SEARCH RESULTS

29625 RESULTS

TREM2, humanized (common variant)

RESEARCH MODELS Summary This mouse model, referred to here as TREM2 CV, expresses the common variant of human TREM2 in the absence of mouse Trem2. Transgenic TREM2 is expressed in microglia and macrophages, where it was shown to function properly in an ex vivo assay. Thi

Psen1 L435F knock-in

RESEARCH MODELS Summary The L435F mutation in PSEN1 was found in affected individuals in a family with early onset AD (Heilig et al., 2010). This knock-in rat model carries the homologous mutation in the rat Psen1 gene and a humanized Aβ sequence within the rat App gene

Trem2 R47H knock-in

RESEARCH MODELS Summary R47H is a rare variant in TREM2 that triples the risk of Alzheimer’s disease in heterozygous carriers. This knock-in rat model carries the R47H mutation in the rat Trem2 gene and a humanized Aβ sequence within the rat App gene (Tambini and D’Adami

App knock‐in (Icelandic mutation and humanized Aβ)

RESEARCH MODELS Summary The A673T (“Icelandic”) mutation in APP is associated with protection against Alzheimer's disease and age-related cognitive decline. This knock-in rat model carries the Icelandic mutation and a humanized Aβ sequence within the endogenous rat

App knock‐in (Swedish mutation and humanized Aβ)

RESEARCH MODELS Summary The KM670/671NL (“Swedish”) double mutation in APP was linked to AD in two large Swedish pedigrees. The mutation is located immediately adjacent to the β-secretase site and results in increased β-secretase processing of APP (Cai et al., 1993; Rabe

App knock-in (humanized Aβ)

RESEARCH MODELS Summary This knock-in model carries a humanized Aβ sequence within the endogenous rat App gene (Tambini et al., 2019). Levels of App mRNA in brain were similar in 21-day-old rats homozygous for the humanized App gene (App h/h) and wild-type animals (App w

Bace1 conditional knockout (Tesco)

RESEARCH MODELS Summary This is the second of two similar models designed to mimic BACE1 inhibition, in which researchers can control the timing of BACE1 deficiency. These conditional knockouts avoid the developmental effects of BACE1 deficiency that are seen in germline

SHRSP/FAD

RESEARCH MODELS Summary Pure Alzheimer’s disease—in which brains contain only the pathological hallmarks of AD, amyloid plaques and neurofibrillary tangles—is rare: In one recent study of nearly 900 autopsy samples with AD pathology, approximately 85 percent also exhibit

APOE4 Knock-In, floxed (CureAlz)

RESEARCH MODELS Summary This knock-in mouse belongs to a set of models designed to allow investigators to compare the effects of the various human APOE isoforms and to conditionally disrupt APOE expression. In this version, “E4F,” the coding region of the mouse Apoe gene

APOE3 Knock-In, floxed (CureAlz)

RESEARCH MODELS Summary This knock-in mouse belongs to a set of models designed to allow investigators to compare the effects of the various human APOE isoforms and to conditionally disrupt APOE expression. In this version, “E3F,” the coding region of the mouse Apoe gene

APOE2 Knock-In, floxed (CureAlz)

RESEARCH MODELS Summary This knock-in mouse belongs to a set of models designed to allow investigators to compare the effects of the various human APOE isoforms and to conditionally disrupt APOE expression. In this version, “E2F,” the coding region of the mouse Apoe gene

Thy1-αSyn “Line 61” Mouse

RESEARCH MODELS Summary The Thy1-αSyn mouse model, a.k.a. Line 61, overexpresses human α-synuclein under the Thy1 promoter (Rockenstein et al., 2002). It is one of the most extensively characterized animal models of Parkinson’s disease (PD), and reproduces several featur

PWK.APP/PS1

RESEARCH MODELS Summary In an effort to mimic the genetic diversity seen in human populations, scientists have crossed popular transgenic mouse models of Alzheimer’s disease with mice of various genetic backgrounds (see 28 Dec 2018 news; 21 Jun 2019 news).  PWK.APP/PS1 m

WSB.APP/PS1

RESEARCH MODELS Summary In an effort to mimic the genetic diversity seen in human populations, scientists have crossed popular transgenic mouse models of Alzheimer’s disease with mice of various genetic backgrounds (see 28 Dec 2018 news; 21 Jun 2019 news). WSB.APP/PS1 mi

CAST.APP/PS1

RESEARCH MODELS Summary In an effort to mimic the genetic diversity seen in human populations, scientists have crossed popular transgenic mouse models of Alzheimer’s disease with mice of various genetic backgrounds (see 28 Dec 2018 news; 21 Jun 2019 news).  CAST.APP/PS1

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