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reMYND, a trusted research partner

Our Contract Research Organization (CRO) helps our clients assess in-vivo characteristics, pharmacokinetics, pharmacodynamics and the effects of their experimental treatments against Alzheimer's disease and other neurodegenerative diseases in our proprietary mouse models.

We serve the majority of the Top 10 pharmaco’s worldwide with clients in the US, Europe and Japan. We have provided pivotal in-vivo proof-of-concept data for several candidate drugs currently in clinical development, and work actively together with Dr. Sugimoto, the inventor of Aricept. We have helped our clients to be the first to demonstrate the synergistic effect of a BACE inhibitor and an aBeta antibody, the effect of Tau antibody on aBeta, the effect of donepezil on brain Abeta,…

The continuous availability of aged mice allows for a short response time and rapid study start. By contributing our extensive expertise and experience we are helping our clients to set up an optimal study design. The CRO offers a broad testing window for our portfolio of behavioral readouts in combination with all routes of administration, as well as immunohistochemical and biochemical read-outs, both in brain and cerebrospinal fluid (CSF).

	Aβ pathology	Tau pathology	Astrocytosis and microgliosis	Neuronal loss	Cognitive impairment	Motoric impairment	Other behavior	LTP deficit	Impaired survival	CSF Biomarker
APP[V717I]
APP[V717I]xPS1[A246E]
Tau[P301L]
Tau[P301S]
APP[V717I]xTau[P301S]
APP[V717I]xTau[P301L]
Seed and spread Tauopathy model

has been investigated and shown to be present

Seed and spread alpha-synuclein

A model to study the prion-like neuron to neuron transmission of Tau pathology

In a wild type model, stereotactically injected into the striatum with sonicated mouse preformed fibrils (mPFFs)
Seeding and progressive spreading of alpha-synuclein pathology to several connected brain regions
Loss of dopaminergic terminals and inflammation in pathology-rich regions

APP[V717I]

APP-London model for studying Alzheimer's disease. Due to the wildtype BACE-cleavage site, a preferred model for testing anti-beta-secretase and anti-gamma-secretase associated approaches

Expression of human APP[V717I] under control of the neuron-specific Thy-1 promoter
Gently progressing AD phenotype

APP[V717I]xPS1[A246E]

A model for studyin gAlzheimer's Disease that develops similar charcteristics as the APP-London model but at an accelerated pace

Expression of human APP[V717I] and human PS1[A246E] under control of the neuron-specific Thy-1 promoter
Faster progressing AD phenotype

Tau[P301L]

Tauopathy model for studying Frontotemperal dementia and Alzheimer’s disease. Additionally, this model has been extensively used to assess experimental treatments that are currently in clinical testing.

Expression of human TAU[P301L] under control of the neuron-specific Thy-1 promotor
A milder Tauopathy model with onset around 7 months
More viariability in onset of Tau pathology, correlating with clasping score

Tau[P301S]

Tauopathy model for Frontotemperal dementia and Alzheimer’s disease.

Expression of human TAU[P301S] under control of the neuron-specific Thy-1 promotor
An aggressive tau-o-pathy model with onset around as of 3-4 months of age
Minor variability in the onset of progressive hyperphosphorylation and conformational change of Tau
Less aggressive heterozygous TAU[P301S] alternative available as well, with onset around 9 months of age

APP[V717I]xTau[P301S]

A combined APP and Tau model for studying Alzheimer’s disease.

Expression of human APP[V717I] and human TAU[P301S] (4R0N) under control of the neuron-specific Thy-1 promotor
Combined and progressive β-amyloid and and Tau pathology with inflammation and cognitive impairment

APP[V717I]xTau[P301L]

A combined APP and Tau model for studying Alzheimer’s disease.

Expression of human APP[V717I] and human TAU[P301S] (4R/2N) under control of the neuron-specific Thy-1 promotor
Combined and progressive β-amyloid and and Tau pathology
No longer being actively bred

Seed and spread

A model to study the prion-like neuron to neuron trans-synaptic transmission of Tau pathology

In the Tau[P301S] or TAU[P301L] model, injected with either brain lysate of each respective model or with synthetic fibrils
Significant seeding and spreading of AT8-positive tangle-like inclusions in the ipsilateral and contralateral hippocampus