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Alzheimer models

reMYND

reMYND's proprietary Alzheimer mouse models are based on the human clinical APP-London allele APP[V717I]- a preferred model for anti-BACE1 approaches - either alone or in combination with the human clinical PS1[A246E] allele, now extended to a TAU[P301L] and APPxTAU model, the latter combining both amyloid plaque and tau tangle pathology.

reMYND’s proprietary APP[V717I] mice, modeling a progressive amyloid-o-pathy and therefore serving as an excellent model for Alzheimer’s disease, is also available in combination with PS1[A246E]; the bigenic APPxPS1 model showing the same pathological hallmarks but with a different timing of onset and severity.

See below for a glance at the difference in pathology progression between both models, for more detailed information download a comprehensive data set here.

remynd

Representative photo collection of anti-Abeta stained sections (proprietary anti-Abeta Nanobody®, reMYND/Ablynx, Belgium) showing total plaque load at different ages in APP[V717I] mice (upper panel) and APP[V717I] x PS1[A246E] mice (lower panel).

reMYND’s proprietary TAU[P301L] transgenic mice, modeling a progressive tau-o-pathy and therefore serving as an excellent model for FTD and Alzheimer’s disease, are now being complemented by the TAU[P301S] model and extended into the bigenic APPxTAU model combining both Abeta and tau pathology.

See below for a glance at a pathological hallmark of both models, for more detailed information download a comprehensive data set here.

remynd

AT100-responsive pathological tau levels (A) in brainstem of 8 month old TAU[P301L] mice, (B) in midbrain of 3-month old APP[V717I] x TAU[P301L] mice.

For more information and all inquiries, please contact Dr. An Tanghe, CRO Manager

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