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29625 RESULTS

MAPT(H1.0*N279K)-GR

RESEARCH MODELS Summary MAPT(H1.0*N279K)-GR mice are among a series of models developed by Michael Koob and colleagues at the University of Minnesota, collectively referred to as Gene Replacement – Alzheimer’s Disease (GR-AD) mice. In GR-AD mice, “genes of interest are p

MAPT(H1.0)-GR

RESEARCH MODELS Summary MAPT(H1.0)-GR mice are among a series of models developed by Michael Koob and colleagues at the University of Minnesota, collectively referred to as Gene Replacement – Alzheimer’s Disease (GR-AD) mice. In GR-AD mice, “genes of interest are precise

Trem2*R47H(NSS)

RESEARCH MODELS Summary R47H is a rare variant in TREM2 that triples the risk of Alzheimer’s disease in heterozygous carriers. In order to study the effects of this variant, several mouse models were created in which the R47H mutation was introduced into the mouse Trem2

Trem2*R47H(HSS)

RESEARCH MODELS Summary R47H is a rare variant in TREM2 that triples the risk of Alzheimer’s disease in heterozygous carriers. In order to study the effects of this variant, several mouse models were created in which the R47H mutation was introduced into the mouse Trem2

hAβ-KI

RESEARCH MODELS Summary This knock-in model, designated “hAβ-KI,” carries a humanized Aβ sequence within the murine App gene. Like the App knock-in (humanized Aβ) model, hAβ-KI mice do not carry any Alzheimer’s disease-linked mutations in APP. hAβ-KI mice exhibit age-dep

AppSAA Knock-in

RESEARCH MODELS Summary The App SAA mouse joins a list of knock-in models that carry a humanized Aβ sequence within the murine App gene (App knock-in (humanized Aβ), APP NL-F Knock-in, APP NL-G-F Knock-in). As in the latter two models, the App gene was further modified t

PA-Rab5

RESEARCH MODELS Summary Rab5 is a small GTPase that regulates endosome trafficking, sorting, and fusion. Enlarged Rab5-positive endosomes are among the earliest neuropathological signs of Alzheimer’s disease and Down’s syndrome (Cataldo et al., 2000), and a body of evide

Atg16LΔWD

RESEARCH MODELS Summary In addition to their roles in canonical autophagy, some protein components of the autophagy machinery are involved in recycling cell-surface receptors in microglia (see Jun 2019 News). Atg16L ΔWD mice express a prematurely truncated version of the

Plcγ2-P522R knock-in

RESEARCH MODELS Summary The PLCG2 gene encodes the enzyme phospholipase C gamma 2 (PLCγ2), a mediator of transmembrane signaling in microglia that acts downstream of TREM2. A rare variant in this gene, P522R, has been associated with reduced risks of Alzheimer’s disease

App knock-in (humanized Aβ)

RESEARCH MODELS Summary App hu/hu mice carry a humanized Aβ sequence within the murine App gene. In this knock-in model, created using CRISPR/Cas9 technology, expression of App is driven by its natural promoter and is expected to show normal cell-type and temporal specif

App knock-in (humanized Aβ) (Leuven)

RESEARCH MODELS Summary App hu/hu rats carry a humanized Aβ sequence within the rat App gene. In this knock-in model, created using CRISPR/Cas9 technology, expression of App is driven by its natural promoter and is expected to show normal cell-type and temporal specifici

App knock-in (humanized Aβ) (Leuven); Psen1 knock-in (M139T)

RESEARCH MODELS Summary App hu/hu;Psen1M139T +/+ rats carry a humanized Aβ sequence within the rat App gene and the AD-linked M139T mutation in the rat Psen1 gene. These knock-in animals are homozygous for both humanized App and Psen1 M139T. Levels of APP and its metabol

PS19 with humanized TREM2 (R47H)

RESEARCH MODELS Summary People who carry one copy of the R47H variant of TREM2 have an approximately threefold greater risk of developing Alzheimer’s disease than do people homozygous for the common variant. Earlier mouse models were generated to explore the effects of t

PS19 with humanized TREM2 (common variant)

RESEARCH MODELS Summary These mice, referred to here as PS19-TREM2 CV, carry transgenes encoding the common variant of human TREM2 and human MAPT with the P301S mutation linked to frontotemporal dementia, on a mouse-Trem2-null background. This model was generated by cros

TREM2, humanized (R47H)

RESEARCH MODELS Summary People who carry one copy of the R47H variant of TREM2 have an approximately threefold greater risk of developing Alzheimer’s disease than do people homozygous for the common variant. This mouse model, referred to here as TREM2 R47H, expresses the

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