Neuronal loss, a pathological hallmark of Alzheimer’s disease, is recapitulated in reMYND’s transgenic human hTauP301L mouse model.
The role of microglia and astrocytes in Alzheimer’s disease and how these contribute to neuronal loss has gained increased interest over the past years. This pathologically feature is recapitulated in reMYND’s transgenic APP, APPxPS1 and hTauP301S mouse models.
The interplay of Ab and Tau is still considered detrimental if not crucial for disease etiology and progression of Alzheimer’s Disease.
VIB is organising its 5th Biotechday. All ages are welcome to this free event at campus Gasthuisberg in Leuven. reMYND will be presenting on the research towards the treatment of Alheimers and diabetes worldwide.
reMYND’s Tau.P301L and Tau.P301S models feature progressive hyperphosphorylation of Tau with age and a strong correlation of Tau pathology with the motor phenotype.
Two-photon imaging allows tracking the formation of Tau aggregates in the same brain-region of a live animal over the course of time. This makes it possible to study the effects of treatment longitudinally in vivo.
The interplay of Abeta and Tau is considered detrimental if not crucial for disease etiology and progression of Alzheimer’s Disease.
Long term potentiation (LTP), a reflection of dendritic spine density and synaptic plasticity, is gaining importance as a functional ex-vivo or even in-vivo read-out related to learning and memory.
reMYND now offers Long Term Potentiation (LTP) measurements to allow clients to assess the effect of their experimental Alzheimer treatment.
Over the last years, more and more tau-treatments are being assessed in mouse models for their potential to treat Alzheimer’s disease. One of the key challenges with many of the tau mouse models is the need for large numbers of animals due to their intrinsic variability.