C promoter. These rats exhibit amyloid pathology, neurodegeneration, and behavior

APP21

RESEARCH MODELS Summary APP21 rats express human APP 695 containing the Swedish and Indiana mutations, driven by the ubiquitin-C promoter (Agca et al., 2008). Although these rats do not spontaneously develop amyloid pathology, they can serve as hosts for exogenously seed

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